glycogen and Starvation

All animals face the possibility of limitations in food resources that could ultimately lead to starvation-induced mortality. The primary goal of this review is to characterize the various physiological strategies that allow different animals to survive starvation. The ancillary goals of this work are to identify areas in which investigations of starvation can be improved and to discuss recent advances and emerging directions in starvation research. The ubiquity of food limitation among animals, inconsistent terminology associated with starvation and fasting, and rationale for scientific investigations into starvation are discussed. Similarities and differences with regard to carbohydrate, lipid, and protein metabolism during starvation are also examined in a comparative context. Examples from the literature are used to underscore areas in which reporting and statistical practices, particularly those involved with starvation-induced changes in body composition and starvation-induced hypometabolism can be improved. The review concludes by highlighting several recent advances and promising research directions in starvation physiology. Because the hundreds of studies reviewed here vary so widely in their experimental designs and treatments, formal comparisons of starvation responses among studies and taxa are generally precluded; nevertheless, it is my aim to provide a starting point from which we may develop novel approaches, tools, and hypotheses to facilitate meaningful investigations into the physiology of starvation in animals.

Topics: Amino Acids; Animals; Body Temperature; Body Weight; Energy Metabolism; Fasting; Glucose; Glycogen; Ketone Bodies; Lipid Metabolism; Organ Size; Proteins; Respiratory Physiological Phenomena; Starvation; Weight Loss

Topics: Animals; Eating; Fasting; Female; Glucose; Glucose Clamp Technique; Glycogen; Glycogen Synthase; Homeostasis; Humans; Insulin; Models, Biological; Muscle Fibers, Fast-Twitch; Muscle Fibers, Slow-Twitch; Muscle, Skeletal; Nutritional Physiological Phenomena; Pregnancy; Rats; Starvation

Parenteral nutrition has been one of the major advances in clinical medicine in the 20th century. By maintaining or re-establishing optimal nutritional status, one can help to ensure an optimal response to appropriate medical or surgical management of the primary disease process. In order to plan an appropriate nutritional regimen, the health-care provider must be equipped to pursue the following thought processes: Understand the consequences of malnutrition. Identify the patient who may benefit from nutritional support. Assess the underlying clinical and metabolic setting. Assess the current nutritional status. Formulate a goal of nutritional intervention--a therapeutic plan. Determine the route and method of administration; the quantity and source of energy and nitrogen; and requirements for fluid, electrolytes, minerals, vitamins, and trace elements. Monitor the patient. Evaluate the efficacy and determine the duration of therapy.

Topics: Catheterization; Dietary Carbohydrates; Dietary Proteins; Energy Metabolism; Female; Glycogen; Heart Failure; Hepatic Encephalopathy; Humans; Intraoperative Period; Kidney Diseases; Male; Metabolic Diseases; Parenteral Nutrition, Total; Pregnancy; Starvation; Stress, Physiological; Triglycerides

Topics: Adenylyl Cyclases; Adrenocorticotropic Hormone; Animals; Cyclic AMP; Epinephrine; Fatty Acids; Female; Fetal Blood; Fetus; Gluconeogenesis; Glycogen; Glyoxylates; Growth; Growth Hormone; Hydrocortisone; Insulin; Liver; Models, Biological; Nutritional Physiological Phenomena; Placenta; Pregnancy; Starvation; Thyroid Hormones

Topics: Amino Acids; Biological Transport; Carbohydrate Metabolism; Dietary Fats; Digestion; Energy Metabolism; Fatty Acids, Nonesterified; Gluconeogenesis; Glucose; Glycogen; Humans; Intestinal Absorption; Lipid Metabolism; Lipolysis; Lipoprotein Lipase; Lipoproteins, VLDL; Proteins; Starvation

Topics: Animals; Brain; Dietary Carbohydrates; Dietary Proteins; Digestive System; Gluconeogenesis; Glucose; Glycogen; Humans; Intestinal Absorption; Keto Acids; Liver; Muscles; Starvation

Topics: Adipose Tissue; Alanine; Animals; Biological Transport; Brain; Diabetes Mellitus; Dogs; Fatty Acids, Nonesterified; Fetus; Glucose; Glycogen; Goats; Humans; Ketone Bodies; Lipid Metabolism; Liver; Lung; Muscles; Myocardium; Rats; Starvation; Tissue Distribution

Topics: Alanine; Amino Acids; Animals; Blood Glucose; Gluconeogenesis; Glycogen; Ketone Bodies; Liver; Models, Biological; Muscles; Rats; Starvation

Starvation entails a progressive selection of fat as body fuel. Soon after a meal glucose utilisation by muscle ceases and fatty acids are used instead. Ketoacid levels in blood become elevated over the first week, and the brain preferentially uses these instead of glucose. The net effect is to spare protein even further, as glucose utilisation by brain is diminished. Nevertheless, there is still net negative nitrogen balance, but this can be nullified by amino acid or protein supplementation. Insulin appears to be the principal regulatory hormone. Recent data suggest that decreased levels of active T3 may play a role by sparing otherwise obligated calories by decreasing metabolic needs.

Topics: Adipose Tissue; Body Weight; Brain; Cyclic AMP; Energy Metabolism; Fatty Acids; Glucagon; Gluconeogenesis; Glycogen; Humans; Insulin; Ketosis; Kidney; Liver; Muscles; Oxygen Consumption; Proteins; Splanchnic Nerves; Starvation; Triglycerides; Urea

Topics: Anesthesia; Anesthetics; Carbohydrate Metabolism; Fructose; Glucose; Glycogen; Halothane; Humans; Ketone Bodies; Metabolism; NAD; Oleic Acids; Oxygen Consumption; Parenteral Nutrition; Starvation; Surgical Procedures, Operative

Topics: Abdomen; Animals; Biopsy; Blood Glucose; Carbohydrate Metabolism; Diabetes Mellitus; Epinephrine; Glucagon; Gluconeogenesis; Glucose; Glycogen; Humans; Insulin; Liver; Muscle Contraction; Muscles; Nucleotides; Physical Exertion; Proteins; Rats; Starvation; Wounds and Injuries

Topics: Adenylyl Cyclases; Adipose Tissue; Animals; Coenzyme A; Cyclic AMP; Diet; Epinephrine; Fatty Acids; Glucose; Glycerophosphates; Glycogen; Insulin; Lactates; Lipid Mobilization; Phosphotransferases; Proteins; Pyruvates; Rats; Starvation

Topics: Biopsy; Blood Glucose; Fats; Glucosyltransferases; Glycogen; Humans; Lactates; Muscles; Physical Exertion; Proteins; Pyruvates; Relaxation; Starvation

Early weight gain by starving patients managed with total parenteral nutrition has been regarded as spurious - that is, merely an increase in body water. We designed an experiment to mimic the starved state in which glycogen stores are depleted and sodium intake is very low. The subjects were then repleted with a sodium-free, high carbohydrate intake. All subjects who received potassium gained weight and switched to a respiratory exchange ratio which suggested mainly carbohydrate oxidation. From changes in weight and total body water the weight gain was calculated to be the consequence of glycogen storage with 1 g of glycogen obligating 3.21 +/- 0.57 g water. Two patients with total dysphagia showed a similar pattern. Two subjects who did not receive potassium showed a rise in respiratory exchange ratio but failed to store glycogen. Early weight gain in patients who received high-carbohydrate feeding after starvation is a normal phenomenon and represents a return to a more hydrated state consequent upon glycogen repletion.

Topics: Body Water; Body Weight; Deglutition Disorders; Dietary Carbohydrates; Female; Glycogen; Humans; Male; Parenteral Nutrition; Parenteral Nutrition, Total; Potassium; Sodium; Starvation

After a meal, excess nutrients are stored within adipose tissue as triglycerides in structures called lipid droplets. Previous genome-wide RNAi screens have identified that mRNA splicing factor genes are required for normal lipid droplet formation in Drosophila cells. We have previously shown that mRNA splicing factors called serine/arginine-rich (SR) proteins are important for triglyceride storage in the Drosophila fat body. SR proteins shuttle in and out of the nucleus with the help of proteins called Transportins (Tnpo-SR); however, whether this transport is important for SR protein-mediated regulation of lipid storage is unknown. The purpose of this study is to characterize the role of Tnpo-SR proteins in regulating lipid storage in the Drosophila fat body. Decreasing Tnpo-SR in the adult fat body resulted in an increase in triglyceride storage and consistent with this phenotype, Tnpo-SR-RNAi flies also have increased starvation resistance. In addition, the lipid accumulation in Tnpo-SR-RNAi flies is the result of increased triglyceride stored in each fat body cell and not due to increased food consumption. Interestingly, the splicing of CPT1, an enzyme important for the β-oxidation of fatty acids, is altered in Tnpo-SR-RNAi fat bodies. The isoform that produces the less catalytically active form of CPT1 accumulates in fat bodies where Tnpo-SR levels are decreased, suggesting a decrease in lipid breakdown, potentially causing the excess triglyceride storage observed in these flies. Together, these data suggest that the transport of splicing proteins in and out of the nucleus is important for proper triglyceride storage in the Drosophila fat body.

Topics: Animals; Animals, Genetically Modified; beta Karyopherins; Carnitine O-Palmitoyltransferase; Drosophila melanogaster; Drosophila Proteins; Fat Body; Female; Glycogen; Lipid Droplets; Lipid Metabolism; RNA Interference; RNA Splicing; Starvation; Triglycerides

Glycogen is an easily accessible source of energy for various processes. In hepatocytes, it can be found in the form of individual molecules (β-particles) and their agglomerates (α-particles). The glycogen content in hepatocytes depends on the physiological state and can vary due to the size and number of the particles. Using biochemical, cytofluorometric, interferometric and morphometric methods, the number of β-particles in rat hepatocytes was determined after 48 h of fasting at different time intervals after glucose refeeding. It has been shown that after starvation, hepatocytes contain ~1.6 × 10

Topics: Animals; Fasting; Glucose; Glycogen; Hepatocytes; Liver; Rats; Starvation

Sexual dimorphism in lifespan, wherein females outlive males, is evident across all animal taxa. The longevity difference between sexes is controlled by multiple physiological processes with complex relationships to one another. In recent years, glycogen, the storage form of glucose, has been shown to cause rapid aging upon forced synthesis in healthy neurons. Glycogen in the form of corpora amylacea in the aging brain is also widely reported. While these studies did suggest a novel role for glycogen in aging, most of them have focused on pooled samples, and have not looked at sex-specific effects, if any. Given the widespread occurrence of sex-biased expression of genes and the underlying physiology, it is important to look at the sex-specific effects of metabolic processes. In the present study, using transgenic fly lines for the human glycogen synthase, we investigated the sex-specific effects of glycogen on stress resistance, fitness, and survival. We demonstrate that Drosophila melanogaster females with altered levels of glycogen in the brain display a shortened lifespan, increased resistance to starvation, and higher oxidative stress than male flies. The present study thus provides a novel insight into the sex-specific effect of glycogen in survival and aging and how differences in metabolic processes could contribute to sex-specific traits.

Topics: Animals; Brain; Drosophila melanogaster; Female; Glycogen; Longevity; Male; Starvation

Fatal starvation is rarely seen in developed countries; when it occurs, it may be associated with medicolegal problems. Forensic pathologists are required to determine leading causes of death and provide opinions on the influence of starvation, especially in cases of suspected child abuse. Recently, starvation-induced steatosis was suggested to be regulated by lipophagy. Here, we report an extremely rare case of death by malnutrition of a 10-year-old boy, who was fed only infant formula throughout his life. The deceased presented with severe hepatic steatosis, probably related to prolonged malnutrition. Fatty liver changes, with deposition of small lipid droplets deposited in the peripheral lobules. High levels of P62 protein (overexpression of which indicates an autophagy impairment) were seen around the central vein region, whereas light-chain-3 (LC3) protein (an indicator of lipophagy activation) was unremarkable. Thus, in our case, impaired lipophagy influenced starvation-induced steatosis. To our knowledge, this article is the first to evaluate the application of lipophagy in forensic investigations as an objective diagnostic criterion.

Topics: Autophagy; Child; Child Nutrition Disorders; Dehydration; Fatal Outcome; Fatty Liver; Glycogen; Humans; Infant; Infant Formula; Liver; Male; RNA-Binding Proteins; Starvation

The storage of excess nutrients as triglycerides is essential for all organisms to survive when food is scarce; however, the mechanisms by which triglycerides are stored are not completely understood. Genome-wide RNAi screens in Drosophila cells have identified genes involved in mRNA splicing that are important in the regulation of triglyceride storage. Our lab has identified a number of splicing factors important for regulating lipid metabolism; however, the full complement of splicing proteins involved in achieving metabolic homeostasis is unknown. Heterogeneous nuclear ribonucleoproteins (hnRNPs), RNA binding proteins that inhibit the splicing of introns by preventing the assembly of splicing complexes, have no established metabolic functions. To assess any metabolic functions of hnRNPs, we used the GAL4/UAS system to induce RNAi to six hnRNP's: hnRNP-K, rumpelstiltskin (rump), smooth (sm), Hrb27C (also referred to as Hrp48), Hrb98DE, and Hrb87F in the Drosophila fat body. Decreasing the levels of hnRNP-K and rump resulted in a decrease in triglyceride storage, whereas decreasing the levels of sm, Hrb27C, and Hrb98DE resulted in an increase in triglyceride storage. The excess triglyceride phenotype in Hrb27C-RNAi flies resulted from both an increase in the number of fat body cells and the amount of fat stored per cell. In addition, both the splicing of the β-oxidation gene, CPT1, and the expression of the lipase brummer (bmm) was altered in flies with decreased Hrb27C, providing insight into the lipid storage phenotype in these flies. Together, these results suggest that the hnRNP family of splicing factors have varying metabolic functions and may act on specific metabolic genes to control their expression and processing.

Topics: Animals; Cell Count; Drosophila melanogaster; Drosophila Proteins; Fat Body; Feeding Behavior; Glycogen; Heterogeneous-Nuclear Ribonucleoproteins; Lipase; Lipids; RNA Splicing; Starvation; Triglycerides

In all eukaryotic organisms, the control of growth, metabolism, reproduction, and lifespan is realized by interactions of genetic and environmental signals. An important player in the regulatory network is the target of rapamycin (TOR) signaling pathway, which is triggered by nutritional cues. Given the pivotal role of TOR in regulating multiple processes in organisms, we inhibited TOR by inducible expression of specific RNAi in Drosophila intestinal stem and progenitor cells or progenitor cells alone. We found that TOR inhibition in stem and progenitor cells shortened the lifespan on both regular diet and under malnutrition. Moreover, flies became more short-lived under starvation or oxidative stress conditions if TOR was inhibited. TOR-RNAi expression resulted in a decrease in body glycogen and TAG levels. All these physiological and metabolic changes might be partially explained by significant changes in mRNA levels for genes encoding the Drosophila insulin-like peptides (dilp2, dilp3 and dilp5) with subsequent effects on insulin signaling to modulate gene expression in peripheral tissues (e.g. tobi and pepck transcripts). In the gut, a strong increase in transcript levels of cytokines upd2, upd3 and downstream target socs36e of the JAK/STAT signaling pathway in the gut indicate an important role for this signaling pathway when TOR is inhibited.

Topics: Animals; Drosophila; Drosophila Proteins; Gene Expression Regulation; Glycogen; Insulins; Janus Kinases; Longevity; Neuropeptides; Oxidative Stress; RNA Interference; Signal Transduction; Starvation; STAT Transcription Factors; Stem Cells; Suppressor of Cytokine Signaling Proteins; TOR Serine-Threonine Kinases; Triglycerides

There is an extensive literature establishing, validating, and quantifying a wide range of responses of fishes to fasting. Our study complements this work by comparing fed and unfed treatments of hatchery-raised Delta Smelt (Hypomesus transpacificus)-an imperiled fish that is endemic to the San Francisco Estuary and its tributaries in California, USA-across a diverse suite of endpoints over a two-month time series. The experiment was conducted at 15.9°C, and individuals were sampled at 12 time points as starvation became increasingly severe. We found that hepatosomatic index and condition factor were relatively sensitive to starvation, becoming significantly depressed at Day 4 and 7, respectively. Histological analysis of liver showed elevated cytoplasmic inclusion bodies at Day 7, followed by increased glycogen depletion, single cell necrosis, and hydropic vacuolar degeneration at Day 14, 21, and 28, respectively. Of four antioxidants measured, glutathione decreased at Day 4, superoxide dismutase increased at Day 14, catalase increased at Day 56, and glutathione peroxidase was not affected by starvation. The net result was a ~2-fold increase in lipid peroxidation (malondialdehyde) in fasted fish that was highly inconsistent through time. RNA to DNA ratio and triglycerides in muscle were relatively insensitive to starvation, only consistently decreasing with fasting after mortality began increasing in the 'No Feeding' treatment, at Day 21. Together, these results suggest that Delta Smelt mobilize hepatic energy stores far more rapidly than lipids in muscle when subjected to fasting, leading to rapid atrophy of liver and the development of cytoplasmic inclusion bodies-possibly autophagosomes-in hepatocytes.

Topics: Animals; Catalase; Glutathione; Glycogen; Inclusion Bodies; Liver; Malondialdehyde; Muscles; Necrosis; Osmeriformes; Starvation; Superoxide Dismutase; Time Factors

Steroid hormones are crucial regulators of life-stage transitions during development in animals. However, the molecular mechanisms by which developmental transition through these stages is coupled with optimal metabolic homeostasis remains poorly understood. Here, we demonstrate through mathematical modelling and experimental validation that ecdysteroid-induced metabolic remodelling from resource consumption to conservation can be a successful life-history strategy to maximize fitness in Drosophila larvae in a fluctuating environment. Specifically, the ecdysteroid-inducible protein ImpL2 protects against hydrolysis of circulating trehalose following pupal commitment in larvae. Stored glycogen and triglycerides in the fat body are also conserved, even under fasting conditions. Moreover, pupal commitment dictates reduced energy expenditure upon starvation to maintain available resources, thus negotiating trade-offs in resource allocation at the physiological and behavioural levels. The optimal stage-specific metabolic shift elucidated by our predictive and empirical approaches reveals that Drosophila has developed a highly controlled system for ensuring robust development that may be conserved among higher-order organisms in response to intrinsic and extrinsic cues.

Topics: Animals; Behavior, Animal; Body Size; Drosophila; Drosophila Proteins; Eating; Ecdysteroids; Glycogen; Insulin-Like Growth Factor Binding Proteins; Larva; Life History Traits; Lipid Metabolism; Metabolomics; Models, Theoretical; Pupa; Starvation; Triglycerides

Adapting to changes in food availability is a central challenge for survival. Glucose is an important resource for energy production, and therefore many organisms synthesize and retain sugar storage molecules. In insects, glucose is stored in two different forms: the disaccharide trehalose and the branched polymer glycogen. Glycogen is synthesized and stored in several tissues, including in muscle and the fat body. Despite the major role of the fat body as a center for energy metabolism, the importance of its glycogen content remains unclear. Here, we show that glycogen metabolism is regulated in a tissue-specific manner under starvation conditions in the fruit fly

Topics: Adaptation, Physiological; Animals; Drosophila; Drosophila Proteins; Fat Body; Glycogen; Homeostasis; Immunohistochemistry; Larva; Real-Time Polymerase Chain Reaction; Starvation; Sugars

The role of adipokinetic hormone (Drome-AKH) in maintaining the levels of basic nutrients, under starvation conditions, was studied using Drosophila melanogaster mutants with AKH deficiency (Akh

Topics: Animals; Animals, Genetically Modified; Carbohydrate Metabolism; Crosses, Genetic; Diglycerides; Drosophila melanogaster; Drosophila Proteins; Energy Metabolism; Enzyme-Linked Immunosorbent Assay; Female; Gene Deletion; Glycogen; Insect Hormones; Lipid Metabolism; Male; Oligopeptides; Pyrrolidonecarboxylic Acid; Random Allocation; Reproducibility of Results; Sex Characteristics; Starvation; Survival Analysis; Triglycerides

In food deprivation assays, several different responses have been observed in crustaceans. However, studying energy reserves utilization among more than one species during the same starvation period has not yet been performed, particularly to discern whether the responses are due to intrinsic and/or environmental factors. We hypothesize that decapod species with similar feeding habits have the same strategies in the use of energetic reserves during starvation, even though they inhabit different environments. The aim of this study was to compare the energy reserves mobilization of three decapods species (Cherax quadricarinatus, Palaemon argentinus and Munida gregaria) with similar feeding habits, exposed to similar food deprivation conditions. The crayfish, shrimp and squat-lobster were experimentally kept at continuous feeding or continuous starvation throughout 15 days. Every 3rd day, the midgut gland index (MGI), and the glycogen, lipid and protein contents were measured in the midgut gland (MG) and pleon muscle. Palaemon argentinus mobilized more reserves during starvation, followed by C. quadricarinatus, and the last M. gregaria. The starved shrimps presented low MGI, whereas MG showed a reduction in glycogen (from day 6 to 15), lipid (from day 3 to 15), and protein levels (at day 9 and 15) while in their muscle, lipid reserves decreased at days 3 and 6. In C. quadricarinatus, the most affected parameters in the MG were MGI, glycogen (from day 6 to 15), and lipids (at day 12 and 15). In the MG of M. gregaria only the glycogen was reduced during fasting from 3 to 15 days. Even though the three studied species have similar feeding habitats, we found that their energetic profile utilization is different and it could be explained by the habitat, life span, temperature, organ/tissue, and metabolism of the species. Our results may be useful to understand the several different responses of crustaceans during starvation.

Topics: Animals; Astacoidea; Crustacea; Energy Metabolism; Environment; Food Deprivation; Glycogen; Lipid Metabolism; Muscles; Phylogeny; Starvation

Animals rely on complex signaling network to mobilize its energy stores during starvation. We have previously shown that the sugar-responsive TGFβ/Activin pathway, activated through the TGFβ ligand Dawdle, plays a central role in shaping the post-prandial digestive competence in the Drosophila midgut. Nevertheless, little is known about the TGFβ/Activin signaling in sugar metabolism beyond the midgut. Here, we address the importance of Dawdle (Daw) after carbohydrate ingestion. We found that Daw expression is coupled to dietary glucose through the evolutionarily conserved Mio-Mlx transcriptional complex. In addition, Daw activates the TGFβ/Activin signaling in neuronal populations to regulate triglyceride and glycogen catabolism and energy homeostasis. Loss of those neurons depleted metabolic reserves and rendered flies susceptible to starvation.

Topics: Activins; Animals; Drosophila; Glycogen; Neurons; Signal Transduction; Starvation; Transforming Growth Factor beta; Triglycerides

Succinyl-CoA synthetase/ligase (SCS) is a mitochondrial enzyme that catalyzes the reversible process from succinyl-CoA to succinate and free coenzyme A in TCA cycle. SCS deficiencies are implicated in mitochondrial hepatoencephalomyopathy in humans. To investigate the impact of SCS deficiencies in Drosophila, we generated a null mutation in Scs alpha subunit (Scsα) using the CRISPR/Cas9 system, and characterized their phenotype. We found that the Drosophila SCS deficiency, designated Scsα

Topics: Acyl Coenzyme A; Animals; Animals, Genetically Modified; Behavior, Animal; Cell Survival; Citric Acid Cycle; Drosophila melanogaster; Drosophila Proteins; Energy Metabolism; Food Deprivation; Glycogen; Glycolysis; Locomotion; Male; Mitochondria; Phenotype; Starvation

We investigated the effect of long-term starvation and posterior feeding on energetic reserves, oxidative stress, digestive enzymes, and histology of C. quadricarinatus midgut gland. The crayfish (6.27 g) were randomly assigned to one of three feeding protocols: continuous feeding throughout 80 day, continuous starvation until 80 day, and continuous starvation throughout 50 day and then feeding for the following 30 days. Juveniles from each protocol were weighed, and sacrificed at day 15, 30, 50 or 80. The lipids, glycogen, reduced glutathione (GSH), soluble protein, lipid peroxidation (TBARS), protein oxidation (PO), catalase (CAT), lipase and proteinase activities, and histology were measured on midgut gland. Starved crayfish had a lower hepatosomatic index, number of molts, specific growth rate, lipids, glycogen, and GSH levels than fed animals at all assay times. The starvation did not affect the soluble protein, TBARS, PO levels and CAT. In starved juveniles the lipase activity decreased as starvation time increased, whereas proteinase activity decreased only at day 80. The histological analysis of the starved animals showed several signs of structural alterations. After 30 days of feeding, the starved-feeding animals exhibited a striking recovery of hepatosomatic index, number of molts, lipids and glycogen, GSH, lipase activity and midgut gland structure.

Topics: Animal Feed; Animals; Astacoidea; Catalase; Glutathione; Glycogen; Intestinal Mucosa; Lipase; Lipid Peroxidation; Lipids; Oxidative Stress; Peptide Hydrolases; Proteins; Starvation

Most organisms are constantly faced with environmental changes and stressors. In diverse organisms, there is an anticipatory mechanism during development that can program adult phenotypes. The adult phenotype would be adapted to the predicted environment that occurred during organism maturation. However, whether this anticipatory mechanism is present in eusocial species is questionable because eusocial organisms are largely shielded from exogenous conditions by their stable nest environment. In this study, we tested whether food deprivation during development of the honey bee (Apis mellifera), a eusocial insect model, can shift adult phenotypes to better cope with nutritional stress. After subjecting fifth instar worker larvae to short-term starvation, we measured nutrition-related morphology, starvation resistance, physiology, endocrinology and behavior in the adults. We found that the larval starvation caused adult honey bees to become more resilient toward starvation. Moreover, the adult bees were characterized by reduced ovary size, elevated glycogen stores and juvenile hormone (JH) titers, and decreased sugar sensitivity. These changes, in general, can help adult insects survive and reproduce in food-poor environments. Overall, we found for the first time support for an anticipatory mechanism in a eusocial species, the honey bee. Our results suggest that this mechanism may play a role in honey bee queen-worker differentiation and worker division of labor, both of which are related to the responses to nutritional stress.

Topics: Adaptation, Physiological; Animals; Bees; Energy Metabolism; Glycogen; Juvenile Hormones; Larva; Lipid Metabolism; Reproduction; Starvation

Environmental changes during development have long-term effects on adult phenotypes in diverse organisms. Some of the effects play important roles in helping organisms adapt to different environments, such as insect polymorphism. Others, especially those resulting from an adverse developmental environment, have a negative effect on adult health and fitness. However, recent studies have shown that those phenotypes influenced by early environmental adversity have adaptive value under certain (anticipatory) conditions that are similar to the developmental environment, though evidence is mostly from morphological and behavioral observations and it is still rare at physiological and molecular levels. In the companion study, we applied a short-term starvation treatment to fifth instar honey bee larvae and measured changes in adult morphology, starvation resistance, hormonal and metabolic physiology and gene expression. Our results suggest that honey bees can adaptively respond to the predicted nutritional stress. In the present study, we further hypothesized that developmental starvation specifically improves the metabolic response of adult bees to starvation instead of globally affecting metabolism under well-fed conditions. Here, we produced adult honey bees that had experienced a short-term larval starvation, then we starved them for 12 h and monitored metabolic rate, blood sugar concentrations and metabolic reserves. We found that the bees that experienced larval starvation were able to shift to other fuels faster and better maintain stable blood sugar levels during starvation. However, developmental nutritional stress did not change metabolic rates or blood sugar levels in adult bees under normal conditions. Overall, our study provides further evidence that early larval starvation specifically improves the metabolic responses to adult starvation in honey bees.

Topics: Adaptation, Physiological; Animals; Basal Metabolism; Bees; Energy Metabolism; Environmental Exposure; Glucose; Glycogen; Juvenile Hormones; Larva; Lipid Metabolism; Reproduction; Starvation; Triglycerides

Glycogen storage in brown adipose tissue (BAT) is generally thought to take place through passive, substrate-driven activation of glycogenesis rather than programmatic shifts favoring or opposing the storage and/or retention of glycogen. This perception exists despite a growing body of evidence suggesting that BAT glycogen storage is actively regulated by covalent modification of key glycogen-metabolic enzymes, protein turnover, and endocrine hormone signaling. Members of one such class of covalent-modification regulators, glycogen-binding Phosphoprotein Phosphatase-1 (PP1)-regulatory subunits (PPP1Rs), targeting PP1 to glycogen-metabolic enzymes, were dynamically regulated in response to 24 hr of starvation and/or 24 hr of starvation followed by ad libitum refeeding. Over-expression of the PPP1R Protein Targeting to Glycogen (PTG), under the control of the aP2 promoter in mice, inactivated glycogen phosphorylase (GP) and enhanced basal- and starvation-state glycogen storage. Total interscapular BAT glycogen synthase and the constitutive activity of GS were conditionally affected. During starvation, glucose-6-phosphate (G-6-P) levels and the relative phosphorylation of Akt (p-Ser-473-Akt) were both increased in PTG-overexpressing (Tg) mice, suggesting that elevated glycogen storage during starvation modifies broader cellular metabolic pathways. During refeeding, Tg and WT mice reaccumulated glycogen similarly despite altered GS and GP activities. All observations during refeeding suggest that the phosphorylation states of GS and GP are not physiologically rate-controlling, despite there being a clear balance of endogenous kinase- and phosphatase activities. The studies presented here reveal IBAT glycogen storage to be a tightly-regulated process at all levels, with potential effects on nutrient sensing in vivo.

Topics: Adipose Tissue, Brown; Animals; Eating; Glycogen; Glycogen Phosphorylase; Glycogen Synthase; Intracellular Signaling Peptides and Proteins; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Oncogene Protein v-akt; Phosphoprotein Phosphatases; Phosphorylation; Signal Transduction; Starvation

To explore the consumption of energy sources and swimming performance of juvenile Gambusia affinis and Tanichthys albonubes after starvation, contents of glycogen, lipid and protein, burst swimming speeds (Uburst), and critical swimming speeds (Ucrit) at different starvation times (0, 10, 20, 30 and 40 days) were evaluated. The results showed that, at 0 day, contents of glycogen and lipid were significantly lower in G. affinis than those in T. albonubes, whereas no significant difference in content of protein between two experimental fish was found. Swimming speeds in G. affinis were significantly lower than those in T. albonubes for all swimming performances. After different starvation scenarios, content of glycogen both in G. affinis and T. albonubes decreased significantly in power function trend with starvation time and were close to zero after starvation for 10 days, whereas the contents of lipid and protein were linearly significantly decreased. The slope of line regression equation between content of lipid and starvation time in G. affinis was significantly lower than that in T. albonubes, whereas there was a significantly higher slope of line equation between content of protein and starvation time in G. affinis. 40 days later, the consumption rate of glycogen both in G. affinis and T. albonubes were significantly higher than that of lipid, while the consumption rate of protein was the least. Consumption amounts of glycogen in all experimental fish were the least, G. affinis consumed more protein than lipid, and T. albonubes consumed more lipid than protein. Uburst and Ucrit decreased significantly linearly with starvation time for all experimental fish. Slope of linear equation between Uburst and starvation time was not significantly different between G. affinis and T. albonubes. However, the straight slope between Ucrit and starvation time was significantly lower in G. affinis than that in T. albonubes. These findings indicated that there was close relationship between the consumption of energy sources and swimming performance in starvation. Although the store amounts of energy sources and swimming performance were lower in G. affinis than those in T. albonubes, G. affinis mainly used protein during starvation. The result of more stable lipid content and Ucrit in G. affinis in starvation compared with that in T. albonubes indicated that G. affinis had a fair endurance to starvation, which helped them to adapt to the poor nutrition environment in

Topics: Animals; Cyprinidae; Cyprinodontiformes; Glycogen; Starvation; Swimming

Animals maximize fitness by modulating sleep and foraging strategies in response to changes in nutrient availability. Wild populations of the fruit fly, Drosophila melanogaster, display highly variable levels of starvation and desiccation resistance that differ in accordance with geographic location, nutrient availability, and evolutionary history. Further, flies potently modulate sleep in response to changes in food availability, and selection for starvation resistance enhances sleep, revealing strong genetic relationships between sleep and nutrient availability. To determine the genetic and evolutionary relationship between sleep and nutrient deprivation, we assessed sleep in flies selected for desiccation or starvation resistance. While starvation resistant flies have higher levels of triglycerides, desiccation resistant flies have enhanced glycogen stores, indicative of distinct physiological adaptations to food or water scarcity. Strikingly, selection for starvation resistance, but not desiccation resistance, leads to increased sleep, indicating that enhanced sleep is not a generalized consequence of higher energy stores. Thermotolerance is not altered in starvation or desiccation resistant flies, providing further evidence for context-specific adaptation to environmental stressors. F2 hybrid flies were generated by crossing starvation selected flies with desiccation selected flies, and the relationship between nutrient deprivation and sleep was examined. Hybrids exhibit a positive correlation between starvation resistance and sleep, while no interaction was detected between desiccation resistance and sleep, revealing that prolonged sleep provides an adaptive response to starvation stress. Therefore, these findings demonstrate context-specific evolution of enhanced sleep in response to chronic food deprivation, and provide a model for understanding the evolutionary relationship between sleep and nutrient availability.

Topics: Adaptation, Physiological; Animals; Body Size; Crosses, Genetic; Desiccation; Disease Resistance; Drosophila melanogaster; Energy Metabolism; Female; Food Deprivation; Glycogen; Hot Temperature; Insect Proteins; Kaplan-Meier Estimate; Male; Motor Activity; Phenotype; Selection, Genetic; Sleep; Starvation; Stress, Physiological; Triglycerides

Dietary compromises, especially food restrictions, possess species-specific effects on the health status and infection control in several organisms, including fish. To understand the starvation-mediated physiological responses in Edwardsiella tarda infected red sea bream, especially in the liver, we performed a 20-day starvation experiment using 4 treatment (2 fed and 2 starved) groups, namely, fed-placebo, starved-placebo, fed-infected, and starved-infected, wherein bacterial exposure was done on the 11th day. In the present study, the starved groups showed reduced hepatosomatic index and drastic depletion in glycogen storage and vacuole formation. The fed-infected fish showed significant (P<0.05) increase in catalase and superoxide dismutase activity in relation to its starved equivalent. Significant (P<0.05) alteration in glucose and energy metabolism, as evident from hexokinase and glucose-6-phosphate dehydrogenase activity, was recorded in the starved groups. Interestingly, coinciding with the liver histology, PPAR (peroxisome proliferator activated receptors) α transcription followed a time-dependent activation in starved groups while PPARγ exhibited an opposite pattern. The transcription of hepcidin 1 and transferrin, initially increased in 0dai (days after infection) starved fish but reduced significantly (P<0.05) at later stages. Two-color immunohistochemistry and subsequent cell counting showed significant increase in P63-positive cells at 0dai and 5dai but later reduced slightly at 10dai. Similar results were also obtained in the lysosomal (cathepsin D) and non-lysosomal (ubiquitin) gene transcription level. All together, our data suggest that starvation exerts multidirectional responses, which allows for better physiological adaptations during any infectious period, in red sea bream.

Topics: Animals; Catalase; Edwardsiella tarda; Energy Metabolism; Enterobacteriaceae Infections; Fish Diseases; Fish Proteins; Food; Gene Expression; Glucose; Glycogen; Host-Pathogen Interactions; Liver; PPAR alpha; PPAR gamma; Reverse Transcriptase Polymerase Chain Reaction; Sea Bream; Starvation; Superoxide Dismutase; Vacuoles

Nitrogen availability is one of the most important factors for the survival of cyanobacteria. Previous studies on Synechocystis revealed a contradictory situation with regard to metabolism during nitrogen starvation; that is, glycogen accumulated even though the expressions of sugar catabolic genes were widely upregulated. Here, we conducted transcript and metabolomic analyses using capillary electrophoresis-mass spectrometry on Synechocystis sp. PCC 6803 under nitrogen starvation. The levels of some tricarboxylic acid cycle intermediates (succinate, malate and fumarate) were greatly increased by nitrogen deprivation. Purine and pyrimidine nucleotides were markedly downregulated under nitrogen depletion. The levels of 19 amino acids changed under nitrogen deprivation, especially those of amino acids synthesized from pyruvate and phosphoenolpyruvate, which showed marked increases. Liquid chromatography-mass spectrometry analysis demonstrated that the amount of NADPH and the NADPH/NADH ratio decreased under nitrogen depletion. These data demonstrate that there are increases in not only glycogen but also in metabolites downstream of sugar catabolism in Synechocystis sp. PCC 6803 under nitrogen starvation, resolving the contradiction between glycogen accumulation and induction of sugar catabolic gene expression in this unicellular cyanobacterium.

Topics: Carbohydrate Metabolism; Carbon; Citric Acid Cycle; Electrophoresis, Capillary; Gene Expression Regulation, Bacterial; Glycogen; Mass Spectrometry; Metabolome; Nitrogen; Purines; Pyrimidines; Starvation; Synechocystis

FoxO proteins are a subgroup of the Forkhead-box family of transcription factors, which function as the main transcriptional effectors of the insulin receptor pathway. This pathway, activated by the binding of insulin or IGFs (or insect insulin-like peptides), promotes the phosphorylation and inactivation of FoxO because of its export from the nucleus to the cytoplasm. The homolog of FoxO in the cockroach Blattella germanica works in a situation of nutrient shortage by inhibiting the endocrine induction of reproduction.. Using Blattella germanica as a model, we studied the functions of FoxO using RNA interference methodologies. We analyzed the mRNA levels of hypertrehalosemic hormone (HTH) and genes related to lipolysis, glycogenolysis and gluconeogenesis and quantified triacylglycerides, glycogen and trehalose.. FoxO knockdown eliminates the starvation-induced expression of HTH in the corpora cardiaca. In addition, FoxO knockdown prevents the activation of the expression of Brummer lipase, glycogen phosphorylase and phosphoenolpyruvate carboxylase in the fat body of starved females.. Starvation-induced activation of FoxO stimulates the transcription of different genes related to catabolic processes, including HTH and genes involved in lipolysis, glycogenolysis and gluconeogenesis.. Our results show conservation in the action of the transcription factor FoxO in the activation of catabolic processes from basal insects to vertebrates. The results also describe a new and essentially different mode of action of transcription factor FoxO, which works through the activation of neuropeptide HTH expression, which will subsequently produce its own catabolic stimulatory function.

Topics: Adipose Tissue; Animals; Cockroaches; Female; Forkhead Transcription Factors; Glycogen; Glycogenolysis; Hemolymph; Neuropeptides; RNA, Small Interfering; Starvation; Triglycerides

Rre37 (sll1330) in a cyanobacterium Synechocystis sp. PCC 6803 acts as a regulatory protein for sugar catabolic genes during nitrogen starvation. Low glycogen accumulation in Δrre37 was due to low expression of glycogen anabolic genes. In addition to low 2-oxoglutarate accumulation, normal upregulated expression of genes encoding glutamate synthases (gltD and gltB) as well as accumulation of metabolites in glycolysis (fructose-6-phosphate, fructose-1,6-bisphosphate, and glyceraldehyde-3-phosphate) and tricarboxylic acid (TCA) cycle (oxaloacetate, fumarate, succinate, and aconitate) were abolished by rre37 knockout. Rre37 regulates 2-oxoglutarate accumulation, glycogen accumulation through expression of glycogen anabolic genes, and TCA cycle metabolites accumulation.

Topics: Citric Acid Cycle; DNA-Binding Proteins; Fructosephosphates; Gene Expression Regulation, Bacterial; Glutamate Synthase; Glycogen; Glycolysis; Ketoglutaric Acids; Nitrogen; Starvation; Synechocystis

Geographically varying starvation stress has often been considered as a natural selector that constrains between-population differences for starvation resistance (SR) in Drosophila species. On the Indian subcontinent, a dozen Drosophila species have shown clinal variations in SR across latitude, but the evolved physiological basis of such contrasting adaptations is largely unknown. In the present study, I untangled the physiological basis of sex-specific as well as between-population divergence for SR in D. leontia, collected across a latitudinal transect of the Indian subcontinent (11°45'-31°19'N). Secondly, I tested the assumptions that hardening to starvation stress facilitates an increased survival under subsequent lethal levels of starvation, and such plastic effects differ between the sexes. I observed several interesting results. In contrast to a steeper cline of starvation-related traits with latitude in females, a shallower gradient was observed for males. Females stored higher (~1.3-fold) dry-mass-specific levels of body lipids and glycogen contents, and utilized these both of these energy resources under starvation stress, whereas the starved males metabolized only body lipids as a source of energy. Conversely, the rate of body lipid utilization and threshold need were considerably higher in females as compared with males. Between-population differences were significant for storage levels of energy reserves only, but not for other avenues (rate of metabolite utilization and threshold need) of SR for both sexes. These findings indicate that multiple pathways shape the physiological basis of sexual dimorphism for SR in D. leontia. Further, single or multiple bouts of starvation hardening conferred an increased longevity (~4-9 h; P<0.001) under subsequent lethal levels of starvation stress for females only, and such plastic responses were consistent with a decrease in rate of metabolite utilization. Nevertheless, between-population effects were non-significant for absolute hardening capacity (AHC=KSR-C). Altogether, these findings suggest that similar evolutionary constraints have resulted in divergent genetic as well as plastic responses to evolve adaptations under starvation stress, and account for the observed sexual dimorphism for basal SR in D. leontia.

Topics: Animals; Drosophila; Energy Metabolism; Female; Geography; Glycogen; India; Longevity; Male; Phenotype; Sex Characteristics; Starvation

The content and structure of glycogen in hepatocytes of normal and cirrhotic rat liver has been studied at definite time intervals after the administration of glucose to starving animals. In the study, an original cytofluorimetric method for detection and quatification of proglycogen (PG) and macroglycogen (MG) content in isolated hepatocytes was applied. This method is based on using Schiff reagents with different spectral characteristics. It has been determined that the content MG content in the hepatocytes of control rats increases in 10 min after initiation of glycogenesis by 52% (P < 0.01). MG content in the cells of cirrhotic liver increased only after 20 min (43%, P < 0.05) after glucose administration to starving animals. The coefficient of correlation between MG content and the total glycogen content in the hepatocytes at different stages of glycogenesis ranged from 0.90 to 0.99 (P < 0.001) in both groups of rats. Increase in PG content in hepatocytes of control rats appeared within 10-30 and 45-70 min. In the case of cirrhosis PG content increased only 60 min after the start of glycogenesis, but after 120 min it was 1.5 times higher than the control values (P < 0.001). The correlation coefficient between the PG and the total glycogen content in rat liver cells averaged 0.86 (P < 0.001) and 0.77 (P < 0.001) in control and experimental groups, respectively. Thus, the change in total glycogen content in hepatocytes of normal and cirrhotic liver is associated mainly with the level of MG. In normal cells, contribution of PG is most significant in the early glycogenesis (10-30 min), and in the cirrhotic liver--in the later stages.

Topics: Animals; Carbon Tetrachloride; Glucose; Glycogen; Hepatocytes; Liver; Liver Cirrhosis; Male; Rats; Rosaniline Dyes; Starvation; Time Factors

The morphological alterations of hepatocytes of cave-dwelling salamander Proteus anguinus anguinus after food deprivation periods of one and 18 months were investigated and the concentrations of glycogen, lipids, and proteins in the liver were determined. Quantitative analyses of the hepatocyte size, the lipid droplets, the number of mitochondria, and volume densities of M and P in the hepatocytes were completed. After one month of food deprivation, the cytological changes in the hepatocytes are mainly related to the distribution and amount of glycogen, which was dispersed in the cytoplasm and failed to form clumps typical of normal liver tissue. After 18 months of food deprivation hepatocytes were reduced in size, lipid droplets were less numerous, peroxisomes formed clusters with small, spherical mitochondria, and specific mitochondria increased in size and lost cristae. Lysosomes, autophagic vacuoles, and clear vacuoles were numerous. The liver integrity was apparently maintained, no significant loss of cytoplasmic constituents have been observed. Biochemical analysis revealed the utilization of stored metabolic reserves in the liver during food deprivation. Glycogen is rapidly utilized at the beginning of the starvation period, whereas lipids and proteins are utilized subsequently, during prolonged food deprivation. In the Proteus liver carbohydrates are maintained in appreciable amounts and this constitutes a very important energy depot, invaluable in the subterranean environment.

Topics: Animals; Caves; Cytoplasm; Female; Food; Food Deprivation; Glycogen; Hepatocytes; Inclusion Bodies; Lipids; Liver; Lysosomes; Mitochondria, Liver; Organelles; Proteidae; Starvation

The present study examines the particular metabolic strategies of the sturgeon Acipenser naccarii in facing a period of prolonged starvation (72 days) and subsequent refeeding (60 days) compared to the trout Oncorhynchus mykiss response under similar conditions. Plasma metabolites, endogenous reserves, and the activity of intermediate enzymes in liver and white muscle were evaluated. This study shows the mobilization of tissue reserves during a starvation period in both species with an associated enzymatic response. The sturgeon displayed an early increase in hepatic glycolysis during starvation. The trout preferentially used lactate for gluconeogenesis in liver and white muscle. The sturgeon had higher lipid-degradation capacity and greater synthesis of hepatic ketone bodies than the trout, although this latter species also showed strong synthesis of ketone bodies during starvation. During refeeding, the metabolic activity present before starvation was recovered in both fish, with a reestablishment of tissue reserves, plasmatic parameters (glucemia and cholesterol), and enzymatic activities in the liver and muscle. A compensatory effect in enzymes regarding lipids, ketone bodies, and oxidative metabolism was displayed in the liver of both species. There are metabolic differences between sturgeon and trout that support the contention that the sturgeon has common characteristics with elasmobranchs and teleosts.

Topics: Animals; Cholesterol; Eating; Enzymes; Fishes; Glycogen; Ketone Bodies; Lipid Metabolism; Liver; Muscle, Skeletal; Oncorhynchus mykiss; Species Specificity; Starvation

Laboratory selection experiments have evidenced storage of energy metabolites in adult flies of desiccation and starvation resistant strains of D. melanogaster but resource acquisition during larval stages has received lesser attention. For wild populations of D. melanogaster, it is not clear whether larvae acquire similar or different energy metabolites for desiccation and starvation resistance. We tested the hypothesis whether larval acquisition of energy metabolites is consistent with divergence of desiccation and starvation resistance in darker and lighter isofemale lines of D. melanogaster. Our results are interesting in several respects. First, we found contrasting patterns of larval resource acquisition, i.e., accumulation of higher carbohydrates during 3rd instar larval stage of darker flies versus higher levels of triglycerides in 1st and 2nd larval instars of lighter flies. Second, 3rd instar larvae of darker flies showed ~40 h longer duration of development at 21°C; and greater accumulation of carbohydrates (trehalose and glycogen) in fed larvae as compared with larvae non-fed after 150 h of egg laying. Third, darker isofemale lines have shown significant increase in total water content (18%); hemolymph (86%) and dehydration tolerance (11%) as compared to lighter isofemale lines. Loss of hemolymph water under desiccation stress until death was significantly higher in darker as compared to lighter isofemale lines but tissue water loss was similar. Fourth, for larvae of darker flies, about 65% energy content is contributed by carbohydrates for conferring greater desiccation resistance while the larvae of lighter flies acquire 2/3 energy from lipids for sustaining starvation resistance; and such energy differences persist in the newly eclosed flies. Thus, larval stages of wild-caught darker and lighter flies have evolved independent physiological processes for the accumulation of energy metabolites to cope with desiccation or starvation stress.

Topics: Animal Nutritional Physiological Phenomena; Animals; Desiccation; Drosophila melanogaster; Energy Metabolism; Female; Glycogen; Larva; Phenotype; Pigmentation; Starvation; Trehalose

Proper assessment of environmental resistance of animals is critical for the ability of researchers to understand how variation in environmental conditions influence population and species abundance. This is also the case for studies of upper thermal limits in insects, where researchers studying animals under laboratory conditions must select appropriate methodology on which conclusions can be drawn. Ideally these methods should precisely estimate the trait of interest and also be biological meaningful. In an attempt to develop such tests it has been proposed that thermal ramping assays are useful assays for small insects because they incorporate an ecologically relevant gradual temperature change. However, recent model-based papers have suggested that estimates of thermal resistance may be strongly confounded by simultaneous starvation and dehydration stress. In the present study we empirically test these model predictions using two sets of independent experiments. We clearly demonstrate that results from ramping assays of small insects (Drosophila melanogaster) are not compromised by starvation- or dehydration-stress. Firstly we show that the mild disturbance of water and energy balance of D. melanogaster experienced during the ramping tests does not confound heat tolerance estimates. Secondly we show that flies pre-exposed to starvation and dehydration have "normal" heat tolerance and that resistance to heat stress is independent of the energetic and water status of the flies. On the basis of our results we discuss the assumptions used in recent model papers and present arguments as to why the ramping assay is both a valid and ecologically relevant way to measure thermal resistance in insects.

Topics: Acclimatization; Analysis of Variance; Animals; Dehydration; Drosophila melanogaster; Endpoint Determination; Glycogen; Starvation; Temperature; Water-Electrolyte Balance

Plasmodium spp. are pathogenic to their vertebrate hosts and also apparently, impose a fitness cost on their insect vectors. We show here, however, that Plasmodium-infected mosquitoes survive starvation significantly better than uninfected mosquitoes. This survival advantage during starvation is associated with higher energy resource storage that infected mosquitoes accumulate during period of Plasmodium oocyst development. Microarray analysis revealed that the metabolism of sated mosquitoes is altered in the presence of rapidly growing oocysts, including the down-regulation of several enzymes involved in carbohydrate catabolism. In addition, enhanced expression of several insulin-like peptides was observed in Plasmodium-infected mosquitoes. Blocking insulin-like signaling pathway resulted in impaired Plasmodium development. We conclude that Plasmodium infection alters metabolic pathways in mosquitoes, epitomized by enhanced insulin-like signaling - thereby conferring a survival advantage to the insects during periods of starvation. Manipulation of this pathway might provide new strategies to influence the ability of mosquitoes to survive and transmit the protozoa that cause malaria.

Topics: Animals; Anopheles; Carbohydrate Metabolism; Cluster Analysis; Down-Regulation; Feeding Behavior; Glucose; Glycogen; Host-Parasite Interactions; Insulin; Molecular Sequence Annotation; Oocysts; Peptides; Plasmodium berghei; RNA Interference; RNA, Messenger; Starvation; Sucrose; Survival Analysis; Triglycerides; Up-Regulation

An indoor exposure experiment with juvenile Babylonia areolata was conducted to study its survival, growth, cadmium (Cd) accumulation, metallothionein (MT) induction, and glycogen content as well as the DNA integrity of hepatopancreas tissue. The juveniles were starved or fed with mussel (Perna viridis) or clamworm (Perinereis aibuhitensis), and exposed to 50 microg x L(-1) of Cd2+ for 10 weeks. Prolonged starvation and simultaneous exposure to Cd reduced the survival rate of B. areolata, and its glycogen was mobilized in great extent. Feeding with P. viridis or P. aibuhitensis helped the B. areolata to combat Cd toxicity and lessen mortality. After exposed to Cd, the damage of the DNA integrity of hepatopancreas tissue for the B. areolata fed with P. viridis or P. aibuhitensis could be recovered with time, but not for the starved B. areolata. Prolonged starvation caused tissue atrophy and led to Cd accumulation and MT increase, while feeding with P. viridis or P. aibuhitensis increased the B. areolata mass and lowered the Cd accumulation and MT level because of the tissue dilution effect. The B. areolata fed with P. viridis had better growth and lower Cd content than that fed with P. aibuhitensis. This study indicated that starvation intensified the toxicity of Cd to B. areolata, while prey type had significant effects on the growth rate of the B. areolata and indirectly affected its Cd accumulation, MT induction, and glycogen consumption. It was suggested that when using gastropods such as B. areolata as the indicator species to monitor marine environmental pollution, it would be necessary to consider the effects of habitat ecological data including food richness and prey type. Moreover, in the high-density cultivation of B. areolata in factory, rational feeding and periodic measurement of Cd concentration in seawater should be made.

Topics: Animals; Cadmium; DNA Damage; Glycogen; Metallothionein; Snails; Starvation; Water Pollutants, Chemical

Potamopyrgus antipodarum is a promising test organism that is often used in ecotoxicology, both in laboratory and field exposures. As no data are available on the physiological variation range of its life-traits and the biomarkers it uses, we studied the variation of fecundity, steroid levels and energy reserves over the course of a year in a field population. The reproductive cycle was described and showed seasonal activity during summer and autumn. Steroid levels (17β-estradiol and testosterone) varied significantly during the year and were correlated with the reproductive cycle, which suggested a potential role for sex-steroids in P. antipodarum reproduction. Energy status also showed seasonal variations. Triglycerides (TG) seemed to be the main energy lipid, whereas cholesterol appeared to be mostly used as a structural lipid. Proteins were also involved in the reproductive cycle, but only when TG were not sufficient to support the reproductive strain, similar to cholesterol. Glycogen seemed to be used as an early reserve. Threshold values under which no reproduction occurred were defined in starved snails. We proposed a range of variation in the measured parameters, allowing for a better understanding and interpretation of their levels during laboratory or in situ exposures. The data suggest that the variability of fecundity in snails has not been fully appreciated in literature.

Topics: Animals; Energy Metabolism; Estradiol; Fertility; Glycogen; Gonadal Steroid Hormones; Individuality; Seasons; Snails; Starvation; Testosterone; Vertebrates

The cAMP-responsive transcription factor CREB functions in adipose tissue and liver to regulate glycogen and lipid metabolism in mammals. While Drosophila has a homolog of mammalian CREB, dCREB2, its role in energy metabolism is not fully understood. Using tissue-specific expression of a dominant-negative form of CREB (DN-CREB), we have examined the effect of blocking CREB activity in neurons and in the fat body, the primary energy storage depot with functions of adipose tissue and the liver in flies, on energy balance, stress resistance and feeding behavior. We found that disruption of CREB function in neurons reduced glycogen and lipid stores and increased sensitivity to starvation. Expression of DN-CREB in the fat body also reduced glycogen levels, while it did not affect starvation sensitivity, presumably due to increased lipid levels in these flies. Interestingly, blocking CREB activity in the fat body increased food intake. These flies did not show a significant change in overall body size, suggesting that disruption of CREB activity in the fat body caused an obese-like phenotype. Using a transgenic CRE-luciferase reporter, we further demonstrated that disruption of the adipokinetic hormone receptor, which is functionally related to mammalian glucagon and beta-adrenergic signaling, in the fat body reduced CRE-mediated transcription in flies. This study demonstrates that CREB activity in either neuronal or peripheral tissues regulates energy balance in Drosophila, and that the key signaling pathway regulating CREB activity in peripheral tissue is evolutionarily conserved.

Topics: Aging; Animals; Cyclic AMP Response Element-Binding Protein; Drosophila melanogaster; Drosophila Proteins; Energy Metabolism; Fat Body; Feeding Behavior; Gene Knockdown Techniques; Glycogen; Lipid Metabolism; Neurons; Oxidative Stress; Receptors, Glucagon; Response Elements; Starvation; Stress, Physiological; Trans-Activators; Transcription, Genetic

Studies in mammals have indicated a connection between circadian clocks and feeding behavior, but the nature of the interaction and its relationship to nutrient metabolism are not understood. In Drosophila, clock proteins are expressed in many metabolically important tissues but have not been linked to metabolic processes. Here we demonstrate that Drosophila feeding behavior displays a 24 hr circadian rhythm that is regulated by clocks in digestive/metabolic tissues. Flies lacking clocks in these tissues, in particular in the fat body, also display increased food consumption but have decreased levels of glycogen and a higher sensitivity to starvation. Interestingly, glycogen levels and starvation sensitivity are also affected by clocks in neuronal cells, but the effects of neuronal clocks generally oppose those of the fat body. We propose that the input of neuronal clocks and clocks in metabolic tissues is coordinated to provide effective energy homeostasis.

Topics: Animals; ARNTL Transcription Factors; Basic Helix-Loop-Helix Transcription Factors; Biological Clocks; Circadian Rhythm; CLOCK Proteins; Drosophila melanogaster; Drosophila Proteins; Eating; Energy Metabolism; Fat Body; Feeding Behavior; Genotype; Glycogen; Homeostasis; Humans; Male; Neurons; Starvation; Transcription Factors

In fasted mammals, glucose homeostasis is maintained through induction of the cAMP response element-binding protein (CREB) coactivator transducer of regulated CREB activity 2 (TORC2), which stimulates the gluconeogenic program in concert with the forkhead factor FOXO1. Here we show that starvation also triggers TORC activation in Drosophila, where it maintains energy balance through induction of CREB target genes in the brain. TORC mutant flies have reduced glycogen and lipid stores and are sensitive to starvation and oxidative stress. Neuronal TORC expression rescued stress sensitivity as well as CREB target gene expression in TORC mutants. During refeeding, increases in insulin signaling inhibited TORC activity through the salt-inducible kinase 2 (SIK2)-mediated phosphorylation and subsequent degradation of TORC. Depletion of neuronal SIK2 increased TORC activity and enhanced stress resistance. As disruption of insulin signaling also augmented TORC activity in adult flies, our results illustrate the importance of an insulin-regulated pathway that functions in the brain to maintain energy balance.

Topics: Animals; Animals, Genetically Modified; Blotting, Western; Brain; Cyclic AMP Response Element-Binding Protein; Drosophila melanogaster; Drosophila Proteins; Female; Glycogen; Hypoglycemic Agents; Insulin; Lipids; Male; Neurons; Oxidative Stress; Peptide Fragments; Phosphorylation; Protein Serine-Threonine Kinases; Starvation; Transcription Factors

The aim of this study was to examine the effects of reduced glycogen concentration on sarcoplasmic reticulum (SR) Ca(2+)-ATPase activity in rat fast-twitch muscles. In the first experiment, the gastrocnemius (GAS) muscle from one leg was removed, followed by starvation for 24-72 h, after which the remaining GAS was removed. Intra-animal comparisons revealed that starvation caused a 25% reduction (P<0.05) in the glycogen concentration but no change in SR Ca(2+)-ATPase activity in the GAS. In the second experiment, the SR was purified from a mixture of the GAS and vastus lateralis muscles. In half of the samples obtained from each animal, glycogen was extracted from the SR by treatment with glucoamylase. Treatment resulted in a 94.1 and 70.2% decrease (P<0.01) in glycogen and glycogen phosphorylase, respectively, and a 41.5% increase (P<0.05) in a fluorescein isothiocyanate (FITC) binding to SR Ca(2+)-ATPase. On the other hand, SR Ca(2+)-ATPase activity and the affinity of the enzyme for ATP were unaltered. These results do not implicate depletion of muscle glycogen as a contributor to impaired SR Ca(2+)-ATPase activity as measured in vitro. Therefore, it is concluded that muscle glycogen does not influence exercise tolerance and work productivity in working muscles by modulating the structure of protein involved in Ca(2+) sequestering. Furthermore, it is suggested that the FITC binding assay may be inappropriate as a method for examining the mechanisms for the altered activity of SR Ca(2+)-ATPase.

Topics: Animals; Glucan 1,4-alpha-Glucosidase; Glycogen; Glycogen Phosphorylase; Male; Muscles; Rats; Rats, Wistar; Sarcoplasmic Reticulum Calcium-Transporting ATPases; Starvation

Changes in body weight and composition are the result of complex interactions among metabolic fluxes contributing to macronutrient balances. To better understand these interactions, a mathematical model was constructed that used the measured dietary macronutrient intake during semistarvation and refeeding as model inputs and computed whole body energy expenditure, de novo lipogenesis, and gluconeogenesis as well as turnover and oxidation of carbohydrate, fat, and protein. Published in vivo human data provided the basis for the model components that were integrated by fitting a few unknown parameters to the classic Minnesota human starvation experiment. The model simulated the measured body weight and fat mass changes during semistarvation and refeeding and predicted the unmeasured metabolic fluxes underlying the body composition changes. The resting metabolic rate matched the experimental measurements and required a model of adaptive thermogenesis. Refeeding caused an elevation of de novo lipogenesis that, along with increased fat intake, resulted in a rapid repletion and overshoot of body fat. By continuing the computer simulation with the prestarvation diet and physical activity, the original body weight and composition were eventually restored, but body fat mass was predicted to take more than one additional year to return to within 5% of its original value. The model was validated by simulating a recently published short-term caloric restriction experiment without changing the model parameters. The predicted changes in body weight, fat mass, resting metabolic rate, and nitrogen balance matched the experimental measurements, thereby providing support for the validity of the model.

Topics: Adipose Tissue; Basal Metabolism; Body Composition; Body Weight; Caloric Restriction; Eating; Energy Metabolism; Glycogen; Humans; Lipid Metabolism; Models, Biological; Nitrogen; Oxygen Consumption; Starvation; Triglycerides

The purpose of the present study was to elucidate the possible role of leptin in food intake and body weight regulation in goldfish. We examined the effects of i.c.v. or i.p. acute leptin administration on food intake in food-deprived goldfish at different time intervals post-injection (0-2, 2-8 and 0-8 h). Food intake was reduced by i.p. administered leptin (1 microg) at 8 h post-injection, without statistically significant differences after i.c.v. treatment. The present study shows for the first time in a teleost that chronic (10 days) leptin treatment (i.p.) reduces food intake, body weight gain, specific growth rate and food efficiency ratio. Moreover, lipid and carbohydrate metabolism seems to be regulated by leptin in fish. Chronic leptin treatment increased lipid mobilization and carbohydrate storage as hepatic and muscle glycogen. Finally, leptin could mediate its actions on energy homeostasis in fish, at least in part, through interactions with hypothalamic catecholamines, since chronic leptin treatment reduced both hypothalamic noradrenergic and dopaminergic turnover without significant modifications in hypothalamic serotoninergic and neuropeptide Y (NPY) systems. In summary, our results suggest that leptin can regulate feeding behaviour and body weight homeostasis in fish.

Topics: Animals; Body Weight; Carbohydrate Metabolism; Catecholamines; Eating; Energy Metabolism; Glycogen; Goldfish; Hypothalamus; Injections, Intraperitoneal; Injections, Intravenous; Leptin; Lipid Metabolism; Liver; Muscles; Neuropeptide Y; Serotonin; Starvation; Time Factors

In some neotropical environments, fishes often experience periods of poor food supply, especially due to extreme fluctuations in rainfall regime. The fish species that experience periods of drought such as the traíra Hoplias malabaricus (Bloch 1794), may stand up to long-term food deprivation. In this study, experiments were performed in order to determine the dynamic of utilization of endogenous reserves in this species during starvation. Adult traíra were both fasted for 30-240 days and re-fed for 30 days following 90 and 240 days of fasting. Glycogen and perivisceral fat were primary energy substrates consumed. During the first 30 days, fish consumed hepatic and muscular glycogen, without exhausting these reserves, and used lipids from perivisceral fat. Hepatic lipids were an important energy source during the first 60 days of starvation and perivisceral fat were consumed gradually, being exhausted after 180 days. Protein mobilization was noticeable after 60 days of fasting, and became the major energy source as the lipid reserves were decreased (between 90 and 180 days). Following the longest periods of food deprivation, fish had utilized hepatic glycogen again. Fish re-fed for 30 days after 90 and 240 days of fasting were able to recover hepatic glycogen stores, but not the other energy reserves.

Topics: Adipose Tissue; Animals; Energy Metabolism; Fishes; Food; Glycogen; Lipid Metabolism; Lipids; Liver Glycogen; Starvation

Newborn piglets were used to study body protein preservation because it is critical to the survival of premature infants. Quantitative estimates of endogenous fuel use were obtained from 12 to 72 h of age in male piglets. Of the 40 piglets used (1300 +/- 205 g, mean +/- SD), 16 served as a 12-h-old body composition reference (R), 16 were starved (S) and received water only, and 8 received supplemental energy (E), obtaining 70% [210 kJ/(kg x d)] of their resting energy requirement as an i.v. mixture of glucose and Intralipid (65:35 energy ratio). Urine was collected continuously from the bladder via an umbilical urachal catheter. Total body water, glycogen, lipid, ash, and Kjeldahl-N were determined on whole-pig homogenates. Comparative slaughter was used to estimate the disappearance of body constituents of S and E pigs from 12 to 72 h of age. Midpoint body weight was used in these calculations. Supplemental energy decreased use of all body energy sources as indicated by the decrease in body dry matter disappearance, 41.6 +/- 8.8 vs. 25.5 +/- 5.9 g/kg (P = 0.0021) and protein (urinary N excretion), 995 +/- 508 vs. 329 +/- 135 mg/kg (P = 0.0119) over 60 h. Supplemental energy did not preferentially spare the percentage of the resting energy expenditure supplied by endogenous body protein (protein 37.6% +/- 9.6 vs. 41.7% +/- 10.4; lipid 25.7% +/- 5.2 vs. 20% +/- 4.1; glycogen 36.8% +/- 7.5 vs. 38.3% +/- 9.9; S vs. E) because it made up approximately 40% of the total in food-deprived and supplemented piglets.

Topics: Animals; Animals, Newborn; Blood Glucose; Blood Urea Nitrogen; Body Composition; Body Water; Energy Intake; Energy Metabolism; Fat Emulsions, Intravenous; Glucose; Glycogen; Lipids; Nitrogen; Proteins; Starvation; Swine

In the present study, the glucose concentration in the haemolymph and glycogen levels were determined in the various body parts of the Helix aspersa snail after feeding lettuce ad libitum and after various periods of starvation. To characterize the effect of starvation on nucleotidase activity, enzyme assays were performed on membranes of the nervous ganglia and digestive gland. Results demonstrated the maintenance of the haemolymph glucose concentration for up to 30 days of starvation, probably due to the consumption of glycogen from the mantle. In the nervous ganglia, depletion of glycogen occurs progressively during the different periods of starvation. No significant changes were observed on ATP and ADP hydrolysis in the membranes of nervous ganglia and no alterations in Ca2+ -ATPase and Mg2+ -ATPase occurred in the membranes of the digestive gland of H. aspersa during the different periods of starvation. Although there were no changes in the enzyme activities during starvation, they could be modulated by effectors in situ with concomitant changes in products/reactants during starvation.

Topics: Adenosine Triphosphatases; Analysis of Variance; Animals; Blood Glucose; Brazil; Calcium; Digestive System; Ganglia, Invertebrate; Glycogen; Helix, Snails; Hemolymph; Nucleotidases; Starvation

The effects of short-term food deprivation (7 days) and refeeding (2 days) on different biochemical and neuroendocrine parameters were studied in tench. A 7-days fast resulted in a significant reduction of plasma glucose and glycogen hepatic content, supporting the key role of liver glycogen as energy depot for being consumed during fasting. The rapid recovery of normal values of blood glucose and glycogen stores by refeeding indicates a rapid replenishment of liver glycogen stores. The short-term starvation decreased circulating thyroid hormones (both T3 and T4) and T4 release from thyroid, supporting an interaction between nutritional state and thyroid function in tench. All these metabolic and hormonal changes were partial or totally reversed under refeeding conditions. An increase in hypothalamic content of norepinephrine and dopamine was found in fasted fish. This result might be a consequence of stress induced by starvation.

Topics: Analysis of Variance; Animals; Blood Glucose; Body Weight; Catecholamines; Cyprinidae; Dopamine; Eating; Epinephrine; Glucose; Glycogen; Hypothalamus; Liver; Norepinephrine; Organ Size; Starvation; Thyroid Gland; Thyroid Hormones; Thyroxine; Triiodothyronine

Patients with malnutrition are susceptible to infection. Polymorphonuclear neutrophils (PMNs) are the major effector of the nonspecific immune response in host resistance to infection. Dietary restriction may impair PMN-mediated immunity in the peritoneal cavity by reducing PMN exudation, adhesion molecule expression on PMNs, and chemokine production.. Randomized study of murine glycogen-induced peritonitis with dietary restriction.. University research laboratory.. Male C57BL/6J mice.. Mice (N = 204) were assigned to ad libitum, moderate, and severe diet-restricted groups receiving mouse chow ad libitum (132 g/kg, 66 g/kg, and 33 g/kg daily for 7 days, respectively). After dietary restriction with or without 1 day of refeeding, mice were administered glycogen intraperitoneally to induce cell exudation.. CD11b, CD18, and CD62L expressions on circulating PMNs, phagocytosis, and reactive oxygen intermediate production by exudative PMNs were measured after glycogen installation. The levels of PMN-specific chemokine, macrophage inflammatory protein 2 (MIP-2), in peritoneal lavage fluid were also measured. These parameters were measured after glycogen installation in the refeeding experiment.. Seven days of dietary restriction decreased CD11b/CD18 expression on circulating PMNs, MIP-2 levels in peritoneal lavage fluid, and subsequent PMN exudation into the peritoneal cavity early in peritonitis. Both CD11b and CD18 expression on circulating PMNs and MIP-2 levels correlated significantly with numbers of exudative PMNs. Seven days of dietary restriction also impaired phagocytosis, while up-regulating reactive oxygen intermediate production by exudative PMNs. Only 1 day of ad libitum refeeding normalized CD11b/CD18 expression with PMN exudation into the peritoneal cavity.. Short-term dietary restriction impairs PMN exudation into local inflammatory sites in murine peritonitis by reducing CD11b/CD18 expression and MIP-2 production. Even brief nutritional replenishment in diet-restricted patients may improve host defense via restoring these PMN functions and chemokine production at local inflammatory sites.

Topics: Animals; CD18 Antigens; Chemokine CXCL2; Chemokines; Glycogen; Immune Tolerance; L-Selectin; Macrophage-1 Antigen; Male; Mice; Mice, Inbred C57BL; Neutrophils; Peritoneal Lavage; Peritonitis; Phagocytosis; Starvation

Female Aedes aegypti of small and large body sizes were fed ad libitum from eclosion with eight different concentrations of sucrose from 0.1% to 50%; females were also starved with access to water. For each experiment we determined the survivorship of such populations. The 90%, 50%, 10%, and maximal survivorships followed linear regressions with the logarithm of the sucrose concentration. For each condition we measured the extent of synthesis of glycogen and lipid reserves. There was a critical sucrose concentration of 0.5% for both size classes: lower concentrations were of no nutritive effect, and all higher concentrations extended survivorship and allowed reserve synthesis. With respect to the teneral value, and normalized for body size, the maximal amounts of glycogen increased 2-3-fold within one week, whereas lipogenesis increased 3-5-fold requiring two weeks. Solid sugar cubes could also be utilized as long as drinking water was available, but synthesis of additional reserves failed. Flight mill experiments revealed the temporal flight pattern, its maturation after eclosion, and the maximal flight performances. Flights shorter than 1000 m per female per night were considered as low activities, whereas flights lower than 1000 m represented strong vigorous flights. Maximal distances were from 11-18 km/female/night. Periods of continuous flights lasted between 2-9 hr per female (mean 2.2 hr). Maximal flight performances were gradually reached within the first and third day of eclosion. Mean caloric energy consumption during flight was 33% to 44% of the pre-flight glycogen, accompanied by lipid reductions of 9%. Evidently, feeding on carbohydrates allows extended flight activities of this species and is essential for survival in the absence of blood meals.

Topics: Aedes; Animals; Biometry; Body Constitution; Energy Metabolism; Female; Flight, Animal; Glycogen; Lipid Metabolism; Movement; Regression Analysis; Starvation; Survival Analysis

Dogwhelks Nucella lapillus feed mainly on mussels and barnacles, and may experience periods of starvation. We report effects of nutritional state and prey type on the survival, growth, cadmium (Cd) accumulation, metallothionein (MT) induction and glycogen stores in N. lapillus exposed to Cd in water. Adult dogwhelks, with similar shell length (30.0+/-1.5 mm), were either starved or fed to satiation with barnacles Semibalanus balanoides, mussels Mytilus edulis or Cd-dosed M. edulis, and kept in filtered natural seawater (< 0.01 microg Cd 1(-1)) or Cd-contaminated (400 microg Cd 1(-1)) seawater for 80 days. Mortality and individual growth rate were determined. Cd, MT and glycogen were measured in different tissues. Prolonged starvation and exposure to Cd significantly reduced the survivorship of N. lapillus, but feeding could help dogwhelks to combat Cd toxicity and minimise mortality. Extended starvation also caused tissue wastage, leading to higher concentrations of Cd and MT in tissues, whereas fed animals increased in weight and had lower Cd and MT concentrations because of the tissue dilution effect. Prey type significantly affected growth rate of dogwhelks and indirectly influenced Cd accumulation, MT induction and glycogen stores. Eating mussels promoted better growth and higher glycogen reserves than eating barnacles. Individual growth rate decreased with increasing Cd accumulation. Cd-exposed survivors grew faster and consumed more than control animals, implying that these survivors may have better fitness and greater tolerance to Cd toxicity. The use of growth, condition index, MT and glycogen as biomarkers of environmental pollution are discussed. These results indicate a need to incorporate biological data including growth (or at least condition index) and prey type into biomonitoring programmes to allow sound interpretation.

Topics: Animals; Body Weight; Cadmium; Environmental Exposure; Food Chain; Glycogen; Metallothionein; Mollusca; Nutritional Status; Predatory Behavior; Starvation; Tissue Distribution; Water Pollutants, Chemical

This study aims at investigating the possible beneficial effect of succinic acid dimethyl ester (SAD), injected intraperitoneally (5.0 micromol/g body wt.), upon the metabolic and hormonal response to a 60 min exercise in both fed and overnight starved rats. In fed rats, the injection of SAD minimized the fall in plasma D-glucose concentration, and the increase in plasma lactate, beta-hydroxybutyrate, free fatty acid and glycerol concentrations, otherwise provoked by exercise. SAD, however, failed to prevent the decrease in plasma insulin concentration and liver glycogen content caused by exercise. Starved rats displayed lower plasma D-glucose and insulin concentrations and higher plasma beta-hydroxybutyrate and free fatty acid concentrations than fed rats. The body weight, liver weight and paraovarian fat weight, as well as the glycogen content of both liver and heart were also decreased in the starved rats. In the latter animals, the injection of SAD again opposed the exercise-induced increase in plasma beta-hydroxybutyrate, free fatty acid and glycerol concentrations, and again failed to prevent the more modest decreases in plasma insulin concentration and liver glycogen content caused by exercise in the starved, as distinct from fed rats. These findings suggest that, independently of any obvious change in plasma insulin concentration, SAD minimizes the exercise-induced mobilization and enhanced utilization of endogenous nutrients, especially fatty acids and glycerol produced by hydrolysis of triglycerides in adipose tissue, presumably through its capacity to act as an oxidizable nutrient in various cell types and as a gluconeogenic precursor in hepatocytes.

Topics: 3-Hydroxybutyric Acid; Animals; Blood Glucose; Body Weight; Fatty Acids; Female; Glycerol; Glycogen; Heart; Hormones; Insulin; Lactic Acid; Liver; Organ Size; Ovary; Physical Conditioning, Animal; Rats; Rats, Wistar; Starvation; Succinates

The starved-to-fed transition is accompanied by rapid glycogen deposition in skeletal muscles. On the basis of recent findings [Bräu, Ferreira, Nikolovski, Raja, Palmer and Fournier (1997) Biochem. J. 322, 303-308] that during recovery from exercise there is a shift from a glucose 6-phosphate/phosphorylation-based control of glycogen synthesis to a phosphorylation-based control alone, this paper seeks to establish whether a similar shift occurs in muscle during re-feeding after starvation in the rat. Chow re-feeding after 48 h of starvation resulted in glycogen deposition in all muscles examined (white, red and mixed quadriceps, soleus and diaphragm) to levels higher than those in the fed state. Although the early phase of re-feeding was associated with increases in glucose 6-phosphate levels in all muscles, there was no accompanying increase in the fractional velocity of glycogen synthase except in the white quadriceps muscle. This finding, together with the observation that the fractional velocity of glycogen synthase in most muscles was already high in the starved state, suggests that in the initial phase of glycogen deposition the phosphorylation state of the enzyme may be adequate to support net glycogen synthesis. In the later phase of re-feeding, the progressive decrease in the fractional velocity of glycogen synthase in association with a decrease in the rate of glycogen deposition suggests that glycogen synthesis is controlled primarily by changes in the phosphorylation state of glycogen synthase. In conclusion, this study suggests that there is a temporal shift in the site of control of glycogen synthesis as glycogen deposition progresses during re-feeding after starvation.

Topics: Animals; Food; Glycogen; Glycogen Synthase; Male; Muscles; Phosphorylases; Rats; Rats, Wistar; Starvation

In immature female rats (21 days), a restricted diet (50% of the daily normal intake for 25 days) interrupts sexual development, leaving animals in a state of sexual immaturity. Food restriction does not affect the use of glycogen in uteri isolated and increases 14CO2 production from U14C-glucose in relation to animals receiving normal feeding that reach sexual maturity. Indomethacin and acetylsalicylic acid stop the increase of glucose metabolism produced by underfeeding, without affecting the uteri of rats receiving normal feeding. The addition of PGE2 and PGF2alpha changes the inhibitory effect of indomethacin. Nordihydroguaiaretic acid produces the opposite effect, increasing glucose metabolism only in uteri isolated from immature animals. These results show that immature animals have a higher glucose metabolism if compared to mature rats. The restricted diet, which slows down sexual maturity, keeps this parameter high due to the influence of some eicosanoids.

Topics: Age Factors; Animals; Carbon Dioxide; Cyclooxygenase Inhibitors; Female; Glucose; Glycogen; Indomethacin; Lipoxygenase Inhibitors; Masoprocol; Prostaglandins; Rats; Rats, Wistar; Sexual Behavior, Animal; Starvation; Uterus

The nutritional reserves and body weight of autogenous and anautogenous strains of Culex tarsalis Coquillett were determined for 4th instars, pupae, females, and males. Starvation tolerance and survivorship of adult females and males also were studied. The autogenous individuals contained significantly greater amounts of total lipids (except the total lipids in 4th instars), total carbohydrates, glycogen, and total proteins, which resulted in a heavier mean body weight of autogenous than anautogenous mosquitoes (except the fresh weight in pupae). Results of the body fluid coefficient determination were inconclusive. Nutritional reserves in the immature stages, especially the pupal stage, were significantly greater (except the total proteins in 4th instars and female adults) than those in the adult stage. There were no significant differences in median longevity between autogenous and anautogenous females, and between autogenous and anautogenous males, provided with distilled water alone after emergence. The median longevity of females and males was significantly different in both autogenous and anautogenous strains. Our findings strongly indicate a relationship between autogenous reproduction and differences in nutritional reserves of autogenous and anautogenous strains.

Topics: Animals; Body Weight; Carbohydrates; Culex; Female; Glycogen; Lipids; Male; Proteins; Starvation

To study the role of glucokinase (GK) in the control of glucose metabolism in the liver, transgenic mice were generated in which GK was overexpressed under control of the P-enolpyruvate carboxykinase gene promoter. Whereas the expression of the GK gene in starved control mice was blocked, this promoter was able to direct the expression of the enzyme to the liver of starved transgenic mice. Furthermore, starved transgenic mice showed levels of GK activity fourfold higher than those of starved control and similar to those of fed control. This activation of GK led to an increase in the intracellular concentration of glucose 6-phosphate, which was also related to an induction of glycogen accumulation. In addition, L-pyruvate kinase (L-PK) activity increased in transgenic mice, which when starved showed similar levels of activity to control fed mice. The induction of L-PK caused an increase in the hepatic lactate concentration. Furthermore, hepatocytes in primary culture from transgenic mice incubated with 20 mM glucose produced levels of lactate threefold higher than controls, but no difference was noted when the hepatocytes from control and transgenic mice were incubated with 2 mM glucose. These results demonstrated in vivo that the activation of GK is a rate-limiting step in the induction of glycolysis and glycogen synthesis. These changes in liver glucose metabolism led to a marked reduction in blood glucose (30%) and insulin (40%) concentrations. Furthermore, transgenic mice showed lower levels of blood glucose after an intraperitoneal glucose tolerance test, indicating that GK overexpression caused an increase in blood glucose disposal by the liver. All these findings show the key role of liver GK in the control of whole-body glucose homeostasis.-Ferre, T., Riu, E., Bosch, F., Valera, A. Evidence from transgenic mice that glucokinase is rate limiting for glucose utilization in the liver.

Topics: Animals; Cells, Cultured; Enzyme Activation; Gene Expression; Glucokinase; Glucose; Glucose-6-Phosphate; Glucosephosphates; Glycogen; Kinetics; Lactates; Lactic Acid; Liver; Mice; Mice, Transgenic; Phosphoenolpyruvate Carboxykinase (GTP); Promoter Regions, Genetic; Pyruvate Kinase; Recombinant Fusion Proteins; Starvation

This study is the first report on the multiexponential T2 relaxation of the 13C-1 carbon of glycogen. In contrast to T1 relaxation, which does not display observable multiexponential decay behavior, T2 relaxation is described by a continuous distribution of T2 times. Changes in molecular weight and sample viscosity, which affect the overall mobility of the glycogen particle have little influence on T1 and T2 relaxation times. This is in contradiction with earlier results that T2 is dominated by the overall motion of the glycogen particles [L.-H. Zang Biochemistry 29, 6815-6820 (1990)]. T1 depends strongly on the external field Bo and is almost temperature independent in the range 23-37 degrees C whereas T2 is field independent and varies appreciably with temperature. The experimental T1 and T2 relaxation data are shown to be consistent with existing theoretical models for relaxation, suitably modified to include a distribution of correlation times for the internal motions. The presence of fast decaying components (short T2) in the FID implies broad line components in the frequency spectrum and the corresponding need to appropriately set the integration limits for the quantification of the glycogen peak.

Topics: Animals; Carbon Isotopes; Chromatography, Gel; Dextrins; Glucose; Glycogen; Liver; Magnetic Resonance Spectroscopy; Male; Models, Chemical; Molecular Biology; Molecular Weight; Rats; Rats, Wistar; Starvation; Sucrose; Temperature; Viscosity

We have performed a comparative analysis of the effects of age of reproduction on the biochemical (protein, lipid, and glycogen content) and stress resistance (ability to survive starvation, desiccation, and exogenous paraquat) parameters on 10 sister lines of five different Drosophila strains. Four pairs of these sister lines were selected under different regimens for either early or delayed reproduction; the fifth pair was maintained in a nonselected state and served as the baseline strain to which all others were compared. It is generally accepted that the early regimens give rise to short-lived phenotypes, whereas the delayed regimens give rise to long-lived phenotypes. Our results suggest that a mechanism involving lipid and starvation resistance is not operative in our long-lived strains. In addition, a mechanism involving glycogen content and desiccation resistance is only weakly supported. Finally, there is strong support for a mechanism that gives rise to enhanced paraquat resistance and therefore may involve regulatory changes in the pattern of ADS gene expression. In addition, the 15-day early age of reproduction regimen (M type) shows qualitatively similar responses to that of the late age at reproduction regimen (L type). These results suggest that correlations between biochemical traits and longevity must be interpreted with caution. We discuss possible reasons for these results, including the possibility of multiple mechanisms, each leading to a different extended longevity phenotype.

Topics: Animals; Body Weight; Drosophila melanogaster; Female; Glycogen; Lipid Metabolism; Longevity; Paraquat; Proteins; Reproduction; Starvation; Water

Physiological insulin stimulation (induced by re-feeding) in late (19 to 20 days) pregnancy in the rat led to only partial reversal of starvation-induced increases in circulating fatty acid concentrations. The impaired suppression of adipose tissue lipolysis was associated with a clear attenuation of the activation of PDHa activity in oxidative skeletal muscles (diaphragm, soleus and adductor longus) in response to physiological insulin stimulation. In contrast, effects of late pregnancy to suppress glucose utilization were only modest in oxidative skeletal muscles, where a predominate fate of glucose under physiological insulin stimulation is glycogen formation. The ability of the pregnant rat to sustain glycogen repletion during physiological insulin stimulation was retained. Glucose utilization by the heart, which in virgin rats is particularly sensitive to increases in lipid-fuel supply and oxidation, bore a significant inverse relationship with the plasma fatty acid concentrations in late-pregnant rats. We conclude that an elevation in circulating fatty acid concentrations in late pregnancy provokes changes in glucose utilization by cardiac and skeletal muscle which are consistent with the operation of the glucose-fatty acid cycle. Importantly, these effects pertain under physiological hyperinsulinaemia. The relative insensitivity of glucose utilization by oxidative skeletal muscle to late pregnancy under conditions of physiological insulin stimulation presumably reflects the predominant use of glucose as a substrate for glycogen synthesis rather than as an energy substrate.

Topics: Animals; Deoxyglucose; Fatty Acids; Female; Food; Glucose; Glycogen; Insulin; Muscles; Myocardium; Oxidation-Reduction; Pregnancy; Pregnancy, Animal; Pyruvate Dehydrogenase Complex; Rats; Rats, Wistar; Starvation

The effect of a period of starvation followed by refeeding on skeletal muscle glycogen was investigated by the use of double-labelled radioactive glucose precursors in rats. Skeletal muscle glycogen, which is not depleted to anything like the extent of liver glycogen, shows a remarkable stability with respect to its overall molecular size distribution during starvation and subsequent refeeding. The experiments also indicate that there is a control mechanism in muscle tissue enabling the synthesis of lysosomal glycogen to be switched off during the initial part of the refeeding process. The results emphasise the inadequacy of the Cori cycle and a modified version is proposed.

Topics: Animals; Carbon Radioisotopes; Eating; Glucose; Glycogen; Liver; Liver Glycogen; Muscles; Organ Specificity; Radioisotope Dilution Technique; Rats; Rats, Wistar; Starvation; Tritium

We have previously reported that fatty liver is easily induced in a novel experimental animal, Suncus murinus (suncus) by withholding food, and that apolipoprotein B (apo B) is not actively synthesized in the liver. In the present paper we describe the effect of starving and refeeding on lipid and lipoprotein metabolism in suncus, in order to explore the mechanisms of induction of fatty liver by starving and of its improvement by refeeding. Starvation induced increase in triglyceride content and decrease in glycogen content of the liver. Although the glycogen content returned to the level before starvation at 12 h after refeeding, the triglyceride content decreased gradually but did not reach the prestarvation level even at 24 h after refeeding in suncus. Plasma lipids, glucose, and insulin levels were decreased by starvation and returned to the levels before starvation between 8 and 24 h after refeeding. On the other hand, the plasma levels of free fatty acid and ketone bodies were elevated significantly by starvation and decreased rapidly by refeeding. These responses to starvation and refeeding, except for the change in hepatic triglyceride, are in common with other experimental animals, suggesting that there are no abnormalities in glucose metabolism or in fatty acid metabolism in suncus. In conclusion, the fatty liver induced by starvation in suncus may be caused by impaired triglyceride transport out of the liver, for which apolipoprotein B is mostly responsible, as reported previously.

Topics: Animals; Blood Glucose; Cholesterol; Eulipotyphla; Food; Glycogen; Insulin; Ketone Bodies; Lipid Metabolism; Liver; Male; Phospholipids; Starvation; Triglycerides

Glucose utilization indices (GUI) were measured in vivo in conjunction with active pyruvate dehydrogenase complex (PDH(a) and glycogen synthase (GS) activities in fast-twitch skeletal muscles [extensor digitorum longus (EDL), tibialis anterior and gastrocnemius] of late-pregnant rats and age-matched virgin control rats in the fed state, after 24 h starvation and at 2 h after re-feeding with standard laboratory chow ad libitum after 24 h starvation. As demonstrated previously [Holness and Sugden (1990) Biochem. J 277, 429-433], GUI values of fast-twitch skeletal muscles of virgin rats were low in the fed ad libitum and the 24 h-starved states, but dramatically increased after subsequent chow re-feeding. GUI values of fast-twitch skeletal muscles of late-pregnant rats were also low in the fed and starved states and were increased by re-feeding, but the increase in GUI values elicited by re-feeding was greatly attenuated. PDHa activities in EDL, tibialis anterior and gastrocnemius in the fed state were unaffected by late pregnancy, and skeletal-muscle PDHa activities were decreased after 24 h of starvation in both groups. Whereas re-feeding of virgin rats with standard diet for 2 h restored PDHa activities in fast-twitch skeletal muscles to values for rats continuously fed ad libitum, PDHa activities in fast-twitch skeletal muscles of late-pregnant rats, although increased in response to re-feeding, remained considerably less than the corresponding fed ad libitum values after 2 h of re-feeding. In contrast, neither skeletal-muscle GS re-activation nor rates of skeletal-muscle glycogen deposition after re-feeding were markedly affected by late pregnancy. The results are discussed in relation to the specific targeting of individual pathways of glucose disposal in fast-twitch skeletal muscles during re-feeding in late pregnancy.

Topics: Animals; Blood Glucose; Fatty Acids, Nonesterified; Female; Food; Glucose; Glycogen; Glycogen Synthase; Insulin; Ketone Bodies; Muscles; Phosphorylation; Pregnancy; Pregnancy, Animal; Pyruvate Dehydrogenase Complex; Rats; Rats, Wistar; Starvation

Tumor necrosis factor-alpha (TNF-alpha) stimulates hepatic lipogenesis. Therefore, it could play a role in the control of ketogenesis. To test this hypothesis, we measured simultaneously free fatty acids (FFA; [1-13C]palmitate) and ketone body (KB; [3,4-13C2]acetoacetate) kinetics, before and after intraperitoneal injection of saline or TNF-alpha, in postabsorptive rats or rats starved for 24 h. In both groups of rats, TNF-alpha injection did not modify insulinemia and induced a moderate increase of FFA concentrations and appearance rates (P < 0.05). Despite increased FFA availability, ketogenesis was impaired after TNF-alpha injection, as shown by lower KB concentrations and appearance rates; this effect was more important in postabsorptive than in starved rats. The percentage of FFA flux used for ketogenesis was decreased by TNF-alpha in the postabsorptive group (P < 0.05) and starved (P < 0.05) rats. In both groups, maximal liver acetyl-coenzyme A carboxylase activity and estimated phosphorylation state were not modified by TNF-alpha injection, but hepatic concentrations of citrate were increased (P < 0.05). This increased citrate level could be related to a mobilization of glucose stored as glycogen since liver glycogen was decreased by TNF-alpha injection (P < 0.05). In conclusion, TNF-alpha injection in rats decreased hepatic ketogenesis. This action could be related to an increased mobilization and utilization of carbohydrate stores.

Topics: Absorption; Animals; Fatty Acids, Nonesterified; Glycogen; Ketone Bodies; Kinetics; Liver; Male; Rats; Rats, Sprague-Dawley; Starvation; Tumor Necrosis Factor-alpha

We have studied the changes in concentration of glycogen, glucose and the bisphosphorylated sugars, glucose 1,6-P2 and fructose 2,6-P2, in several rat brain regions during 72 h of starvation. The animals were killed by focused microwave irradiation. The activities of glycogen metabolizing enzymes in the different areas were measured. A large decrease in glycogen and glucose concentration was observed in all areas. The concentrations of bisphosphorylated sugars changed, suggesting that an increase in glycolysis could take place at the beginning of starvation, with blood glucose as a major energy source. Differences in metabolite concentration before starvation disappeared after 72 h. The activities of glycogen synthase, glycogen phosphorylase and glycogen phosphorylase kinase were similar in all areas, and they did not change during starvation.

Topics: Animals; Brain; Fructosediphosphates; Glucose; Glucose-6-Phosphate; Glucosephosphates; Glycogen; Glycogen Synthase; Male; Microwaves; Phosphorylase Kinase; Phosphorylases; Rats; Rats, Sprague-Dawley; Starvation

The pattern of glycogen deposition in individual cardiothoracic and skeletal muscles in response to oral and intraperitoneal glucose administration was examined in 40 h-starved rats. Rates of glycogen synthesis were consistently higher in oxidative muscles than in non-oxidative muscles. Intragastric ethanol administration was associated with an impaired glycaemic response and the almost total abolition of glycogen deposition in oxidative muscles in response to oral or intraperitoneal glucose re-feeding. This effect was dose-dependent and differential, in that ethanol produced no equivalent impairment in glycogen deposition in non-oxidative muscles. Ethanol treatment also selectively promoted glycogenolysis in oxidative muscles in the starved state. There was positive correlation (P < 0.001) between the decrease in glycogen levels in soleus and diaphragm muscles in response to increasing ethanol doses and blood glucose and lactate concentrations after intraperitoneal glucose administration, implying that the basis for the impairment in glycogen synthesis may be diminished glucose availability. The mechanism whereby ethanol may differentially compromise carbohydrate metabolism in oxidative muscles is discussed.

Topics: Animals; Dose-Response Relationship, Drug; Ethanol; Glucose; Glycogen; Insulin; Male; Muscles; Rats; Rats, Wistar; Starvation

1. Starvation of rats for 40 hr decreased the body weight, liver weight and blood glucose concentration. The hepatic and skeletal muscle glycogen concentrations were decreased by 95% (from 410 mumol/g tissue to 16 mumol/g tissue) and 55% (from 40 mumol/g tissue to 18.5 mumol/g tissue), respectively. 2. Fine structural analysis of glycogen purified from the liver and skeletal muscle of starved rats suggested that the glycogenolysis included a lysosomal component, in addition to the conventional phosphorolytic pathway. In support of this the hepatic acid alpha-glucosidase activity increased 1.8-fold following starvation. 3. Refeeding resulted in liver glycogen synthesis at a linear rate of 40 mumol/g tissue per hr over the first 13 hr of refeeding. The hepatic glycogen store were replenished by 8 hr of refeeding, but synthesis continued and the hepatic glycogen content peaked at 24 hr (approximately 670 mumol/g tissue). 4. Refeeding resulted in skeletal muscle glycogen synthesis at an initial rate of 40 mumol/g tissue per hr. The muscle glycogen store was replenished by 30 min of refeeding, but synthesis continued and the glycogen content peaked at 13 hr (approximately 50 mumol/g tissue). 5. Both liver and skeletal muscle glycogen synthesis were inhomogeneous with respect to molecular size; high molecular weight glycogen was initially synthesised at a faster rate than low molecular weight glycogen. These observations support suggestions that there is more than a single site of glycogen synthesis.

Topics: Animals; Body Weight; Food; Glycogen; Kinetics; Liver; Male; Molecular Weight; Muscles; Organ Size; Rats; Rats, Inbred Strains; Starvation

Submandibular glands of rats injected with NaF solution (10 mg F-/kg body weight) were analysed for glycogen content and phosphorylase activity after various time intervals. In contrast to what has been reported for the liver, sodium fluoride caused increased glycogen content. Phosphorylase (a and total) activity was not affected, suggesting a different mechanism of action of F- in the submandibular gland. In vivo experiments demonstrated stimulation of glycogenesis.

Topics: Animals; Drug Administration Schedule; Glycogen; Male; Phosphorylase a; Rats; Rats, Inbred Strains; Sodium Fluoride; Starvation; Submandibular Gland; Time Factors

The effects of selenium (Se) deficiency on urinary ketone body excretion in starved rats were examined. Rats were fed a basal diet which was Se-deficient (Se content: 0.011 micrograms/g) or a Se-adequate diet (the basal diet supplemented with 0.1 micrograms Se/g as sodium selenite). On the 11th and 22nd week of the feeding period, Se-deficient status in rats fed the basal diet was verified by the observation that the Se content and glutathione peroxidase activity in their plasma, erythrocytes, and livers were markedly lowered. On the 4th, 6th, 11th, 15th, and 22nd week, the rats were starved for 48 h and the urinary excretion of ketone bodies (acetoacetate (AcAc) and 3-hydroxybutyrate (3-OHBA)), urea, and creatinine were examined. The urinary excretion of AcAc and 3-OHBA during the second 24 h of the 48-h starvation period were markedly higher in the Se-deficient rats than in the Se-adequate rats for all weeks examined, while the urine volume and the excretion of urea and creatinine were similar in the Se-deficient and Se-adequate rats, irrespective of the feeding period and the number of hours of starvation. On the 22nd week, the plasma ketone body levels were also determined and significantly higher plasma 3-OHBA levels were observed in the Se-deficient rats than in the Se-adequate rats 72 h after starvation began. These results indicate that Se deficiency causes an increase of urinary ketone body excretion in starved rats and that the increase is ketone-specific with no changes in major urinary profiles.

Topics: 3-Hydroxybutyric Acid; Acetoacetates; Animals; Blood Glucose; Body Weight; Creatinine; Erythrocytes; Glutathione Peroxidase; Glycogen; Hydroxybutyrates; Ketone Bodies; Liver; Male; Rats; Rats, Inbred Strains; Selenium; Starvation; Urea

Attempts have been made to determine the reason for the depletion of glycogen reserves in tumour-bearing rats. The possible roles of anorexia, competition for glucose by the tumour, and lack of hormonal control of glycogen biosynthesis have been investigated. The glycogen content of the liver, skeletal muscle, and brain, and the levels of glucose and the hormones corticosterone, insulin, and glucagon were determined in healthy rats which had been starved for various periods and in tumour-bearing rats carrying the fast-growing Zajdela ascites hepatoma or the slow-growing solid hepatoma 27. It was found that towards the terminal stages of tumour development there was an increase in the content of corticosterone and glucagon in the blood serum and also an increase in the glycogen reserves in skeletal muscle and brain despite the presence of hypoglycaemia and hypo-insulinaemia. There was at this time a sharp fall in the level of liver glycogen. It is shown that neither anorexia nor excessive competition for glucose by the tumour were the main reasons for liver glycogen depletion and hypoglycaemia. A strong correlation was observed, however, between the occurrence of anaemia and the loss of liver glycogen, which suggests that the former may be an important factor in the changes in host tissue observed in response to tumour growth.

Topics: Animals; Blood Glucose; Brain; Corticosterone; Glucagon; Glycogen; Hematocrit; Insulin; Liver Glycogen; Liver Neoplasms, Experimental; Male; Muscles; Rats; Rats, Inbred Strains; Reference Values; Starvation; Time Factors

1. The metabolic patterns in the livers of rats of the Wistar, August and Wag strains were evaluated 4, 8, 12 and 24 hr after food withdrawal. 2. In the fed state (4 hr) there were large differences in the liver's contents of ATP, phosphate potential values, glycogen contents and blood FFA. These distinctions disappeared in the fasted state (12 hr). 3. There are large differences between the strains in the dynamics of transition of the liver metabolic patterns from the fed to the starved states. 4. The results obtained show that the three strains of the laboratory animals strongly differ in the organization of the liver energy metabolism.

Topics: Acyl Coenzyme A; Adenine Nucleotides; Animals; Glycogen; Kinetics; Liver; Male; Rats; Rats, Inbred Strains; Species Specificity; Starvation

We investigated the extent to which increases in glucose utilization indices (GUIs) in individual skeletal muscles during chow re-feeding after 6 h, 24 h or 48 h starvation are related to the antecedent duration of starvation. Chow re-feeding after either acute or prolonged starvation led to an increase in glucose disposal by the muscle mass. Glucose intolerance after prolonged starvation was not associated with lower values of GUI in skeletal muscle. In both working and non-working muscles, the increment in GUI during the first 2 h of re-feeding was less after acute than after prolonged starvation. In non-working muscles the differential responses to re-feeding were due to higher GUI values after re-feeding rather than lower pre-prandial GUI values. Therefore the contribution of non-working muscles to glucose clearance is higher as the antecedent period of starvation is extended. Rates of glycogen deposition in non-working muscles after refeeding were similar to absolute values of GUI, and a strong relationship existed between measured GUI values and rates of glycogen deposition.

Topics: Animals; Blood Glucose; Deoxyglucose; Eating; Fasting; Female; Glucose; Glycogen; Insulin; Muscles; Organ Specificity; Rats; Rats, Inbred Strains; Starvation; Time Factors

Glycogen synthase (GS) activity was characterized in rat brown adipose tissue (BAT) and the activity was found to be much higher than that in white adipose tissue. Prolonged starvation had no effect on the active form of GS, as found in the liver and muscle. The GS activity was similar in BAT of rats housed in an animal room (21 +/- 1 degree) whether they were fed on high-carbohydrate, high-fat, or stock diets. Acclimatization of rats to cold (4 +/- 1 degree) for 2 weeks significantly increased GS activity. This increase in the cold was fivefold greater when rats were fed on high-carbohydrate diets than in control rats at room temperature fed on an identical diet. The increase was accompanied by a large accumulation of glycogen in BAT. It was concluded that GS may play an important role in BAT and may contribute to the control of blood glucose in a cold environment. Its relevance to thermogenesis requires further elucidation.

Topics: Acclimatization; Adipose Tissue, Brown; Animals; Blood Glucose; Cholesterol; Cold Temperature; Dietary Carbohydrates; Glycogen; Glycogen Synthase; Homeostasis; Male; Pyruvate Dehydrogenase Complex; Rats; Rats, Inbred Strains; Starvation; Time Factors; Triglycerides

Glucose homeostasis and fatty acid metabolism are abnormal in patients with cirrhosis. To assess the metabolic response to starvation in an animal model of cirrhosis, glycogen and fuel metabolism were characterized in rats with CCl4-induced cirrhosis studied 2 wk after 10 weekly doses of CCl4. Plasma concentrations of glucose and beta-hydroxybutyrate were not different between fed CCl4-treated and control rats, but plasma nonesterified fatty acid concentrations were higher in cirrhotic animals (0.25 +/- 0.01 vs. 0.39 +/- 0.04 mmol/L; p less than 0.05). After 12 hr of starvation, the plasma nonesterified fatty acid concentration had reached 0.58 +/- 0.04 mmol/L in CCl4-treated rats, compared with 0.38 +/- 0.04 mmol/L in control rats (p less than 0.05). The redistribution of the hepatic carnitine pool toward acylcarnitines, which is characteristic of starvation, was complete after fasting for 12 hr in the CCl4-treated rats, compared with the 24 hr required in control rats. In fed cirrhotic rats, liver glycogen content per gram liver was decreased by 64% compared with control rats (30.0 +/- 5.1 vs. 10.8 +/- 1.1 mg/gm liver wet wt; p less than 0.05). After 12-hr fasting, hepatic glycogen content had fallen to 14.3 +/- 3.9 and 4.8 +/- 0.4 mg/gm liver wet wt (p less than 0.05) in control and cirrhotic animals, respectively. To further characterize the status of glycogen metabolism in cirrhotic livers, activities of glycogen synthase and glycogen phosphorylase were determined. Hepatic active and total glycogen phosphorylase activities normalized to hepatocellular content were unaffected by CCl4 treatment, whereas total glycogen synthase activity was increased by 45%.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Carbon Tetrachloride; Carnitine; Energy Metabolism; Glycogen; Glycogen Synthase; Homeostasis; Liver; Liver Cirrhosis, Experimental; Male; Phosphorylases; Rats; Rats, Inbred Strains; Starvation

Adult Culex quinquefasciatus, maintained from emergence on sugar, were fed blood and then fed either sugar (control) or water (starving) for 7 days. Analysis of ovaries and egg rafts for protein, lipids and glycogen showed that only glycogen levels were diminished by starvation. Eggs from both control and starving females, however, were equally viable. Nonbloodfed starving females lived longer than bloodfed starving females. These results suggest that the blood meal maximizes fertility, not longevity.

Topics: Animals; Body Composition; Culex; Dietary Carbohydrates; Egg Proteins; Egg Yolk; Feeding Behavior; Female; Fertility; Glycogen; Lipids; Ovary; Oviposition; Proteins; Starvation

Female rats were mated and thyroidectomized on the same day. Some animals were kept without treatment and killed on day 12 or 21 of gestation (T). Others were subsequently treated daily with 1.8 micrograms L-T4/100 g BW for either the first 12 days and then not treated from that time until day 21 [T+T4(I+0)] or else not treated for the first 12 days and then treated from days 12-21 [T+T4(0+II)]. A final group received treatment during the entire 21-day study [T+T4(I+II)] and was used as the control. The net maternal body weight increased until day 12 of gestation in T+T4(I+II) rats, but not in T animals. On day 21 net maternal body weight was significantly lower in T and T+T4(0+II) than in T+T4(I+II) rats. Lipoprotein lipase activity in the lumbar fat pads increased from days 0 to 12 of gestation and decreased on day 21, whereas in the heart the change was in the opposite direction, and these changes were greater in T+T4(I+II) rats than in T rats. Incorporation of [U-14C]glucose administered in vivo into liver [14C]fatty acids or [14C]glycogen was significantly lower in T rats than in T+T4(I+II) on either the 12th or 21st day of gestation. The response of plasma triglyceride, glycerol, or beta-hydroxybutyrate levels to 24 h of starvation was similar in 12-day pregnant rats regardless of whether they were treated with T4, whereas on day 21 the change was greater in T+T4(I+II) or T+T4(I+0) animals than in T or T+T4(0+II) animals. Results show that maternal hypothyroidism during the first half of gestation impaired the anabolic events occurring during this phase and compromised the normal catabolic response during late gestation even when T4 treatment was restored. However, once maternal metabolic stores were built up normally during the first half of gestation, maternal hypothyroidism during late gestation did not affect the mother's normal metabolic adaptation, including the accelerated response to starvation.

Topics: Adipose Tissue; Animals; Blood Glucose; Fatty Acids; Female; Glucose; Glycogen; Hypothyroidism; Insulin; Lipoprotein Lipase; Liver; Myocardium; Pregnancy; Pregnancy Complications; Rats; Rats, Inbred Strains; Starvation; Thyrotropin; Thyroxine; Time Factors; Weight Gain

Alanine metabolism in 24 hour starved 20-day pregnant rats, following intravenously administered C14-alanine, in trace dose that does not affect the normal availability of this amino acid, has been studied. The steady state levels of alanine and glucose in blood, liver and skeletal muscle, together with the tissue glycogen, metabolites and amino acid composition pools, are given in both the maternal and foetal compartments compared with the virgin control rats. The utilization of alanine as a gluconeogenetic precursor is not increased in late pregnancy under 24-hour starvation and it depends on the lower blood substrate availability.

Topics: Administration, Oral; Alanine; Animals; Blood Glucose; Female; Fetus; Glucose; Glycogen; Liver; Liver Glycogen; Male; Muscles; Pregnancy; Pregnancy, Animal; Rats; Rats, Inbred Strains; Starvation

Topics: Animals; Eating; Glycogen; Male; Molecular Weight; Muscles; Rats; Rats, Inbred Strains; Reference Values; Starvation

Topics: Animals; Eating; Glucose; Glycogen; Hyperthyroidism; Kinetics; Muscles; Rats; Rats, Inbred Strains; Starvation

About 90% of the glycogenin in skeletal muscle extracts prepared from fed, 24-h starved or alloxan-diabetic rabbits sedimented at 140,000 x g with the glycogen/sarcovesicular fraction, from which it was released by glycogenolysis, but not by 1% SDS. Glycogenin in the glycogen/sarcovesicular fraction is therefore bound covalently to glycogen, and not associated (covalently or non-covalently) with the sarcoplasmic reticulum. The same proportion of glycogen synthase was also recovered in the glycogen/sarcovesicle fraction, was solubilised by glycogenolysis, and copurified with glycogenin to yield a heterodimer composed of a 1:1 complex between these proteins. Glycogen synthase and glycogenin are therefore present in equimolar amounts in skeletal muscle and there is an average of one glycogen synthase catalytic subunit associated with each molecule of glycogen in vivo. Glycogenin and glycogen synthase released into the muscle cytosol by degradation of glycogen did not form a complex initially, and only 50% reassociation took place after storage for several hours or overnight dialysis. This suggests that the muscle cytosol may contain a factor(s) which regulates glycogen biogenesis by modulating the association of glycogenin and glycogen synthase. Only glycogen synthase that was complexed to glycogenin was capable of elongating the primer formed by incubation of glycogenin with Mn2+ and micromolar concentrations of UDP-glucose, demonstrating the critical importance of this complex for glycogen biogenesis.

Topics: Animals; Carbon Radioisotopes; Diabetes Mellitus, Experimental; Electric Stimulation; Epinephrine; Glucosyltransferases; Glycogen; Glycogen Synthase; Glycoproteins; Kinetics; Macromolecular Substances; Molecular Weight; Muscle Proteins; Muscles; Organ Specificity; Propranolol; Rabbits; Reference Values; Starvation; Uridine Diphosphate Glucose

A gastric [U-14C]glucose load (4.8 mg/g body wt.) was delivered to unrestrained post-absorptive or 30 h-starved rats bearing peripheral and portal vein catheters and continuously perfused with [3-3H]glucose, in order to compare their metabolic and hormonal responses. In the basal state, portal and peripheral glycaemia were less in starved rats than in rats in the post-absorptive period (P less than 0.01), whereas blood lactate was similar. Portal insulinaemia (P less than 0.05) and protal glucagonaemia (P less than 0.005) were lower in starved rats, but insulin/glucagon ratio was higher in post-absorptive rats (P less than 0.005). The glucose turnover rate was decreased by starvation (P less than 0.005). After glucose ingestion, blood glucose was similar in post-absorptive and starved rats. A large portoperipheral gradient of lactate appeared in starved rats. Portal insulinaemia reached a peak at 9 min, and was respectively 454 +/- 68 and 740 +/- 65 mu-units/ml in starved and post-absorptive rats. Portal glucagonaemia remained stable, but was higher in post-absorptive rats (P less than 0.05). At 60 min after the gastric glucose load, 30% of the glucose was delivered at the periphery in both groups. The total glucose appearance rate was higher in starved rats (P less than 0.05), as was the glucose utilization rate (P less than 0.05), whereas the rate of appearance of exogenous glucose was similar. This was due to a non-suppressed hepatic glucose production in the starved rats, whereas it was totally suppressed in post-absorptive rats. At 1 h after the glucose load, the increase in both liver and muscle glycogen concentration was greater in starved rats. Thus short-term fasting induces an increased portal lactate concentration after a glucose load, and produces a state of liver insulin unresponsiveness for glucose production, whereas the sensitivity of peripheral tissues for glucose utilization is unchanged or even increased. This might allow preferential replenishment of the peripheral stores of glycogen.

Topics: Animals; Blood Glucose; Female; Food; Gastrostomy; Glucagon; Glucose; Glycogen; Insulin; Kinetics; Lactates; Lactic Acid; Liver; Muscles; Portal Vein; Rats; Starvation

In the fed state, hyperthyroidism increased glucose utilization indices (GUIs) of skeletal muscles containing a lower proportion of oxidative fibres. Glycogen concentrations were unchanged, but active pyruvate dehydrogenase (PDHa) activities were decreased. Hyperthyroidism attenuated the effects of 48 h of starvation to decrease muscle GUI. Glycogen concentrations and PDHa activities after 48 h of starvation were low and similar in euthyroid and hyperthyroid rats. The increase in glucose uptake and phosphorylation relative to oxidation and storage in skeletal muscle induced by hyperthyroidism may contribute to increased glucose re-cycling in the fed hyperthyroid state and to glucose turnover in the starved hyperthyroid state.

Topics: Animals; Blood Glucose; Fatty Acids, Nonesterified; Female; Food; Glucose; Glycogen; Hyperthyroidism; Insulin; Muscles; Oxidation-Reduction; Phosphorylation; Pyruvate Dehydrogenase Complex; Pyruvates; Pyruvic Acid; Rats; Rats, Inbred Strains; Starvation; Triiodothyronine

LY177507 is representative of a series of phenacyl imidazolium compounds that cause marked lowering of blood glucose levels in animal models of noninsulin-dependent diabetes mellitus. In studies conducted with isolated rat hepatocytes, LY177507 inhibited net glucose production from a variety of substrates, inhibited glycolysis from exogenous glucose and endogenous glycogen, inhibited glycogenolysis, and stimulated glycogenesis. These effects of LY177507 appear to be the consequence of activation of glycogen synthase and inactivation of glycogen phosphorylase. In vivo studies with normal fed rats demonstrated a decrease in blood glucose, an increase in hepatic glycogen stores, and an inactivation of glycogen phosphorylase. Phenacyl imidazolium compounds appear to lower blood glucose levels and affect hepatic carbohydrate metabolism by a mechanism unlike other known hypoglycemic compounds.

Topics: Animals; Eating; Gluconeogenesis; Glycogen; Glycogen Synthase; Hypoglycemic Agents; Imidazoles; Lactates; Liver; Male; Phosphorylases; Rats; Rats, Inbred Strains; Starvation

Erythropoietic responses of fed and starved species of teleosts, viz., Clarias batrachus and Heteropneustes fossilis, to human urinary erythropoietin and thyroxine have been examined. The effects of these hormones on energy reserves have also been evaluated. Twenty-four C. batrachus were divided into two groups: half were fed regularly; the remaining fish were starved 20 days. On the 21st day each group was further divided into three subgroups of four each and received either saline, thyroxine (8 micrograms), or erythropoietin (6 IU) over 4 consecutive days. The experimental protocol was identical for H. fossilis; however, for H. fossilis two identical studies were conducted approximately 1 year apart. A decline in the rate of erythropoiesis and a stimulatory response to human urinary erythropoietin followed starvation in both species of teleosts. In addition, erythropoietin had a pronounced effect on hepatic glycogenesis of fed H. fossilis and stimulated erythropoiesis in the fed teleosts of both species. Prolonged starvation drastically depleted hepatic glycogen in C. batrachus. In contrast, it had no effect on hepatic glycogen in H. fossilis and on muscle glycogen and protein in both species. In general, while both species could respond to erythropoietin and withstand prolonged starvation, H. fossilis alone exhibited remarkable tolerance to fasting.

Topics: Animals; Energy Metabolism; Erythrocyte Count; Erythropoietin; Fish Diseases; Fishes; Food; Glycogen; Hematocrit; Hemoglobins; Liver Glycogen; Muscle Proteins; Muscles; Starvation; Thyroxine

1. The effect of starvation for 12 months on organo-somatic indices, glycogen, protein and water contents of several organs and the Na+/K+ ratio in muscle was studied in the South African clawed toad Xenopus laevis Daudin. 2. The liver- and ovary-somatic index were reduced by 30 and 70% of the initial value after 12 months. Fat bodies had disappeared after approximately 6 months of starvation. The indices of heart and kidney were not changed. 3. Glycogen concentration of the liver, ovaries and muscle were depleted nearly totally during the first half of the experimental time, whereas glycogen in the kidney seemed to be unaffected. 4. Protein concentration increased in the liver, decreased in the muscle and remained constant in the kidney. 5. Starvation caused an increase of the water concentration of the whole animal and different organs, especially at the end of the experiment. 6. The Na+/K+ ratio of the muscle increased significantly after 6 months of starvation and reached a maximum after 10 months.

Topics: Animals; Body Water; Glycogen; Muscles; Osmolar Concentration; Potassium; Proteins; Sodium; Starvation; Time Factors; Xenopus laevis

The effects of starvation and of a short period of refeeding on energy-linked metabolic processes, as well as the effects of insulin administration, were investigated in an omnivorous fish (catfish, Rhamdia hilarii) previously adapted to a carbohydrate-rich diet. Following food deprivation blood sugar levels declined progressively to about 50% of fed values after 30 days. During the same period plasma free fatty acid (FFA) concentration increased twofold. Starvation resulted in reduced concentrations of lipid and glycogen in the liver and of glycogen, lipid, and protein in white muscle. However, taking into account the initial and final concentrations of tissue constituents, the liver weight, and the large fractions of body weight represented by muscle, it could be estimated that most of the energy utilized during starvation derived from the catabolism of muscle lipid and protein. Refeeding starved fishes for 48 hr induced several-fold increases in the rates of in vivo and in vitro incorporation of [14C]glucose into liver and muscle lipid and of [14C]glycine into liver and muscle protein. Incorporation of [14C]glucose into liver glycogen was also increased. However; refeeding did not affect the incorporation of labeled glucose into muscle glycogen, neither in vivo nor in vitro. Administration of pharmacological doses of insulin to normally fed catfishes resulted in marked increases in the in vivo incorporation of 14C from glucose into lipid and protein in both liver and muscle. In contrast, labeled glucose incorporation into muscle glycogen was not affected by insulin and label incorporation into liver glycogen was actually lower than that in noninjected controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adaptation, Physiological; Animal Feed; Animals; Blood Glucose; Carbon Radioisotopes; Catfishes; Dietary Carbohydrates; Energy Metabolism; Fatty Acids, Nonesterified; Food; Glycogen; Insulin; Lipid Metabolism; Liver; Male; Muscles; Starvation

The urinary excretion of a glucose-containing oligosaccharide, Glc alpha[1-6Glc alpha[1-4Glc alpha[1-4Glc, (Glc4) has been measured in various physiological and pathological conditions. The Glc4 content of 24 h samples from the same individual was relatively constant, whereas 2 h samples showed up to 4-fold variations in Glc4 concentration. This variation is associated mainly with increased excretion of Glc4 after meals. A carbohydrate-rich diet, starvation or a protein-rich diet, and intense physical activity all affected the urinary excretion of Glc4. Both oral and intravenous administration of glycogen in a Rhesus monkey resulted in increased excretion of Glc4. When Glc4 itself was injected intravenously in small amounts renal clearance was rapid and complete. In contrast, injection of a larger amount resulted in incomplete (approximately 10%) renal clearance, probably due to uptake and metabolism of the oligosaccharide. In patients with glycogen storage diseases, certain malignancies, and pancreatitis, 24 h urinary Glc4 excretion exceeded the normal range. The diagnostic implications of these observations deserve evaluation. The results presented suggest a need for standardization of nutritional status and physical activity when monitoring urinary Glc4 excretion for diagnostic purposes.

Topics: Adult; Circadian Rhythm; Dietary Carbohydrates; Female; Glucose; Glycogen; Humans; Male; Middle Aged; Oligosaccharides; Starvation

The effect of starvation on blood glucose, muscle glycogen and liver glycogen concentration was measured in a group of newborn piglets. Liver biopsies were obtained by using a modified version of the Menghini technique. No difference in length of survival time was observed between piglets that received water and those that did not. Piglets with higher birth weight survived longer. No relationship was found between initial liver glycogen content and survival time. Moreover, we concluded that plasma glucose levels are not reliable indicators of length of survival time. The interrelated changes in liver glycogen, muscle glycogen, and plasmaglucose concentrations found in this study correspond with those reported elsewhere. Moreover, the number of experimental animals needed for the study was markedly reduced. We conclude that the liver biopsy technique is valuable in longitudinal hypoglycaemia studies of piglets.

Topics: Animals; Animals, Newborn; Biopsy, Needle; Blood Glucose; Glycogen; Liver; Liver Glycogen; Starvation; Swine; Time Factors

1. Intragastric administration of ethanol (75 mmol/kg body wt.) at 1 h before glucose refeeding of 24 h-starved rats inhibited hepatic glycogen deposition (by 69%) and synthesis (by approx. 70%), but was without significant effect on muscle glycogen deposition and synthesis. 2. Treatment of ethanol-administered rats with methylpyrazole (an inhibitor of alcohol dehydrogenase) did not significantly diminish the inhibitory effect of ethanol on hepatic glycogen deposition after glucose refeeding, suggesting that the inhibition was not dependent on ethanol metabolism. 3. Ethanol delayed and diminished intestinal glucose absorption, at least in part by delaying gastric emptying. 4. At a lower dose (10 mmol/kg body wt.), ethanol inhibited hepatic glycogen repletion and synthesis without compromising intestinal glucose absorption. Ethanol inhibited glycogen deposition (by 40%) in hepatocytes from starved rats provided with glucose + lactate + pyruvate as substrates, consistent with it having a direct effect to diminish hepatic glycogen synthesis by inhibition of gluconeogenic flux at a site(s) between phosphoenolpyruvate and triose phosphate in the pathway. 5. It is concluded that ethanol acutely impairs hepatic glycogen repletion by inhibition at at least two distinct sites, namely (a) intestinal glucose absorption and (b) hepatic gluconeogenic flux.

Topics: Animals; Dietary Carbohydrates; Dose-Response Relationship, Drug; Ethanol; Fomepizole; Food; Glucose; Glycogen; Intestinal Absorption; Liver Glycogen; Male; Muscles; Pyrazoles; Rats; Rats, Inbred Strains; Starvation

The label distribution in control and cafeteria-diet fed rats, either in basal conditions or after 24 hours of food deprivation, 10 minutes after the i.v. injection of carrier-free D-14C-(U)-glucose, has been studied. The radioactivity recovered in the different fractions of liver, kidney, heart, striated muscle and white adipose tissue showed comparable patterns of change with starvation in both dietary groups. Most of the radioactivity was found in the free amino acid fraction as well as in proteins, with significant proportions also in lipid and liver glycogen. However, most of the label was lost due to its oxidation, remaining in the combined indicated tissues 10-20% of the injected label. On the whole, cafeteria rats consumed more glucose than controls, the lowest oxidation corresponding to the starved-control group. The amount of glucose oxidized by cafeteria rats was actually comparable to that of fed controls. The availability of other energetic sources--i.e. lipid--allows for an increased glucose utilization in cafeteria rats, even in the starved state.

Topics: Adipose Tissue; Amino Acids; Animals; Blood Glucose; Diet; Glucose; Glycogen; Kidney; Lipid Metabolism; Liver; Male; Muscles; Myocardium; Proteins; Rats; Starvation

The pattern of glycogen deposition in skeletal muscles of varying fibre composition was examined in rats during the starved-to-fed transition. In all the muscles studied, glycogen concentrations steadily increased during the first 8 h after chow re-feeding, and the fed value was exceeded. Rates of glycogen deposition varied, not with muscle fibre composition, but with the extent of glycogen depletion during starvation. There was no evidence for skeletal-muscle glycogen breakdown during the period of hepatic glycogenesis, making it unlikely that recycling of carbon from muscle glycogen to lactate is quantitatively important for the provision of glycogenic precursors to the liver, but moderate glycogen loss was observed from 8 to 24 h after re-feeding, when the liver is in the lipogenic mode. The factors influencing glucose disposal by skeletal muscle after re-feeding are discussed.

Topics: Animals; Female; Food; Glycogen; Liver Glycogen; Muscles; Rats; Rats, Inbred Strains; Starvation

1. Starvation for 48 hr doubled the rate of gluconeogenesis from lactate and pyruvate in perfused chicken kidney, but did not change the rate of production of glucose from malate, succinate, or alpha-ketoglutarate. 2. Amino-oxyacetate and D-malate inhibited the production of glucose from lactate and from pyruvate by 55% in each case. Quinolinate reduced the production of glucose from lactate and from pyruvate by 50% in both fed and starved chickens, but had no effect on the production of glucose from intermediates in the citric acid cycle. 3. Starvation increased the rate of formation of mitochondrial phosphoenolpyruvate from pyruvate, but had no effect on the rate of formation of mitochondrial phosphoenolpyruvate from malate.

Topics: Animals; Chickens; Eating; Gluconeogenesis; Glycogen; In Vitro Techniques; Kidney; Male; Mitochondria; NAD; Perfusion; Phosphoenolpyruvate; Phosphoenolpyruvate Carboxykinase (GTP); Starvation

1. Responses of enzymic characteristics of gastrocnemius muscle were studied when frogs (Rana pipiens) were exposed to cold environment (4 degrees C). 2. The content of adenosine triphosphate (ATP) decreased significantly after cold exposure. This decrease was greater in starved than in fed frogs. 3. Although the glycogen content did not change, lactate levels were lower in cold-exposed than room-temperature (control) frogs. No change was observed in glycogen and lactate between fed and unfed frogs kept at 4 degrees C for 2 months. Lactate dehydrogenase activity tended to increase during chronic cold exposure, but not significantly. 4. The activities of citrate synthase, cytochrome oxidase, and beta-hydroxyacyl CoA dehydrogenase were higher in gastrocnemius of chronically cold-exposed frogs than in room-temperature controls. This increase was statistically significant only in the muscles of starved frogs; these muscles had the greatest decrease in ATP. 5. It was suggested that chronic cold exposure decreases skeletal muscle ATP content but may not affect glycolysis. The data also suggested that the decrease in ATP content stimulates mitochondrial biogenesis which increases enzyme activities.

Topics: Adenosine Triphosphate; Animals; Cold Temperature; Glycogen; Lactates; Lactic Acid; Mitochondria, Muscle; Muscles; Rana pipiens; Starvation

We examined the long-term effects of nutritional status and the acute effects of changes in exogenous carbohydrate- and lipid-substrate supply and utilization on fructose 2,6-bisphosphate (Fru-2,6-P2) concentrations in heart, gastrocnemius and soleus. Starvation decreased Fru-2,6-P2 concentrations in all three muscles. The acute administration of insulin and glucose increased skeletal-muscle Fru-2,6-P2 in the fed, but not in the starved, state, but cardiac Fru-2,6-P2 was unchanged. Cardiac and skeletal-muscle Fru-2,6-P2 concentrations were unaffected by acute increases in fatty acid supply produced by the administration of corn oil plus heparin, or by acute decreases in fatty acid supply produced by inhibition of lipolysis. Differences in cardiac and skeletal-muscle Fru-2,6-P2 concentrations observed in response to starvation were not reversed by administration of glucose or glucose plus insulin, or by inhibition of lipolysis, even though changes in citrate (heart), acylcarnitine (heart) and glycogen (skeletal muscle) were observed. Concentrations remained low for at least 8 h after chow re-feeding, but the fed value was restored by 24 h.

Topics: Animals; Carnitine; Citrates; Citric Acid; Food; Fructosediphosphates; Glucose; Glycogen; Heart; Hexosediphosphates; Insulin; Muscles; Myocardium; Pyrazoles; Pyruvate Dehydrogenase Complex; Rats; Rats, Inbred Strains; Starvation

The levels of glycogen, protein and lactate in the tissues of 3- and 5-day-old domestic fowl chicks either starved or fed a protein diet (hard-boiled egg white) have been studied. The patterns of change in the parameters studied were much similar in both experimental groups compared to fed controls. Tissue and circulating levels of lactate were very low in protein-fed chicks, they are lowest in the starved ones. Plasma glucose levels were diminished in starved and protein-fed groups vs. controls, as were their tissue glycogen levels, the latter being lowest in starved chicks. The availability of dietary amino acids could not prevent the effects of the lack of dietary carbohydrate observed in starved chicks, as the weight of liver, circulating glucose and lactate levels were significantly lowered in these animals compared with controls.

Topics: Animals; Chickens; Dietary Proteins; Glycogen; Homeostasis; Lactates; Starvation

1. Glycogen concentrations in Richardson's ground squirrels of the weight-loss phase were 1/4-1/2 those in animals of the weight-gain phase. White adipose lipid content was similar in animals in the two phases when total body weight was similar. 2. Specific activity of 14C in muscle glycogen of fed, starved and refed ground squirrels in the weight-loss phase was similar to that in starved weight-gain phase animals. Activity in adipose lipids of fed, starved, and refed ground squirrels in the weight-gain phase was 5-8 times greater than that in the same nutritional states in weight-loss phase animals. 3. In addition to a voluntary reduction in food intake, a depressed synthetic activity in lipids and glycogen may account in part for the rapid decrease in body weight during the weight-loss phase of the circannual cycle.

Topics: Adipose Tissue; Animals; Body Weight; Glycogen; Lipid Metabolism; Male; Muscles; Periodicity; Sciuridae; Starvation

A method is presented which allows simultaneous estimation of rates of glycogen synthesis and glycogenolysis in an isolated incubated skeletal muscle, thus allowing measurement of the glycogen/glucose-1-phosphate substrate cycling rate. In the absence of hormonal additions, the measured rates of glycogen synthesis and breakdown were similar [respectively, 0.54 +/- 0.12 (8) and 0.74 +/- 0.10 (8) mumol glucosyl equiv. h-1 (g tissue)-1]. Incremental addition of insulin stimulated glycogen synthesis up to threefold and reduced glycogenolysis by about sevenfold; the half-maximally effective concentration of insulin on both processes was about 100 microU/ml (0.7 nM). Incremental addition of adrenaline (in the presence of 1 mU insulin/ml) caused a dramatic increase in the glycogenolytic rate (about 15-fold), but a much less marked inhibition of glycogen synthetic rate. In addition to hormonal manipulation of the muscle preparation in vitro, the effects of cold exposure, the hyperthyroid state, a single exercise bout and exercise-training of animals in vivo on the rates of glycogen synthesis and breakdown in the isolated incubated muscle preparation have been investigated. Significant changes in measured glycogen synthesis, breakdown and glycogen/glucose-1-phosphate cycling have been observed, both under basal conditions and in response to hormonal additions in vitro. The results are discussed with respect to the possible physiological importance of this substrate cycle.

Topics: Adaptation, Physiological; Animals; Cold Temperature; Epinephrine; Glucosephosphates; Glycogen; Hyperthyroidism; Insulin; Male; Models, Biological; Muscles; Physical Exertion; Rats; Rats, Inbred Strains; Starvation

In mice, the response of carcass glycogen to glucose re-feeding after starvation is biphasic. The initial repletive phase is followed by partial (greater than 50%) glycogen mobilization. This turnover of carcass glycogen in response to carbohydrate re-feeding may play an important role in the provision of C3 precursors for hepatic glycogen synthesis.

Topics: Animals; Blood Glucose; Food; Glucose; Glycogen; Lactates; Lactic Acid; Liver Glycogen; Male; Mice; Mice, Inbred BALB C; Starvation; Tissue Distribution

A method was developed for the hemoglobin-free perfusion of the rabbit psoas muscle in situ. This muscle consists almost exclusively of fast-twitch (type IIb) glycolytic fibres and was therefore used as a model of a homogeneous muscle of the glycolytic, metabolic type.

Topics: Adenosine Triphosphatases; Adenosine Triphosphate; Animals; Glucose; Glycogen; Glycolysis; In Vitro Techniques; Insulin; Kinetics; Male; Muscles; Perfusion; Phosphocreatine; Rabbits; Starvation

With regard to the protein content, as analysed cytophotometrically, of hepatocytes from rats kept under a 12L 12D photoperiod (photophase 7:00-19:00), the following facts have been established: 1) Hepatocytes of different classes of ploidy all demonstrate, more or less equally, daily variations in protein content and also its reduction after 24-h fasting. 2) With computer analysis of data obtained at eight time points during a period of 24 h, a sinusoidal curve of the protein content of individual mononuclear tetraploid hepatocytes throughout the day could be demonstrated with a maximum at 6:20 and a minimum at 18:20. 3) Animals, fed with meals via a dispensing machine from 23:00 to 24:00 only, show a similar sinusoidal curve but with higher amplitude, and a virtually identical mean value as those fed ad libitum. The maximum was found at 10:40, revealing a time lag of 12 h after food intake, the minimum at 22:40. 4) Trained animals deprived of food during the standardized feeding time revealed a moderate reduction of their hepatocyte protein content in the first 6 h, then a 6-h period with a steep fall followed by a slower reduction. After 24 h, the mean hepatocyte protein mass had decreased to 72% of that at the commencement of fasting at 23:00.

Topics: Animals; Circadian Rhythm; Computers; Cytophotometry; Food; Glycogen; Liver; Male; Naphthalenesulfonates; Ploidies; Proteins; Rats; Rats, Inbred Strains; Starvation; Time Factors

Both starvation of and feeding a high linoleic acid content diet to rats during late pregnancy resulted in marked differences in the metabolism of the fed offspring immediately after birth when compared to control neonates (mother fed the normal high carbohydrate content laboratory diet during pregnancy). In particular differences in postnatal changes in blood glucose, non esterified fatty acids and ketone bodies and in hepatic triglyceride content were observed. Many of the differences appeared to be related to the variations in blood and hepatic metabolites present at birth in the various groups of animals. A similar situation also existed with respect to postnatal changes in the activity of hydroxymethylglutaryl-CoA synthase.

Topics: Animals; Animals, Newborn; Diet; Dietary Fats; Fatty Acids, Nonesterified; Female; Glycogen; Hydroxymethylglutaryl-CoA Synthase; Hypoglycemia; Ketone Bodies; Liver; Mitochondria, Liver; Oxo-Acid-Lyases; Pregnancy; Proteins; Rats; Rats, Inbred Strains; Starvation; Succinate Dehydrogenase; Triglycerides

The insulin sensitivity of protein synthesis and glucose incorporation into glycogen by the soleus and epitrochlearis muscles from fed rats and 24 h-starved rats was determined in vitro during the first and second hours of incubation after isolation of the muscles. Rates of protein synthesis by both muscles from fed rats in the first hour of incubation were 2-fold higher than in the second hour and were not increased by insulin. Rates of protein synthesis during the first hour in the presence of 6000 microunits of insulin/ml were increased in soleus, but not in epitrochlearis, muscles from starved rats. Rates of protein synthesis in both muscles from fed and starved rats were increased significantly by insulin during the second hour. High concentrations of insulin caused a marked stimulation of the rates of glucose incorporation by both muscles from fed and starved rats in both the first and second hours of incubation. The insulin sensitivity of glucose incorporation during the second hour, defined as the concentration of insulin causing half-maximal stimulation, was increased 10-fold for both muscle types from starved rats (soleus, 65 microunits/ml; epitrochlearis, 45 microunits/ml) relative to muscles from fed rats (soleus, 600 microunits/ml; epitrochlearis, 500 microunits/m). The insulin sensitivity of protein synthesis in the second hour was greater for soleus muscles from starved rats (65 microunits/ml) than from fed rats (500 microunits/ml). In contrast, the insulin sensitivity of protein synthesis in epitrochlearis muscles from starved rats was significantly decreased (225 microunits/ml) compared with fed rats (25 microunits/ml Maximal rates achieved by high concentrations of insulin were not different from those in the same muscle from fed rats. It is suggested that protein synthesis, in distinction to glucose utilization, may be resistant to insulin stimulation during periods of acute starvation in muscles with fibre compositions similar to the epitrochlearis, but not in muscles with fibre compositions similar to the soleus. Partial reversal of the resistance observed in vitro for epitrochlearis muscles from starved rats may be due to the loss of factors which suppress the effect of insulin in vivo.

Topics: Animals; Dose-Response Relationship, Drug; Female; Glucose; Glycogen; In Vitro Techniques; Insulin; Muscle Proteins; Muscles; Rats; Rats, Inbred Strains; Starvation

Carbohydrate metabolism was examined in different organs of rats with dietary potassium deprivation for 4 weeks. Thereafter, a 24- or 48-hour starvation period caused a significant decrease of skeletal muscle and liver glycogen content in K+-depleted (KD) rats, whereas kidney glycogen concentration increased and heart glycogen remained unchanged. In contrast, liver glucose concentration was significantly higher in starved KD animals without changes in muscle, heart, and kidney glucose concentrations. Potassium depletion caused a highly significant decrease of plasma and muscle potassium concentrations, metabolic alkalosis, reduced plasma insulin, and increased creatine phosphokinase levels. Blood lactate, pyruvate, and oxoglutarate levels were significantly enhanced in fasted KD rats, whereas blood citrate, beta-hydroxybutyrate, and glucose concentrations were unchanged. Blood acetoacetate level, however, was significantly reduced following potassium depletion. Therefore, beta-hydroxybutyrate/acetoacetate ratio increased significantly, whereas lactate/pyruvate ratio was not influenced. Our results clearly indicate impaired carbohydrate metabolism in potassium-depleted rats.

Topics: Acetoacetates; Animals; Blood Glucose; Carbohydrate Metabolism; Female; Glucose; Glycogen; Insulin; Ketoglutaric Acids; Kidney; Lactates; Lactic Acid; Liver; Muscles; Myocardium; Potassium; Potassium Deficiency; Pyruvates; Pyruvic Acid; Rats; Rats, Inbred Strains; Starvation

In quarter-diaphragms from 40 h-starved rats the rate of glycogen mobilization is sufficient to account for the rate of lactate+pyruvate+alanine production. It is concluded, therefore, that alanine derives its carbon skeleton predominantly via glycolysis and not via synthesis de novo from tricarboxylic acid-cycle intermediates and related amino acids.

Topics: Alanine; Amino Acids, Branched-Chain; Animals; Diaphragm; Glycogen; Glycolysis; In Vitro Techniques; Male; Muscles; Rats; Rats, Inbred Strains; Starvation

Concentrations of citrate, hexose phosphates and glycogen were measured in skeletal muscle and heart under conditions in which plasma non-esterified fatty acids and ketone bodies were physiologically increased. The aim was to determine under what conditions the glucose-fatty acid cycle might operative in skeletal muscle in vivo. In keeping with the findings of others, starvation increased the concentrations of glycogen, citrate and the fructose 6-phosphate/fructose 1,6-bisphosphate ratio in heart, indicating that the cycle was operative. In contrast, it decreased glycogen and had no effect on the concentration of citrate or the fructose 6-phosphate/fructose 1,6-bisphosphate ratio in the soleus, a slow-twitch red muscle in which the glucose-fatty acid cycle has been demonstrated in vitro. In fed rats, exercise of moderate intensity caused glycogen depletion in the soleus and red portion of gastrocnemius muscle, but not in heart. In starved rats the same exercise had no effect on the already diminished glycogen contents in skeletal muscle, but it decreased cardiac glycogen by 25-30%. After exercise, citrate and the fructose 6-phosphate/fructose 1,6-bisphosphate ratio were increased in the soleus of the starved rat. Significant changes were not observed in fed rats. The data suggest that in the resting state the glucose-fatty acid cycle operates in the heart, but not in the soleus muscle, of a starved rat. In contrast, the metabolite profile in the soleus was consistent with activation of the glucose-fatty acid cycle in the starved rat during the recovery period after exercise. Whether the cycle operates during exercise itself is unclear.

Topics: Animals; Citrates; Citric Acid; Diabetes Mellitus, Experimental; Fatty Acids; Glucose; Glycogen; Hexosephosphates; Liver Glycogen; Male; Muscles; Myocardium; Physical Exertion; Rats; Rats, Inbred Strains; Starvation

Rats were fasted 24, 48 or 72 hours to determine the effect of several days without food on glycogen synthase and synthase phosphatase activity in heart. The basal percentage of synthase I decreased gradually from approximately 20% in fed animals to approximately 6% in rats starved for 72 hours. Glycogen increased progressively from 4.6 mg/g wet weight in fed rats to 7.6 mg/g wet weight in 72-hour starved rats. Thus, there was an inverse relationship between the glycogen concentration and the basal percentage of synthase I. The total synthase phosphatase activity measured at a standardized glycogen concentration decreased 50% by 24 hours of starvation and then was unchanged up to 72 hours. The 50% decrease in phosphatase activity correlated directly with insulin concentration in rats fasted 24-72 hours. The rapid stimulatory effect of insulin on synthase activity observed in fed rats was delayed in rats starved 24 and 48 hours. This correlated with a progressively slower synthase phosphatase response to insulin. The stimulatory effect of insulin was lost completely in 72-hour fasted rats. The proposed mechanism for the delayed response in rats starved 24 and 48 hours and lack of response in rats starved 72 hours is insulin resistance. The mechanism remains to be elucidated.

Topics: Animals; Blood Glucose; Glycogen; Glycogen Synthase; Glycogen-Synthase-D Phosphatase; Insulin; Insulin Resistance; Male; Myocardium; Phosphoprotein Phosphatases; Rats; Starvation; Time Factors

The effects of a restricted-diet (50% of the normal intake during 25 days) on the isometric developed tension (IDT) of uterine horns isolated from diestrous non-cycling rats, were explored. After 60 minutes following isolation and mounting the IDT of controls suspended in glucose containing solution was higher than in preparations from underfed animals but this was no the case in the absence of glucose. Glycogen levels of controls at 60 minutes were smaller in substrate-free than in the presence of glucose whereas no change was detected in horns from restricted-diet rats. Preparations from underfed animals had a significantly augmented basal concentration of triglycerides which diminished at 60 minutes following the removal of glucose from the suspending solution. This effect was abolished by the addition of 3-O-methyl glucose and by blockers of beta-adrenoreceptors such as propranolol or MJ-1999. A similar situation occurs when the animals were injected prior killing with 6-hydroxydopamine.

Topics: 3-O-Methylglucose; Animals; Female; Glycogen; Hydroxydopamines; Methylglucosides; Oxidopamine; Propranolol; Rats; Rats, Inbred Strains; Starvation; Triglycerides; Uterine Contraction; Uterus

Although the glycogen content of mouse tail skin was decreased during starvation and was restored on re feeding, the proportion of glycogen synthase in the I form remained constant throughout at about 10% of the total. During the phase of net glycogen synthesis 1.5h after access to food was restored, the concentration of UDP glucose was markedly increased and the proportion of phosphorylase in the a form was significantly decreased.

Topics: Animals; Blood Glucose; Food; Glucose; Glycogen; Glycogen Synthase; Male; Mice; Mice, Inbred BALB C; Phosphorylases; Skin; Starvation

The ischemic myocardium utilizes glycogen as metabolic substrate. The effects of oral nutrition on the levels of glycogen in the myocardium and of myocardial glycogen content on myocardial tolerance to ischemia were studied. Rats were divided into groups and fed (a) rat chow, (b) rat chow plus 5% dextrose, and elemental diets (c) Flexical (Mead Johnson) or (d) Vital (Ross Laboratories). Another group was starved. All fed groups gained weight normally while the starved rats lost 23% of their body weight. Compared with the effect on rat chow, myocardial glycogen levels were elevated in the Flexical and starvation groups, while Vital depressed the level (P less than 0.01). Thus, both caloric intake and diet affected myocardial glycogen content. Elevation of myocardial glycogen content after starvation contrasted with glycogen disappearance from the liver. The level of myocardial glycogen and left ventricular function after global ischemia were correlated in dogs under cardiopulmonary bypass conditions. During 30 minutes of normothermic aortic cross-clamping, hearts with a preischemic myocardial glycogen content greater than 0.4 g% had less asystole or ventricular fibrillation. Their left ventricular function (stroke work index, myocardial contractility) upon reperfusion was substantially better than those with a myocardial glycogen level of less than 0.4 g%. Dietary manipulation and the nutritional status can thus affect the myocardial glycogen content and may be useful in protecting the myocardium from ischemia.

Topics: Animals; Coronary Disease; Energy Intake; Food, Formulated; Glycogen; Heart Ventricles; Liver Glycogen; Male; Myocardial Contraction; Myocardium; Nutritional Requirements; Rats; Rats, Inbred Strains; Starvation; Stroke Volume

The rates of glycolysis and glycogenolysis an the rate of lactate formation from glucoso-6-phosphate (G-6-Ph) in the liver were reduced during stress (starvation). On the contrary, these activities in the adrenals were increased. The rates of lactate formation from fructose diphosphate remained unchanged in both organs. The results obtained attest to the inhibition in the liver and activation in the adrenals of phosphorylase, hexokinase and phosphofructokinase. The degree of hexokinase inhibition in the liver depended on the presence of cAMP, ATP and MgCl2 in the incubation medium and was a consequence of enzymatic phosphorylation. Unlike 2', 3'-AMP, the inhibitory effect of CAMP was highly specific. The protein inhibitor of protein kinase completely reversed the inhibitory effect of cAMP on hexokinase. In the adrenals, cAMP slightly increased the rates of glycolysis and lactate formation from G-6-Ph because of allosteric effects of cAMP. The activation rather than inhibition of glycolysis in the adrenals during stress is probably caused by the absence in this tissue of cAMP-dependent protein kinase which phosphorylates hexokinase.

Topics: Adrenal Glands; Animals; Cyclic AMP; Female; Fructosediphosphates; Glucosephosphates; Glycogen; Glycolysis; Liver; Rats; Rats, Inbred Strains; Starvation; Stress, Physiological

The role of glucocorticoid (GC) in the diurnal variation of glycogenesis, glycogenolysis and hepatic glycogen levels was studied in starved-refed rats. Intact, adrenalectomized (ADX) and ADX-GC supplemented rats were either ad libitum fed a 65% glucose diet or starved for 48 hours and refed the glucose diet. At the end of the starvation period and at 4-hour intervals thereafter, rats from all six treatment groups were killed and hepatic glycogen levels, glycogen synthase and phosphorylase activity determined. Ad libitum-fed animals displayed the usual diurnal glycogen and enzyme activity rhythms. Adrenalectomy was without effect in the ad libitum-fed rats on glycogen level and glycogen synthase activity and, at most points, on phosphorylase activity. Starvation-refeeding profoundly affected both the synthesis and degradation of glycogen and these effects could, in part, be attributed to the presence or absence of the adrenals. The phosphorylase activity and the hepatic glycogen level appeared to be cued by GC, whereas GC was without effect on glycogen synthase. Starvation-refeeding stimulated glycogen synthase activity within the first 4 hours of refeeding in the intact rats and within the first 8 hours of refeeding in the ADX-GC rats. These results suggest that the glycogen response to starvation refeeding is, in part, mediated by the adrenal hormones.

Topics: Adrenalectomy; Animals; Circadian Rhythm; Food; Glucocorticoids; Glycogen; Glycogen Synthase; Liver; Male; Phosphorylase a; Phosphorylases; Rats; Starvation

The glycogen content of muscle was correlated with the activity of glycogen synthase and glycogen phosphorylase from the parasitic roundworm Ascaris suum maintained in vitro. Adult female worms were maintained in the laboratory in a perfusion system during periods of starvation and feeding. During starvation, the levels of glucogen decreased at a rate of 0.1 to 0.2 mumoles/min/g wet weight of muscle-cuticle. During this time, 95% of the glycogen synthase (E.C. 2.4.1.11) was in the active D-form, and 48% of the phosphorylase (E.C. 2.4.1.1) was in the active a-form. Upon feeding, the rate of incorporation of glycosyl residues into glycogen proceeded at a rate of 0.75 to 1.0 mumoles/min/g muscle-cuticle. Glycogen synthase was 22% in the active I-form and phosphorylase a-levels remained virtually unchanged at 41% as compared with the starved worm. Total levels of both enzymes remained constant over the starvation-feeding period with 3.9 units/g phosphorylase and 0.4 units/g glycogen synthase. The apparent Km value for the substrate UDPG for glycogen synthase was 0.22 +/- 0.02 mM. For glycogen phosphorylase the Km value for G-1-P was 1.76 +/- 0.38 mM.

Topics: Animals; Ascaris; Female; Food; Glycogen; Glycogen Synthase; Kinetics; Phosphorylase a; Phosphorylase b; Phosphorylases; Starvation

In contrast to adipose tissue and heart, the in vitro sensitivity of skeletal muscle to insulin is enhanced by starvation. To determine the basis for this, insulin binding and its ability to stimulate glucose metabolism were examined in the incubated rat soleus. In solei from 50-g rats, starvation for 48 h enhanced insulin binding by 50-100% at concentrations of 100 ng/ml or less. Starvation also resulted in higher basal and insulin-stimulated rates of glycogen synthesis, glycolysis, and glucose uptake. The enhanced effect of insulin only occurred at concentrations less than 50-75 ng/ml, in keeping with the increased binding of insulin in this concentration range. On the other hand, under conditions in which binding at equilibrium was the same, glucose uptake was still higher in the starved group, suggesting that some postreceptor event may have been more sensitive to insulin. These studies confirm that the in vitro sensitivity of rat skeletal muscle to insulin is enhanced by 48 h of starvation. They suggest that this is due at least partially to an increase in insulin binding at physiological concentrations.

Topics: Animals; Deoxyglucose; Female; Glucose; Glycogen; Insulin; Muscles; Rats; Receptor, Insulin; Starvation

Pregnant dogs were starved for 72 hr before a term delivery. Maternal (1.68 +/- 0.39 versus 0.74 +/- 0.20 mM) and fetal (0.39 +/- 0.03 versus 0.22 +/- 0.07) circulating free fatty acids and maternal (2.99 +/- 0.79 versus 1.04 +/- 0.84) and fetal (2.53 +/- 0.35 versus 1.01 +/- 0.32) ketones were elevated whereas blood glucose values remained unchanged at the time of delivery. After birth, pups born to starved mothers had significantly lower blood glucose values during 3, 6, 9, and 24 hours of neonatal fasting. Intracerebral glucose concentrations paralleled those in the blood as they were depressed at 3, 6, and 9 hours of age. Cerebral glycogen content was lower in pups born to starved mothers at 6 (2.72 +/- 0.43 versus 4.32 +/- 0.56 mumoles/g) and 24 (2.31 +/- 0.17 versus 3.48 +/- 0.39 mumoles/g) hr, whereas UDP-glucose concentrations were significantly elevated in these pups during fetal, 3, 9, and 24 hr of age. Phosphoenolpyruvate was higher after maternal starvation in the fetus and at 6 and 9 hr, whereas cerebral pyruvate concentrations were elevated at 3, 6, and 9 hr of age. The elevation of pyruvate with no alteration of lactate concentration resulted in an elevated cytoplasmic NAD/NADH ratio at 3 hr of age (1381 +/- 194 versus 792 +/- 198). Cerebral alpha-ketoglutarate and calculated oxaloacetate concentrations were elevated throughout the day after maternal starvation whereas malate concentrations were depressed at 3 and 9 hr of age. Cerebral energy charge was unaffected, whereas the calculated energy reserve was lower at 3, 6, and 24 hours. Cerebral amino acids demonstrated elevated aspartate concentrations at 3 and 6 hr. Cerebral glutamine concentrations were lower during fetal stage (7.86 +/- 0.52 versus 10.01 +/- 0.41 mumoles/g) and 3, 6, and 9 hr of life.

Topics: Adenine Nucleotides; Amino Acids; Animals; Animals, Newborn; Cerebellum; Citric Acid Cycle; Dogs; Energy Metabolism; Female; Fetus; Glucose; Glycogen; Hypoglycemia; Pregnancy; Pregnancy Complications; Starvation; Time Factors

A series of experiments were conducted with turkey poults to ascertain the effects of supplemental chromium or excess of nicotinic acid on growth and carbohydrate metabolism. A 23% protein starter diet was selected to emphasize the effect of chromium under basal, starvation for 48 hr, and refeeding periods. Thirty percent protein diets were also used to determine if the effects were compounded by protein levels. Supplemental chromium (20 ppm) significantly increased (P less than .05) weight at 3 weeks of age of poults consuming 23% protein diets, while an additional 250 ppm of nicotinic acid had little effect on poult weight at 3 weeks (P greater than .05). Supplemental chromium did not increase (P greater than .05) feed consumption of poults consuming both 23 and 30% protein diets. Supplemental chromium increased liver glycogen at 3 weeks of age and following refeeding after the 48 hr fast (P less than .05). Blood glucose was significantly affected by starvation-refeeding (P less than .05) but was not affected by either chromium or nicotinic acid. Supplemental chromium increased (P less than .01) active glycogen synthetase, while nicotinic acid increased (P less than .01) active phosphorylase at both protein levels. Synthetase was not decreased by starvation but was increased (P less than .01) by refeeding regardless of protein level fed. Phosphorylase was not affected by a starvation-refeeding regimen. Chromium supplementation increased in the vitro incorporation of (14C) glucose into glycogen during basal, starvation and refeeding periods (P less than .01), again, regardless of protein level.

Topics: Animal Feed; Animals; Body Weight; Chromium; Glucose; Glycogen; Liver; Niacin; Nicotinic Acids; Starvation; Turkeys

In the snail, Achatina fulica, parasitized by the rat lungworm Angiostrongylus cantonensis, levels of carbohydrate in hemolymph and digestive glands were determined. The normal level of hemolymph glucose of 11.7 mg% dropped to 4.25 mg% in the infected snails, a significant difference after only one week of infection. The level of total reducing sugar in the hemolymph also decreased significantly (12.3 mg% to 3.6 mg%) in this period. Later on, the snails were capable of adapting themselves to the parasitic infection and the concentration of hemolymph sugars returned to the normal range. Starvation caused a decrease in the carbohydrate reserves of the digestive gland only when the starved snails had been previously infected.

Topics: Angiostrongylus; Animals; Carbohydrate Metabolism; Glucose; Glycogen; Hemolymph; Metastrongyloidea; Snails; Starvation

The levels of isometric developed tension (IDT) in portal veins from starved and diabetic rats in glucose medium were of the same magnitude but significantly reduced compared with veins from normal rats. Glucose removal led to contractile depression, more marked in starved veins (-74%; p < 0.001 vs. diabetics and normals). Addition of glucose, pyruvate, acetate, lactate, or butyrate counteracted this depression in all groups but in diabetics butyrate significantly stimulated IDT over controls whereas in starved veins lactate overcame IDT reduction only partially. Added insulin significantly enhanced contractile recovery with glucose in normal and diabetic preparations but was ineffective in starved veins. Glycogen content was significantly lower in diabetics; however, in no group did changes occur in incubated veins as compared with unincubated ones. Glycerol production was significantly higher in diabetic veins. It would appear that, although experimental diabetes induces a shift to fatty acid utilization, aerobic glycolysis and mitochondrial respiration are somehow preserved as reflected by the IDT recovery with pyruvate or lactate.

Topics: Animals; Diabetes Mellitus, Experimental; Glucose; Glycerol; Glycogen; In Vitro Techniques; Male; Muscle Contraction; Muscle, Smooth, Vascular; Portal Vein; Rats; Starvation

Bovine adipose-tissue glycogen metabolism was studied during food deprivation and re-feeding. Changes in the specific activity of adipose-tissue glycogen synthase paralleled changes in tissue glycogen content: both parameters increased during food deprivation and remained so during the first 10 days of re-feeding. The values for the A0.5 (activation constant) for glucose 6-phosphate of the freshly isolated enzyme from adipose tissue from fed and starved steers were 2.9 +/- 0.1 mM and 0.90 +/- 0.05 mM respectively. Additionally, whereas incubation of adipose-tissue extracts from fed steers did not activate endogenous glycogen synthase (through a presumed phosphoprotein phosphatase mechanism), the enzyme from starved or re-fed (up to 3 days re-feeding) steers was reversibly activated as measured by changes in the value for the A0.5 for glucose 6-phosphate. Thus activation of bovine adipose-tissue glycogen synthase during food deprivation appears to be related to expression of glycogen synthase phosphatase activity. These effects of food deprivation on bovine glycogen metabolism contrast markedly with the effects observed in rat adipose tissue.

Topics: Adipose Tissue; Animals; Cattle; Enzyme Activation; Feeding Behavior; Food Deprivation; Glycogen; Glycogen Synthase; Glycogen-Synthase-D Phosphatase; Kinetics; Male; Starvation

1. Effects of acute starvation on enzymes of carbohydrate metabolism were determined in rat submandibular and parotid glands. 2. Activities of glycolytic enzymes were high in submandibular gland, but those of pentose phosphate pathway and glycogen metabolism were high in parotid gland. 3. Enzyme activities were lowered by acute starvation. Refeeding the rats with solid diet restored the enzyme activities, but with liquid diet, only partial recoveries were found in submandibular gland.

Topics: Animals; Carbohydrate Metabolism; Food; Fructose-Bisphosphate Aldolase; Glucosephosphate Dehydrogenase; Glycogen; Glycolysis; Hexokinase; Male; Parotid Gland; Pentose Phosphate Pathway; Phosphofructokinase-1; Phosphoglucomutase; Phosphogluconate Dehydrogenase; Rats; Salivary Glands; Starvation; Submandibular Gland

The influence of starvation has been studied on tissue and serum G-6Pase F-D-Pase and alkaline phosphatase activities and on the muscle and liver glycogen content of the freshwater catfish H. fossilis (Bloch). A marked increase in G-6Pase and F-D-Pase activities and a fall in the muscle and liver glycogen content recorded during 40 day starvation. The rise in gluconeogenic enzymes during starvation may be due to glucocorticoid stimulation. Alkaline phosphatase activity was found to decline markedly during starvation. The decline in enzyme activity is attributed to some factors like a fall in the rate of synthesis caused by lowered metabolic demands and to electrolyte imbalance caused by tissue overhydration. The fall in glycogen content may be related to the starved condition of the fish. Elevation in glycogen content and alkaline phosphatase activity and a fall in gluconeogenic enzymes were noted when feeding had been resumed.

Topics: Alkaline Phosphatase; Animals; Fishes; Fresh Water; Fructose-Bisphosphatase; Glucose-6-Phosphatase; Glycogen; Kidney; Liver; Liver Glycogen; Muscles; Starvation

Addition of 10 micron of the alpha-adrenergic agonist phenylephrine to polymorphonuclear leukocytes suspended in glucose-free Krebs-Ringer bicarbonate buffer (pH 6.7) activated phosphorylase, inactivated glycogen synthase R maximally within 30 s, and resulted in glycogen breakdown. Phenylephrine increased 45Ca efflux relative to control of 45Ca prelabelled cells, but did not affect cyclic adenosine 3',5'-monophosphate (cAMP) concentration. The effects of phenylephrine were blocked by 20 micron phentolamine and were absent in cells incubated at pH 7.4. The same unexplained dependency of extracellular pH was observed with 2.5 nM--2.5 micron glucagon, which activated phosphorylase and inactivated synthase-R, but in addition caused a 30-s burst in cAMP formation. 25 nM glucagon also increased 45Ca efflux. The activation of phosphorylase by phenylephrine and possibly also by glucagon are thought mediated by an increased concentration of cytosolic Ca2+ activating phosphorylase kinase. The effects of 5 micron isoproterenol or 5 micron epinephrine were independent of extracellular pH 6.7 and 7.4 and resulted in a sustained increase in cAMP, an activation of phosphorylase and inactivation of synthase-R within 15 s, and in glycogenolysis. The effects of both compounds were blocked by 10 micron propranolol, whereas 10 micron phentolamine had no effect on the epinephrine action. The efflux of 45Ca was not affected by either isoproterenol or epinephrine. The beta-adrenergic activation of phosphorylase is consistent with the assumption of a covalent modification of phosphorylase kinase by the cAMP dependent protein kinase. Phosphorylation of synthase-R to synthase-D can thus occur independently of increase in cAMP, but the evidence is inconclusive with respect to the cAMP dependent protein kinase also being active in this phosphorylation.

Topics: Calcium; Catecholamines; Cyclic AMP; Epinephrine; Glucagon; Glycogen; Glycogen Synthase; Humans; Hydrogen-Ion Concentration; In Vitro Techniques; Isoproterenol; Neutrophils; Phenylephrine; Phosphorylases; Starvation

Topics: Alcohol Oxidoreductases; Animals; Glucosephosphate Dehydrogenase; Glycogen; Guinea Pigs; L-Lactate Dehydrogenase; Male; Myocardium; NADH Tetrazolium Reductase; Starvation; Succinate Dehydrogenase

Incubation of human polymorphonuclear leukocytes in a glucose-free Krebs-Ringer bicarbonate buffer for 2 h resulted in glycogen depletion, decreased phosphorylase activity and increased synthase-R activity. Addition of dialyzed latex particles to starved leukocytes revealed a very rapid ingestion rate (half-maximal ingestion within 30 s). This uptake is followed by glycogenolysis associated with an immediate two-fold increase in phosphorylase a activity and a synthase-R to -D conversion within 30 s. Furthermore, in rapid time-course experiments with phagocytozing cells we found that the concentration of cyclic AMP increased by 93% within 15 s and returned to baseline values at 1 min. In a medium without added calcium and with 1 mM ethyleneglycol-bis-(beta-aminoethylether)-N,N'-tetraacetic acid, phagocytosis was blocked, cyclic AMP formation decreased by 50% and phosphorylase activation was abolished, but the conversion of synthase-R to -D was preserved. Addition of calcium ions to cells suspended in a calcium-free buffer without added latex results in phosphorylase activation and glycogenolysis, but not in cyclic AMP increase or synthase-R to -D conversion. Measurements of 45Ca efflux during phagocytosis suggest an initial increase in cytosolic calcium obtained by a release of membrane-bound 45Ca. Activation of phosphorylase during phagocytosis is thus presumably due to an increase in cytosol Ca2+ and subsequent activation of phosphorylase kinase, and is independent of the simultaneous increase in concentration of cyclic AMP. Phosphorylation of synthase R to the D form does not depend on the presence of Ca2+ in the extracellular phase.

Topics: Calcium; Cyclic AMP; Egtazic Acid; Glycogen; Glycogen Synthase; Humans; In Vitro Techniques; Latex; Magnesium; Microspheres; Neutrophils; Phagocytosis; Phosphorylases; Starvation; Time Factors

Effects of induced starvation on the morphology of the oocytic nucleus in Cyprinus carpio have been studied to assess the nature of structural aberrations caused and the adaptations induced in the oocytes during the period of stress on account of inanition. An attempt has also been made to study the fate of a number of metabolites during this period. It has also been observed that the nuclear membrane undergoes partial or complete degeneration and there is a proliferation in the number of nucleoli which tend to move into the cytoplasm. In addition, the degenerating oocytes tend to release most of the metabolites into the interstitial tissue surrounding the oocytes.

Topics: Animals; Ascorbic Acid; Carps; Cell Nucleus; Cyprinidae; Female; Glycogen; Lipid Metabolism; Nuclear Envelope; Nucleic Acids; Oocytes; Ovum; Starvation

Topics: Animals; Blood Glucose; Catechol O-Methyltransferase; Feeding Behavior; Glycogen; Liver; Monoamine Oxidase; Myocardium; Rats; Starvation; Time Factors

In the presence of 5mM glucose insulin only modestly activated rates of glucose uptake by rat epitrochlearis muscles while the rate of glycogen formation from D(U-14C) glucose was markedly stimulated by the hormone. No effect of insulin on lactate output could be detected under these conditions. The activation of labeled glycogen formation by insulin occurred in a dose-dependent manner and a maximal effect was noted at hormone concentrations greater than 4 mU/ml. However, glycogen accumulation by epitrochlearis muscles obtained from old, spontaneously obese rats was activated by only 38 +/- 15% by a supermaximal insulin concentration (200 mU/ml) compared to a 123 +/- 43% stimulation observed in muscles from small rats. This impaired responsiveness to the hormone could not be explained by inhibition of the glycogen synthetase system by increased amounts of endogenous glycogen in the epitrochlearis muscle of spontaneously obese rats. The magnitude of this resistance greatly exceeds the modest reduction in insulin receptor number reported for msucle membranes in obese rats which suggests that other defective cellular components contribute to this syndrome.

Topics: Animals; Dose-Response Relationship, Drug; Glucose; Glycogen; Insulin; Insulin Resistance; Lactates; Male; Muscles; Obesity; Rats; Starvation

Topics: Alanine; Animals; Cyclic AMP; Fructose; Glucose; Glycerol; Glycogen; Lactates; Lipid Metabolism; Liver; Male; Phosphorylases; Pyruvates; Rats; Starvation

In the parenchymal cells of the liver of adult male rats re-fed on the evening of the fifth day after a period of absolute starvation, a nearly complete absence of autophagic vacuoles (AV) has been found by the morphometric determination of the fractional cytoplasmic volume of AV. The mean value for that parameter increased only gradually during periods of re-feeding. The value was found to be in the range of the control values only on, or after, the fifth day of re-feeding. As in previous experiments, in the control animals the number of AV was again found to be dependent on a circadian rhythm with maxima during the light, and minima during the dark, periods. This rhythm reappeared in the period of re-feeding without a shift in phase. In the controls as well as in the re-fed animals the "segregated fraction" was highest for microbodies, intermediate for mitochondria and glycogen, but rather low for the remaining components of the cytoplasm. It is suggested that the long term inhibition of cellular autophagy, found in the present study, plays an important role in the restorative cellular growth of the liver during the recovery from the atrophy induced by starvation.

Topics: Animals; Atrophy; Circadian Rhythm; Glycogen; Liver; Male; Microbodies; Mitochondria, Liver; Rats; Starvation; Time Factors

Topics: Animals; Female; Glycogen; Guinea Pigs; Heart; Heart Atria; Heart Ventricles; Lipids; Male; Myocardium; Papillary Muscles; Phospholipids; Reserpine; Starvation; Time Factors; Tissue Preservation; Triglycerides

Studies in man and experimental animals suggest that the metabolism of glucose by skeletal muscle is depressed during starvation. To investigate the basis for this, the effect of starvation on the uptake and disposition of glucose in skeletal muscle was studied in the isolated perfused rat hindquarter. In contrast to earlier work carried out in heart, neither glucose uptake, whether stimulated by insulin or exercise, nor glycolysis were depressed by 48 hr of starvation or by perfusion of the hindquarter with acetoacetate, palmitate, or octanoate. Glucose oxidation, assessed from the oxidation of 1-[14C]lactate, was depressed by approximately 75% in starved rats and by 30% in fed rats perfused with acetoacetate. Exercise increased lactate oxidation 10-fold in both fed and starved rats; however, the relative difference between the groups persisted. In general, changes in lactate oxidation were paralleled by changes in the activity of pyruvate dehycrogenase (active form). The data suggest that glucose metabolism in skeletal muscle is inhibited during starvation at the step of pyruvate oxidation and that this inhibition persists during exercise. The also suggest that the diminution of glucose uptake that occurs in skeletal muscle of intact organisms during starvation may not be related to the presence of high concentrations of free fatty acids and ketone bodies.

Topics: Acetyl Coenzyme A; Alanine; Animals; Blood Glucose; Fatty Acids, Nonesterified; Glucose; Glycogen; Insulin; Ketone Bodies; Lactates; Muscle Proteins; Muscles; Perfusion; Physical Exertion; Pyruvate Dehydrogenase Complex; Rats; Starvation

Glycogen reserves are entirely consumed during total starvation of Bombyx mori L. larvae. While the storage of glycogen is lowering and the dietary supply of carbohydrates stopped, the amount of trehalose also decreases but less rapidly than this of glycogen. Relative homeostasis is maintained but only for the ten first hours of inanition. Quantitative evaluation of blood trehalose, which is preformed more rapidly than glycogen analysis, might be used as an efficient test to characterized some physiopathological states.

Topics: Animals; Bombyx; Disaccharides; Glycogen; Larva; Starvation; Trehalose

1. Tissue glycogen contributes, maximally, only 10% of the respiratory fuel of the rat spleen slice in the absence of an added carbon source, and makes no significant contribution when glucose (3mM) is added. 2. The reserves of fatty acid in the form of triglyceride (35.5mumol of fatty acid/g dry wt. of tissue) fall by approx. 25% after incubation of spleen slices with or without added glucose for 2h, and , on this basis, account for 32% of the oxidative fuel. 3. In contrast, the total oxidative contribution of fatty acid reserves to the respiratory fuel, determined on the basis of inhibiton of respiration by 2-bromostearate, is 42-52%. This range includes tissue from both starved and well-fed animals and is not significantly altered by the presence of added glycose (3mM). 4. Large quantities of NH3 (31-35mumol//h per g dry wt. of tissue) are produced by spleen slices incubated in the absence of added substrates, and this value is suppressed by approx. 50% on incubation with glucose (3mM). Adenine nucleotide breakdown can account for only 17% of the total ammonia produced. 5. Individual free amino acid concentrations in spleen were determined, both in vivo and in slices before and after 60 min of incubation. Although the total free amino acid pool size increases by 45% during incubation, owing to protein breakdown, the tissue concentrations of aspartate, glutamate, glutamine and alanine do not increase. It is suggested that these amino acids areoxidized in a net sense to CO2 and water with the liberation of free NH3 via transamination reactions, glutaminase, the purine nucleotide cycle and the tricarboxylic acid cycle. 6. It is concluded that the normal endogenous metabolism of sliced rat spleen (43-52% due to lipids, 30% due to amino acids and 10% due to glycogen) is modified by added glycose only to the extent that glycogen oxidation and 50% of the contribtion made by ino acids are suppressed; endogenous lipid metabolism is unaffected.

Topics: Amino Acids; Ammonia; Animals; Carbohydrate Metabolism; Fatty Acids, Nonesterified; Glucose; Glycogen; In Vitro Techniques; Models, Biological; NAD; Oxygen Consumption; Rats; Spleen; Starvation; Stearates

In small rats deprived of food for 19h (or 43h), 36% (or 39%) of the glycogen that disappeared was lost from the carcass and 64% (or 61%) from liver. Carcass glycogen is potentially a substantial source of glucose during short-term starvation via the Cori cycle.

Topics: Animals; Glucose; Glycogen; Liver Glycogen; Male; Muscles; Rats; Starvation; Time Factors

Topics: Body Weight; Child; Diet Fads; Female; Glycogen; Humans; Male; Nutrition Disorders; Nutritional Physiological Phenomena; Obesity; Physical Fitness; Sports Medicine; Starvation

Topics: Animals; Calcium; Catheterization; Cell Separation; Epinephrine; Glucagon; Gluconeogenesis; Glycogen; In Vitro Techniques; Liver; Male; Microbial Collagenase; Microscopy, Electron; Perfusion; Protein Biosynthesis; Rats; Starvation

Topics: Animals; Female; Glucose-6-Phosphatase; Glycogen; Histocytochemistry; In Vitro Techniques; Liver; Phosphorylases; Rats; Starvation; Time Factors

Topics: Animals; Bird Diseases; Birds; Fish Diseases; Fishes; Glycogen; Starvation; Trematoda; Trematode Infections

The amount of fat available as substrate to provide the energy needed for submaximal exercise is almost unlimited; therefore, it stands to reason that the organism will adapt so that it uses fat as the major energy substrate during very prolonged exercise. Nevertheless, the quantitatively smaller body stores of carbohydrate, which contain only one to two percent as many calories as the fat stores, play a very important role during exercise, since depletion of either muscle or liver glycogen will force an individual to terminate strenuous muscular work. In normal dogs during long-lasting exercise, at energy expenditures ranging from the resting state of 0.73 kcal/m2 min to a work load of 4.66 kcal/m2 min, the FFA mobilization, and participation of FFA oxidation in total energy expenditure increases. During prolonged exercise in trained dogs, 50-90% of the energy may derive from plasma FFA, while plasma glucose contributes not more than 10% to the energy expenditure. However, there is an inverse relationship between the amount of glycogen stored inside the muscle, its rate of depletion, and muscular endurance during prolonged strenuous work. Oxidation of FFA spares muscle glycogen and in this way increases work endurance.

Topics: Animals; Blood Glucose; Cold Temperature; Dogs; Energy Metabolism; Fatty Acids, Nonesterified; Female; Glucose; Glycogen; Lactates; Male; Muscles; Oxidation-Reduction; Physical Conditioning, Animal; Rest; Starvation; Time Factors

Topics: Alanine; Amino Acids; Animals; Blood Glucose; Carbon Radioisotopes; Citrates; Female; Gluconeogenesis; Glucosephosphates; Glycerol; Glycerophosphates; Glycogen; Heterozygote; Homozygote; Lactates; Lipids; Liver; NADP; Obesity; Starvation; Triglycerides

Topics: Adrenergic beta-Agonists; Adrenergic beta-Antagonists; Animals; Blood Glucose; Epinephrine; Gluconeogenesis; Glucose; Glycogen; Glycosuria; Isoproterenol; Kidney; Norepinephrine; Propranolol; Rats; Regional Blood Flow; Starvation; Stimulation, Chemical

1. Rates of insulin secretion, glucose utilization, lactate output, incorporation of glucose into glycogen, contents of glucose 6-phosphate, fructose 1,6-diphosphate and ATP, and maximally extractable enzyme activities of hexokinase, high-K(m) glucose-phosphorylating activity (;glucokinase'), glucose 6-phosphatase and unspecific acid phosphatase were measured in isolated pancreatic islets from fed and 48-h-starved mice. 2. In the fed state insulin secretion from isolated islets was increased five- to six-fold when the extracellular glucose concentration was raised from 2.5mm to 16.7mm; 5mm-caffeine potentiated this effect. The secretory response to glucose of islets from mice starved for 48h was diminished at all glucose concentrations from 2.5mm up to approx. 40mm. Very high glucose concentrations (60mm and above) restored the secretory response to that found in the fed state, suggesting that the K(m) value for the overall secretory process had been increased (approx. fourfold) by starvation. Addition of 5mm-caffeine to islets from starved mice also restored the insulin secretory response to 2.5-16.7mm-glucose to normal values. 3. Extractable hexokinase, ;glucokinase', glucose 6-phosphatase and unspecific phosphatase activities were not changed by starvation. 4. Glucose utilization and glycolysis (measured as the rate of formation of (3)H(2)O from [5-(3)H]glucose over a 2h period) was decreased in islets from starved mice at all glucose concentrations up to approx. 55mm. At still higher glucose concentrations up to approx. 100mm, there was no difference between the fed and starved state, suggesting that the K(m) value for the rate-limiting glucose phosphorylation had been increased (approx. twofold) by starvation. Preparation of islets omitting substrates (glucose, pyruvate, fumarate and glutamate) from the medium during collagenase treatment lowered the glucose utilization measured subsequently at 16.7mm-glucose by 38 and 30% in islets from fed and starved mice respectively. Also the 2h lactate output by the islets at 16.7mm extracellular glucose was diminished by starvation. Incorporation of glucose into glycogen was extremely low, but the rate of incorporation was more than doubled by starvation. 5. After incubation for 30min at 16.7mm-glucose the content of glucose 6-phosphate was unchanged by starvation, that of ATP was increased and the concentration of (fructose 1,6-diphosphate plus triose phosphates) was decreased. 6. Possible mechanisms behind t

Topics: Acid Phosphatase; Adenosine Triphosphate; Animals; Caffeine; Fructosephosphates; Fumarates; Glucokinase; Glucose; Glucose-6-Phosphatase; Glucosephosphates; Glutamates; Glycogen; Glycolysis; Hexokinase; In Vitro Techniques; Insulin; Insulin Secretion; Islets of Langerhans; Kinetics; Male; Mice; NADP; Pyruvates; Starvation; Tritium

Topics: Age Factors; Animal Nutritional Physiological Phenomena; Animals; Animals, Newborn; Brain; Diet Therapy; Female; Glycogen; Haplorhini; Kidney; Liver; Liver Glycogen; Lung; Macaca; Muscles; Nutrition Disorders; Organ Specificity; Pregnancy; Spleen; Starvation; Time Factors

Topics: Animals; Brain; Brain Edema; Brain Neoplasms; Central Nervous System; Dogs; Glycogen; Guinea Pigs; Haplorhini; Hibernation; Humans; Hypoglycemia; Hypoxia; Ischemia; Mice; Microscopy, Electron; Neuroglia; Neurons; Physical Exertion; Rabbits; Radiation Effects; Rats; Seizures; Shock; Starvation

1. The effects of starvation and diabetes on brain fuel metabolism were examined by measuring arteriovenous differences for glucose, lactate, acetoacetate and 3-hydroxybutyrate across the brains of anaesthetized fed, starved and diabetic rats. 2. In fed animals glucose represented the sole oxidative fuel of the brain. 3. After 48h of starvation, ketone-body concentrations were about 2mm and ketone-body uptake accounted for 25% of the calculated O(2) consumption: the arteriovenous difference for glucose was not diminished, but lactate release was increased, suggesting inhibition of pyruvate oxidation. 4. In severe diabetic ketosis, induced by either streptozotocin or phlorrhizin (total blood ketone bodies >7mm), the uptake of ketone bodies was further increased and accounted for 45% of the brain's oxidative metabolism, and the arteriovenous difference for glucose was decreased by one-third. The arteriovenous difference for lactate was increased significantly in the phlorrhizin-treated rats. 5. Infusion of 3-hydroxybutyrate into starved rats caused marked increases in the arteriovenous differences for lactate and both ketone bodies. 6. To study the mechanisms of these changes, steady-state concentrations of intermediates and co-factors of the glycolytic pathway were determined in freeze-blown brain. 7. Starved rats had increased concentrations of acetyl-CoA. 8. Rats with diabetic ketosis had increased concentrations of fructose 6-phosphate and decreased concentrations of fructose 1,6-diphosphate, indicating an inhibition of phosphofructokinase. 9. The concentrations of acetyl-CoA, glycogen and citrate, a potent inhibitor of phosphofructokinase, were increased in the streptozotocin-treated rats. 10. The data suggest that cerebral glucose uptake is decreased in diabetic ketoacidosis owing to inhibition of phosphofructokinase as a result of the increase in brain citrate. 11. The inhibition of brain pyruvate oxidation in starvation and diabetes can be related to the accelerated rate of ketone-body metabolism; however, we found no correlation between the decrease in glucose uptake in the diabetic state and the arteriovenous difference for ketone bodies. 12. The data also suggest that the rates of acetoacetate and 3-hydroxybutyrate utilization by brain are governed by their concentrations in plasma. 13. The finding of very low concentrations of acetoacetate and 3-hydroxybutyrate in brain compared with plasma suggests that diffusion across the blood-brain barrier

Topics: Acetoacetates; Acetyl Coenzyme A; Adenine Nucleotides; Animals; Biological Transport; Blood Glucose; Blood-Brain Barrier; Brain; Citrates; Diabetes Mellitus; Female; Glucose; Glycogen; Hydroxybutyrates; Ketone Bodies; Lactates; Pentobarbital; Phlorhizin; Phosphocreatine; Rats; Spectrometry, Fluorescence; Starvation; Streptozocin; Time Factors

Topics: Acetoacetates; Animals; Blood Glucose; Caprylates; Cattle; Diabetes Mellitus; Fatty Acids, Nonesterified; Female; Glucose; Glucose Tolerance Test; Glycogen; Glycolysis; Insulin; Ketone Bodies; Muscles; Oleic Acids; Oxidation-Reduction; Perfusion; Pyruvates; Rats; Rest; Starvation; Streptozocin; Swine

Topics: Adaptation, Physiological; Animals; Carbon Dioxide; Carbon Radioisotopes; Cytochrome c Group; Dietary Proteins; Energy Metabolism; Glucose; Glycogen; Hypertrophy; In Vitro Techniques; Leucine; Liver; Male; Mitochondria, Muscle; Muscles; Myofibrils; Organ Size; Oxidation-Reduction; Palmitic Acids; Proteins; Rats; Starvation; Time Factors; Water

Topics: Adenosine Triphosphate; Anaerobiosis; Brain; Carbohydrate Metabolism; Cyclic AMP; Dietary Carbohydrates; Epinephrine; Glucagon; Gluconeogenesis; Glucose; Glycogen; Glycogen Synthase; Humans; Hyperglycemia; Hypoxia; Insulin; Ketone Bodies; Lactates; Liver; Muscles; Oxidative Phosphorylation; Physical Exertion; Postoperative Complications; Pyruvates; Starvation; Wounds and Injuries

Topics: Animals; Calcium; Coronary Circulation; Dose-Response Relationship, Drug; Glycogen; Heart; Heart Rate; Mice; Mitochondria, Muscle; Myocardium; Starvation; Temperature

Topics: Animals; Cycloheximide; Fructose; Glucagon; Glucose; Glycogen; Glycolysis; In Vitro Techniques; Insulin; Lactates; Liver; Oxygen Consumption; Rats; Starvation; Stimulation, Chemical

Topics: Acetates; Animals; Carbon Radioisotopes; Culture Media; Dinitrophenols; Glucose; Glycogen; Glycolysis; Hydrogen-Ion Concentration; Hypoxanthines; Iodoacetates; Methods; Oxidative Phosphorylation; Phosphates; Phosphorus; RNA; Spectrophotometry; Starvation; Tetrahymena; Uracil

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Bivalvia; Carbohydrate Metabolism; Cytoplasmic Granules; Ecology; Glucose; Glycogen; Hemolymph; Histocytochemistry; Starvation; Temperature; Trematoda

Topics: Animals; Aspartate Aminotransferases; Blood Glucose; Blood Proteins; Body Weight; Chlorides; Cholesterol; Eels; Fatty Acids, Nonesterified; Glycerides; Glycogen; Hematocrit; Hemoglobinometry; Lactates; Liver; Liver Glycogen; Muscles; Organ Size; Phosphates; Seasons; Starvation

Topics: Adipose Tissue; Amino Acids; Animals; Blood; Chickens; Fatty Acids, Nonesterified; Glucagon; Glucose; Glycogen; Guanidines; Hypoglycemic Agents; In Vitro Techniques; Kinetics; Lipid Metabolism; Liver Glycogen; Muscles; Pancreas; Pancreatectomy; Reserpine; Starvation

Topics: Animals; Brain; Glycogen; Haplorhini; Hypoxia; Kidney; Liver Glycogen; Macaca; Muscles; Spleen; Starvation; Time Factors

Topics: Animals; Biomphalaria; Body Water; Body Weight; Cell Nucleus; Connective Tissue Cells; Cytoplasmic Granules; Endoplasmic Reticulum; Epithelium; Female; Genitalia; Glycogen; Golgi Apparatus; Histocytochemistry; Inclusion Bodies; Lipoproteins; Lysosomes; Male; Microscopy, Electron; Mitochondria; Organ Size; Pigments, Biological; Polysaccharides; Starvation; Time Factors

Topics: Animals; Biometry; Body Weight; Cell Nucleus; Circadian Rhythm; Epithelial Cells; Glycogen; Inclusion Bodies; Kupffer Cells; Liver; Lysosomes; Male; Microbodies; Microscopy; Microscopy, Electron; Mitochondria, Liver; Phagocytosis; Rats; Starvation; Time Factors

Topics: Acid Phosphatase; Alkaline Phosphatase; Aminopeptidases; Animals; Digestive System; Esterases; Fasciola hepatica; Glucosidases; Glucuronidase; Glycogen; Glycosaminoglycans; Hexosaminidases; Histocytochemistry; Inclusion Bodies; Lymnaea; Lysosomes; Starvation; Sulfatases; Time Factors

Topics: Animals; Anura; Endoplasmic Reticulum; Fasting; Fatty Liver; Glycogen; Inclusion Bodies; Lipids; Liver; Lysosomes; Microscopy, Electron; Mitochondria; Necrosis; Seasons; Starvation

Topics: Adipose Tissue; Adipose Tissue, Brown; Animals; Cell Count; Connective Tissue; Connective Tissue Cells; Epididymis; Esterases; Glycogen; Histocytochemistry; Male; Mice; Obesity; Rats; Starvation

Topics: Animals; Cold Temperature; Environmental Exposure; Female; Glycogen; Isoenzymes; Kinetics; L-Lactate Dehydrogenase; Lactates; Muscles; Myocardium; Starvation; Turtles

Topics: Animals; Animals, Newborn; Blood Glucose; Brain; Dietary Fats; Female; Glutamates; Glutamine; Glycine; Glycogen; Liver Glycogen; Maternal-Fetal Exchange; Pregnancy; Rats; Starvation; Time Factors

Topics: Animals; Carbon Isotopes; Fructosephosphates; Gluconeogenesis; Glycogen; Guinea Pigs; Intestinal Mucosa; Jejunum; Ligases; Male; Phosphoenolpyruvate Carboxykinase (GTP); Pyruvates; Starvation

Topics: Aging; Animals; Blood Glucose; Body Weight; DNA; Fatty Acids; Female; Glycogen; Ketone Bodies; Lactation; Liver; Male; Organ Size; Pregnancy; Rats; Starvation; Time Factors

Topics: Adult; Biopsy, Needle; Blood Glucose; Blood Pressure; Body Weight; Depression, Chemical; Dietary Carbohydrates; Female; Glycogen; Humans; Liver; Male; Middle Aged; Pulse; Starvation; Stimulation, Chemical; Time Factors

Topics: Acetoacetates; Adult; Blood Flow Velocity; Blood Glucose; Dietary Carbohydrates; Female; Glycogen; Humans; Hydroxybutyrates; Ketone Bodies; Lactates; Liver; Male; Nitrogen; Starvation; Urea

Topics: Alanine; Animals; Blood Glucose; Brain Chemistry; Diabetes Mellitus; Gluconeogenesis; Glutamates; Glycine; Glycogen; Hyperglycemia; Injections, Intravenous; Ketones; Male; Rats; Starvation; Streptozocin

Topics: Acetates; Animals; Cytoplasmic Granules; Germ-Free Life; Glucose; Glutamates; Glycerophosphates; Glycogen; Inclusion Bodies; Latex; Microspheres; Peptones; Pinocytosis; RNA; Starch; Starvation; Stimulation, Chemical; Tetrahymena pyriformis

1. The purpose of this study was to determine the nature of the metabolic changes associated with carbohydrate and fat metabolism that occurred in the blood and liver of lactating dairy cows during starvation for 6 days. 2. During starvation, the blood concentrations of the free fatty acids and ketone bodies increased, whereas that of citrate decreased. After an initial increase, the blood concentration of glucose subsequently declined as starvation progressed. Starvation caused a significant decrease in the plasma concentration of serine and a significant increase in that of leucine. 3. After 6 days of starvation the hepatic concentrations of oxaloacetate, citrate, phosphoenolpyruvate, 2-phosphoglycerate, 3-phosphoglycerate, glucose, glycogen, ATP and NAD(+) had all decreased, as had the hepatic activities of phosphopyruvate carboxylase (EC 4.1.1.32) and pyruvate kinase (EC 2.7.1.40). 4. The above metabolic changes are similar to those previously found to occur in cows suffering from spontaneous ketosis (Baird et al., 1968; Baird & Heitzman, 1971). 5. Milk yield decreased progressively during starvation. 6. There were marked differences in the ability of individual animals to resist the onset of severe starvation ketosis.

Topics: Acidosis; Adenosine Triphosphate; Animals; Blood Glucose; Cattle; Cattle Diseases; Citrates; Fatty Acids, Nonesterified; Female; Glucose; Glycogen; Ketone Bodies; Lactation; Leucine; Liver; NAD; Oxaloacetates; Phosphoenolpyruvate; Pregnancy; Serine; Starvation

Topics: Animals; Arthropods; Blood Cells; Calcium; Cell Nucleolus; Cell Nucleus; Collagen; Endoplasmic Reticulum; Enzymes; Exocrine Glands; Glycogen; Hemolymph; Inclusion Bodies; Intercellular Junctions; Lipids; Microscopy, Electron; Microtubules; Mitochondria; Pinocytosis; Protein Biosynthesis; Starvation

Topics: Adipose Tissue, Brown; Animals; Body Temperature Regulation; Cold Temperature; Female; Glycogen; Hibernation; Histocytochemistry; Lipids; Male; Mice; Microscopy, Electron; Mitochondria; Starvation; Temperature; Time Factors

Topics: Adrenal Glands; Adrenocorticotropic Hormone; Animals; Corticosterone; Diabetes Mellitus, Experimental; Epinephrine; Glucagon; Glucose; Glycogen; Hormones; Hypophysectomy; Insulin; Insulin Antibodies; Male; Pancreatectomy; Rats; Starvation

Topics: Adipose Tissue; Animal Nutritional Physiological Phenomena; Animals; Carbon Dioxide; Carbon Isotopes; Catalysis; Cytoplasm; Depression, Chemical; Dietary Carbohydrates; Epididymis; Fatty Acids; Glycerol; Glycogen; Hydrogen; Lactates; Lipids; Male; NAD; Oxidation-Reduction; Phenazines; Protons; Pyruvates; Rats; Species Specificity; Starvation; Sulfuric Acids; Time Factors; Tritium; Water

Topics: Acclimatization; Animals; Aspartate Aminotransferases; Blood Glucose; Blood Proteins; Diet; Eels; Fatty Acids, Nonesterified; Female; Glucose; Glycerol; Glycogen; Kidney; Lactates; Lipid Metabolism; Liver Glycogen; Muscles; Ovary; Pyruvates; Starvation; Temperature

Topics: Adipose Tissue; Amides; Ammonium Chloride; Animals; Blood Glucose; Butyrates; Carbon Isotopes; Diabetes Mellitus, Experimental; Diaphragm; Glucose; Glucose Tolerance Test; Glycogen; Guanidines; Insulin; Insulin Antibodies; Insulin Secretion; Islets of Langerhans; Liver; Liver Glycogen; Metabolism; Mice; Muscles; Ornithine; Phenformin; Rabbits; Radioimmunoassay; Rats; Seizures; Starvation; Stimulation, Chemical; Urea

Topics: Adipose Tissue; Animal Nutritional Physiological Phenomena; Animals; Blood Glucose; Circadian Rhythm; Diaphragm; Fatty Acids, Nonesterified; Glycogen; Glycolysis; Lactates; Lipids; Liver; Liver Glycogen; Male; Muscles; Nitrogen; Oxygen Consumption; Pyruvates; Rats; Starvation; Time Factors

1. In aerobic conditions the isolated perfused liver from well-fed rats rapidly formed lactate from endogenous glycogen until the lactate concentration in the perfusion medium reached about 2mm (i.e. the concentration of lactate in blood in vivo) and then production ceased. Pyruvate was formed in proportion to the lactate, the [lactate]/[pyruvate] ratio remaining between 8 and 15. 2. The addition of 5mm- or 10mm-glucose did not affect lactate production, but 20mm- and 40mm-glucose greatly increased lactate production. This effect of high glucose concentration can be accounted for by the activity of glucokinase. 3. The perfused liver released glucose into the medium until the concentration was about 6mm. When 5mm- or 10mm-glucose was added to the medium much less glucose was released. 4. At high glucose concentrations (40mm) more glucose was taken up than lactate and pyruvate were produced; the excess of glucose was probably converted into glycogen. 5. In anaerobic conditions, livers of well-fed rats produced lactate at relatively high rates (2.5mumol/min per g wet wt.). Glucose was also rapidly released, at an initial rate of 3.2mumol/min per g wet wt. Both lactate and glucose production ceased when the liver glycogen was depleted. 6. Addition of 20mm-glucose increased the rate of anaerobic production of lactate. 7. d-Fructose also increased anaerobic production of lactate. In the presence of 20mm-fructose some glucose was formed anaerobically from fructose. 8. In the perfused liver from starved rats the rate of lactate formation was very low and the increase after addition of glucose and fructose was slight. 9. The glycolytic capacity of the liver from well-fed rats is equivalent to its capacity for fatty acid synthesis and it is pointed out that hepatic glycolysis (producing acetyl-CoA in aerobic conditions) is not primarily an energy-providing process but part of the mechanism converting carbohydrate into fat.

Topics: Animals; Coenzyme A; Fatty Acids; Female; Fructose; Glucokinase; Glucose; Glycogen; Glycolysis; Hypoxia; In Vitro Techniques; Lactates; Liver; Male; Perfusion; Pyruvates; Rats; Starvation

Topics: Aconitate Hydratase; Adenosine Triphosphate; Animals; Citrates; Female; Fluorine; Fluoroacetates; Glycogen; Liver; Male; Microscopy; Mitochondria, Liver; Models, Biological; Oxygen; Oxygen Consumption; Polarography; Rats; Starvation; Time Factors

Topics: Adipose Tissue; Animals; Blood Glucose; Body Weight; Cholesterol; Chromatography, Gas; Creatinine; Dietary Carbohydrates; Dietary Fats; Dietary Proteins; Fatty Acids; Fatty Acids, Essential; Fatty Acids, Nonesterified; Glycogen; Growth; Insulin; Lipids; Liver Glycogen; Male; Muscles; Nitrogen; Rats; Starvation; Triglycerides

Topics: Abdominal Injuries; Animals; Animals, Newborn; Autoradiography; Blood Glucose; Carbon Isotopes; Fatty Acids, Nonesterified; Gluconeogenesis; Glucose; Glucose Tolerance Test; Glycogen; Laparotomy; Rabbits; Starvation

Topics: Adenine Nucleotides; Adenosine Triphosphate; Animals; Animals, Newborn; Body Weight; Diet; Glucose; Glycogen; Growth; Growth Disorders; Hindlimb; Lactates; Male; Muscle Development; Muscles; Organ Size; Oxidoreductases; Pyruvates; Rats; Starvation

Topics: Animals; Carbon Isotopes; Gluconeogenesis; Glycogen; Hydrocortisone; Injections, Intravenous; Liver; Oligosaccharides; Perchlorates; Rats; Starvation; Time Factors; Uracil Nucleotides

Topics: Adipose Tissue; Calorimetry; Central Nervous System; Fasting; Gluconeogenesis; Glucose; Glycogen; Humans; Insulin; Insulin Secretion; Kidney; Lipid Metabolism; Liver; Muscles; Proteins; Starvation

Topics: Animals; Blood Glucose; Carbohydrate Metabolism; Centrifugation; Epinephrine; Female; Glycogen; Guinea Pigs; Lactates; Liver Glycogen; Rotation; Starvation; Time Factors

Topics: Adipose Tissue; Animals; Enzyme Activation; Glucosyltransferases; Glycogen; Hyperglycemia; Insecta; Male; Neurosecretory Systems; Starvation

Topics: Animals; Digestive System; Echinodermata; Fucose; Galactose; Glucose; Glycogen; Mannitol; Mannose; Starvation; Time Factors

Topics: Cell Division; Cell Membrane; Cell Wall; Cycloheximide; Cytoplasmic Granules; Dactinomycin; Glycogen; Microscopy, Electron; Myxomycetes; Plant Proteins; RNA; Spores; Starvation; Time Factors

Topics: Adrenal Medulla; Blood Glucose; Caseins; Diarrhea, Infantile; Diet Therapy; Dietary Carbohydrates; Ephedrine; Epinephrine; Female; Glucagon; Glucose Tolerance Test; Glycogen; Humans; Hypoglycemia; Infant; Infant, Newborn; Injections, Intravenous; Insulin; Liver; Malabsorption Syndromes; Monosaccharides; Pregnancy; Starvation; Time Factors

Topics: Adipose Tissue; Animals; Body Weight; Carbohydrate Metabolism; Glycogen; Hemolymph; Insecta; Larva; Lipid Metabolism; Muscles; Organ Size; Starvation

Topics: Acetates; Acetoacetates; Adipose Tissue; Animal Nutritional Physiological Phenomena; Animals; Carbohydrate Metabolism; Carbon Dioxide; Carbon Isotopes; Cholesterol; Citrates; Citric Acid Cycle; Depression, Chemical; Diaphragm; Drug Synergism; Epididymis; Esters; Fatty Acids; Glucose; Glycerides; Glycerol; Glycogen; Hydroxybutyrates; Insulin; Lipids; Male; Muscles; Oxygen Consumption; Pyruvates; Rats; Rats, Inbred Strains; Starvation; Stimulation, Chemical

1. Glycerol and dihydroxyacetone, both antiketogenic and readily metabolized, but differing in their effects on the redox state of the hepatic NAD couples, were given to starved rats and the contents of metabolites were measured in freezeclamped liver and in the blood. The object was to study the effects of changes in the redox state and of the availability of oxidizable substrates on the rate of ketone-body formation. 2. Intramuscular administration of dihydroxyacetone, glycerol or glucose to starved rats decreased the concentrations of acetoacetate and 3-hydroxybutyrate in the blood by 70-80% within 60min., whereas there was no major change in the free fatty acid concentration. 3. Dihydroxyacetone, but not glucose or glycerol, caused an immediate and sustained twofold increase in the blood lactate concentration. 4. Dihydroxyacetone and glycerol caused a rapid fall in the hepatic concentrations of ketone bodies, dihydroxyacetone being more effective. 5. This decrease was not accompanied by significant changes in the concentrations of acetyl-CoA, long-chain acyl-CoA or free CoA. 6. The hepatic glycerophosphate concentration rose about 40-fold on administration of glycerol, whereas with dihydroxyacetone the increase was only about 50%. The large increase in glycerophosphate concentration after administration of glycerol was completely prevented by pretreatment of the rats with tri-iodothyronine. Triiodothyronine-treated rats showed the same decrease in ketone-body concentrations after administration of glycerol as the untreated rats. 7. Glycerol and dihydroxyacetone caused an increase in the hepatic lactate concentration; the pyruvate concentration rose only after injection of dihydroxyacetone. 8. Both compounds increased liver glycogen. 9. Calculation of the [free NAD(+)]/[free NADH] ratios indicated that dihydroxyacetone increased the ratio in cytoplasm and mitochondria, whereas glycerol caused a prompt fall in both compartments, followed at 10min. by a slight rise in the mitochondrial compartment. 10. Dihydroxyacetone did not alter the hepatic content of ATP. 11. The findings suggest that the main reason for the antiketogenic effect of glycerol and dihydroxyacetone was a consequence of their ready metabolism and the provision of an increased supply of C(3) intermediates for conversion into oxaloacetate. Under the test conditions, neither the hepatic content of alpha-glycerophosphate nor the redox state of the NAD couples appeared to play a major role in

Topics: Acetoacetates; Acetone; Animals; Coenzyme A; Fatty Acids, Nonesterified; Glucose; Glycerol; Glycerophosphates; Glycogen; Hydroxybutyrates; Ketone Bodies; Lactates; Liver; Mitochondria, Liver; NAD; Oxidation-Reduction; Pyruvates; Rats; Starvation; Triiodothyronine

Topics: Animals; Carbon Isotopes; Culicidae; Disaccharides; Female; Fructose; Glucose; Glycogen; Kinetics; Sorbitol; Starvation

Topics: Acid Phosphatase; Adipose Tissue; Alkaline Phosphatase; Animals; Epididymis; Esterases; Glycogen; Histocytochemistry; Male; Mesentery; Nutritional Physiological Phenomena; Rats; Starvation

Topics: Animals; Chickens; Fasting; Glycogen; Liver Glycogen; Male; Starvation

Topics: Acid-Base Equilibrium; Animals; Carbohydrate Metabolism; Carbon Dioxide; Diabetes Mellitus, Experimental; Fasting; Gluconeogenesis; Glucose; Glycogen; In Vitro Techniques; Kidney; Liver; Male; Rats; Starvation

Topics: Age Factors; Animals; Animals, Newborn; Blood Glucose; Fatty Acids, Nonesterified; Gluconeogenesis; Glycogen; Growth Hormone; Hypoglycemia; Insulin; Liver Glycogen; Myocardium; Radioimmunoassay; Starvation; Swine

Topics: Animals; Cell Nucleolus; Cell Nucleus; Cytoplasm; Glycogen; Lipid Metabolism; Microscopy, Electron; Mitochondria; Proteins; Starvation; Tetrahymena

Topics: Acclimatization; Adaptation, Physiological; Animals; Crustacea; Glycogen; Liver Glycogen; Muscles; Myocardium; Oxygen Consumption; Starvation; Temperature

Topics: Animals; Carbohydrate Metabolism; Cold Temperature; Disaccharides; Glycogen; Insecta; Starvation

Topics: Adrenal Glands; Animals; Carbohydrate Metabolism; Diaphragm; Drug Antagonism; Glucose; Glycogen; Histamine; Hyperglycemia; Hypoglycemia; In Vitro Techniques; Insulin; Liver Glycogen; Male; Muscles; Oxygen Consumption; Rats; Starvation

Topics: Acetoacetates; Acute Disease; Adenosine Triphosphate; Animals; Blood Glucose; Chronic Disease; Citrates; Diabetes Mellitus, Experimental; Fatty Acids, Nonesterified; Fructose; Glucose; Glycogen; Hexosephosphates; Hydroxybutyrates; Ketoglutaric Acids; Lactates; Malates; Myocardium; Pyruvates; Rats; Starvation; Statistics as Topic

Topics: Adenosine Triphosphate; Animals; Chlorothiazide; Diabetes Mellitus, Experimental; Glucose; Glycogen; Hexosephosphates; Insulin; Ischemia; Kidney; Lactates; Male; Organomercury Compounds; Phlorhizin; Phosphocreatine; Rats; Starvation

Topics: Acclimatization; Adipose Tissue; Animals; Body Composition; Body Weight; Chorionic Gonadotropin; Female; Fetus; Glycogen; Liver; Mice; Myocardium; Organ Size; Placenta; Pregnancy; Pregnancy, Animal; Starvation; Temperature; Water

Topics: Adaptation, Physiological; Arteries; Brain; Carbohydrate Metabolism; Carbohydrates; Gluconeogenesis; Glucose; Glycogen; Humans; Keto Acids; Lipid Metabolism; Obesity; Oxygen Consumption; Proteins; Starvation; Time Factors; Veins

Topics: Animals; Body Composition; Body Weight; Carbon Isotopes; Cestoda; Chromatography, Thin Layer; Dietary Fats; Esterases; Fatty Acids; Fatty Acids, Essential; Glycogen; Linoleic Acids; Lipase; Lipid Metabolism; Male; Oleic Acids; Palmitic Acids; Phosphatidylcholines; Phosphatidylethanolamines; Phospholipids; Proteins; Rats; Spectrum Analysis; Starvation; Stearic Acids; Triglycerides

Topics: Animals; Calcium; Cartilage; Glycogen; Growth Plate; Phosphates; Rats; Rats, Sprague-Dawley; Starvation; Vitamin D; Wound Healing

Topics: Animals; Atrial Function; Glucose; Glycogen; Heart; Muscle Contraction; Rats; Starvation

Topics: Animals; Carbohydrate Metabolism; Emulsions; Fatty Acids; Female; Glycogen; Gonadotropins; Pregnancy; Pregnancy, Animal; Rats; Sesame Oil; Starvation

Topics: Acid Phosphatase; Cell Nucleolus; Cell Nucleus; Cytoplasm; Dihydrolipoamide Dehydrogenase; Feeding Behavior; Glycogen; Histocytochemistry; Inclusion Bodies; Insecta; Larva; Lipid Metabolism; Lipids; Methods; Microscopy, Electron; Mitochondria; Mitochondrial Swelling; Mitosis; Nucleoproteins; Oxygen Consumption; RNA; Staining and Labeling; Starvation; Time Factors

1. Glucose uptake or glucose formation has been studied in kidney cortex slices to investigate metabolic control of phosphofructokinase and fructose-diphosphatase activities. 2. Glucose uptake is increased and glucose formation is decreased by anoxia, cyanide or an uncoupling agent. Under these conditions the intracellular concentrations of glucose 6-phosphate and ATP decreased whereas that of fructose diphosphate either increased or remained constant, and the concentrations of AMP and ADP increased. 3. Glucose uptake was decreased, and glucose formation from glycerol or dihydroxyacetone was increased, by the presence of ketone bodies or fatty acids, or after starvation of the donor animal. Under these conditions, the concentrations of glucose 6-phosphate and citrate were increased, whereas those of fructose diphosphate and the adenine nucleotides were unchanged (see also Newsholme & Underwood, 1966). 4. It is concluded that anoxia and cell poisons increase glucose uptake and decrease gluconeogenesis by stimulating phosphofructokinase and inhibiting fructose diphosphatase, whereas ketone bodies, fatty acids or starvation increase gluconeogenesis and decrease glucose uptake through the citrate inhibition of phosphofructokinase.

Topics: Acetoacetates; Adenine Nucleotides; Adenosine Triphosphate; Animals; Butyrates; Cyanides; Fructose-Bisphosphatase; Gluconeogenesis; Glycogen; Glycolysis; Hexosephosphates; In Vitro Techniques; Kidney; Palmitic Acids; Phosphofructokinase-1; Rats; Starvation

1. The rates of gluconeogenesis from most substrates tested in the perfused livers of well-fed rats were about half of those obtained in the livers of starved rats. There was no difference for glycerol. 2. A diet low in carbohydrate increased the rates of gluconeogenesis from some substrates but not from all. In general the effects of a low-carbohydrate diet on rat liver are less marked than those on rat kidney cortex. 3. Glycogen was deposited in the livers of starved rats when the perfusion medium contained about 10mm-glucose. The shedding of glucose from the glycogen stores by the well-fed liver was greatly diminished by 10mm-glucose and stopped by 13.3mm-glucose. Livers of well-fed rats that were depleted of their glycogen stores by treatment with phlorrhizin and glucagon synthesized glycogen from glucose. 4. When two gluconeogenic substrates were added to the perfusion medium additive effects occurred only when glycerol was one of the substrates. Lactate and glycerol gave more than additive effects owing to an increased rate of glucose formation from glycerol. 5. Pyruvate also accelerated the conversion of glycerol into glucose, and the accelerating effect of lactate can be attributed to a rapid formation of pyruvate from lactate. 6. Butyrate and oleate at 2mm, which alone are not gluconeogenic, increased the rate of gluconeogenesis from lactate. 7. The acceleration of gluconeogenesis from lactate by glucagon was also found when gluconeogenesis from lactate was stimulated by butyrate and oleate. This finding is not compatible with the view that the primary action of glucagon in promoting gluconeogenesis is an acceleration of lipolysis. 8. The rate of gluconeogenesis from pyruvate at 10mm was only 70% of that at 5mm. This ;inhibition' was abolished by oleate or glucagon.

Topics: Animal Nutritional Physiological Phenomena; Animals; Carbohydrate Metabolism; Fatty Acids; Glucagon; Gluconeogenesis; Glucose; Glycerol; Glycogen; Lactates; Liver; Perfusion; Phlorhizin; Pyruvates; Rats; Starvation

Topics: Ascaris; Body Composition; Chromatography; Fatty Acids; Glucose; Glycogen; Male; Starvation

Topics: Animals; Chiroptera; Female; Glycogen; Hibernation; Liver; Male; Microscopy, Electron; Mitochondria; Nutritional Physiological Phenomena; Starvation

Topics: Acceleration; Adrenal Medulla; Adrenalectomy; Amino Acids; Animals; Blood; Blood Glucose; Carbohydrate Metabolism; Corticosterone; Diabetes Mellitus, Experimental; Fatty Acids; Glycogen; Hypophysectomy; Lipids; Liver Glycogen; Muscles; Rats; Research; Starvation; Stress, Physiological

Topics: Animals; Dietary Proteins; Glucokinase; Glucosephosphate Dehydrogenase; Glycogen; Isocitrate Dehydrogenase; Lipid Metabolism; Liver; Male; Organ Size; Rats; Starvation

Topics: Alanine Transaminase; Animals; Arginase; Aspartate Aminotransferases; Colorimetry; Estivation; Fishes; Glycogen; Hibernation; Hypothermia, Induced; Lipids; Liver Glycogen; Manometry; Metabolism; Muscles; Peptide Hydrolases; Research; Starvation; Urea

Topics: Acetates; Animals; Butyrates; Carbon Isotopes; Coenzyme A; Glucose; Glycogen; Guinea Pigs; Lactates; Lactic Acid; Metabolism; Myocardium; Perfusion; Propionates; Pyruvates; Radiometry; Research; Starvation

Topics: Animals; Arabinose; Carbon Dioxide; Diabetes Mellitus, Experimental; Diaphragm; Fatty Acids; Glucose; Glycogen; Glycolysis; Heart; Hydroxybutyrates; Hypoxia; In Vitro Techniques; Muscles; Myocardium; Perfusion; Phosphofructokinase-1; Pyruvates; Rats; Salicylates; Starvation

Topics: Acetates; Animals; Coenzyme A; Glycogen; Heart; In Vitro Techniques; Insulin; Lactates; Myocardium; NAD; Perfusion; Pyruvates; Rats; Starvation

Topics: Administration, Intravenous; Cholesterol; DNA; Glucose; Glycerides; Glycogen; Injections; Lipids; Liver; Nitrogen; Phospholipids; Starvation

Topics: Animals; Carbohydrate Metabolism; Carbon Isotopes; Dialysis; Glycine; Glycogen; Guinea Pigs; Liver; Liver Glycogen; Renal Dialysis; Research; Starvation

Topics: Animals; Chlorpropamide; Glycogen; Hypoglycemic Agents; Liver; Muscles; Rats; Starvation

Topics: Glycogen; Guinea Pigs; Starvation

Topics: Carbohydrate Metabolism; Glucose; Glycogen; Insulin; Liver; Oligosaccharides; Starvation

Topics: Animals; Carbohydrate Metabolism; Cestoda; Cestode Infections; Glucose; Glycogen; Hymenolepis; Starvation

Topics: Animals; Fasting; Glycogen; Glycogenolysis; Liver; Mice; Muscles; Starvation

Topics: Animals; Gluconeogenesis; Glycogen; Glycogenolysis; Liver; Starvation

Topics: Acclimatization; Animals; Glycogen; Glycogenolysis; Liver; Rats; Starvation

Topics: Animals; Fasting; Glycogen; Glycogenolysis; Liver; Mice; Muscles; Starvation

Topics: Animals; Estrogens; Fasting; Female; Glycogen; Humans; Rats; Starvation; Uterus

Topics: Animals; Glycogen; Helminths; Starvation