glycogen and Weight-Gain

The edematogenic properties of insulin have long been documented, although they have been underestimated despite current trends toward intensive insulin therapy. Insulin treatment has been associated with weight gain, mild or moderate edema, and, rarely, generalized edema and cardiopulmonary congestion. In addition, the use in recent years of thiazolidinediones, which improve insulin sensitivity, has been associated with weight gain and peripheral edema, which can progress to pulmonary edema, particularly when thiazolidinediones are used in combination with insulin. This article attempts to raise awareness about the overlooked edematogenic action of insulin. In addition, the potential role of edema-provoking properties of insulin in the development of vascular complications in patients with diabetes is discussed.

Topics: Capillary Permeability; Diabetic Angiopathies; Drug Interactions; Edema; Glycogen; Humans; Hyperinsulinism; Hypoglycemic Agents; Insulin; Mitochondria; Sodium; Thiazolidinediones; Water-Electrolyte Balance; Weight Gain

In this study, we compared the effects of endurance training in the fasted state (F) vs. the fed state [ample carbohydrate intake (CHO)] on exercise-induced intramyocellular lipid (IMCL) and glycogen utilization during a 6-wk period of a hypercaloric (∼+30% kcal/day) fat-rich diet (HFD; 50% of kcal). Healthy male volunteers (18-25 yrs) received a HFD in conjunction with endurance training (four times, 60-90 min/wk) either in F (n = 10) or with CHO before and during exercise sessions (n = 10). The control group (n = 7) received a HFD without training and increased body weight by ∼3 kg (P < 0.001). Before and after a HFD, the subjects performed a 2-h constant-load bicycle exercise test in F at ∼70% maximal oxygen uptake rate. A HFD, both in the absence (F) or presence (CHO) of training, elevated basal IMCL content by ∼50% in type I and by ∼75% in type IIa fibers (P < 0.05). Independent of training in F or CHO, a HFD, as such, stimulated exercise-induced net IMCL breakdown by approximately twofold in type I and by approximately fourfold in type IIa fibers. Furthermore, exercise-induced net muscle glycogen breakdown was not significantly affected by a HFD. It is concluded that a HFD stimulates net IMCL degradation by increasing basal IMCL content during exercise in type I and especially IIa fibers. Furthermore, a hypercaloric HFD provides adequate amounts of carbohydrates to maintain high muscle glycogen content during training and does not impair exercise-induced muscle glycogen breakdown.

Topics: Acetyl-CoA Carboxylase; Adolescent; Adult; AMP-Activated Protein Kinases; Analysis of Variance; Belgium; Dietary Carbohydrates; Dietary Fats; Energy Intake; Energy Metabolism; Exercise; Exercise Test; Fasting; Fatty Acids, Nonesterified; Gene Expression Regulation, Enzymologic; Glycogen; Humans; Lipid Metabolism; Male; Muscle Fibers, Skeletal; Oxygen Consumption; Phosphorylation; Physical Endurance; Protein Serine-Threonine Kinases; Pyruvate Dehydrogenase Acetyl-Transferring Kinase; RNA, Messenger; Time Factors; Weight Gain; Young Adult

The aim of this study was to lower the glycogen stores in pork muscle in order to improve pork muscle quality by feeding an ultra-high-protein/low-carbohydrate (HIPRO) diet. Forty-eight barrows (average live weight = 92 kg) were assigned across five treatments and two replications (four or five pigs per treatment by replication combination). All barrows were fed a control diet (13.1% CP) until their assigned treatment began. A treatment was the number of days the barrows were fed the HIPRO diet prior to slaughter (0, 2, 4, 7, or 14 d). The HIPRO diet (35.9% CP) was 97% extruded soybeans. Daily feed intake and weekly live weights were recorded for all barrows. At-death blood glucose levels were determined. Muscle pH, temperature, and electrical impedance were measured in the longissmus lumborum and semimembranosus muscles at 45 min, 3 h, and 24 h postmortem. Glycolytic potential; Minolta L*a*b* values; visual scores for color, firmness, and marbling; water-holding capacity traits (drip loss, purge loss, and cooking loss); and Warner-Bratzler shear force values were determined in the longissmus thoracis et lumborum. Weight gain per day decreased the longer the pigs were fed the HIPRO diet (P < 0.05). Daily feed intake decreased during the 1st wk on the HIPRO diet but returned to near-control levels during the 2nd wk, which when coupled with the continued decreases in daily gain resulted in substantial decreases in feed efficiency during the 2nd wk on the HIPRO diet (P < 0.05). Blood glucose levels and glycolytic potentials were not lowered by feeding the HIPRO diet (P > 0.05); therefore, no differences in rate of pH decline or ultimate pH among dietary treatments were found (P > 0.05). Likewise, there were no differences among dietary treatments in any of the measured meat quality attributes (P > 0.05). Feeding barrows the HIPRO diet for a time period prior to slaughter decreased feed intake, rate of gain, and feed efficiency and was not effective at lowering glycolytic potential or improving pork muscle quality.

Topics: Animals; Dietary Carbohydrates; Dietary Proteins; Glycine max; Glycogen; Male; Meat; Muscle, Skeletal; Swine; Weight Gain

Fatty liver is an abnormal metabolic condition of excess intrahepatic fat. This condition, referred to as hepatic steatosis, is tightly associated with chronic liver disease and systemic metabolic morbidity. The most prevalent form in humans, i.e. non-alcoholic fatty liver, generally develops due to overnutrition and sedentary lifestyle, and has as yet no approved drug therapy. Previously, we have developed a relevant large-animal model in which overnourished sheep raised on a high-calorie carbohydrate-rich diet develop hyperglycemia, hyperinsulinemia, insulin resistance, and hepatic steatosis. Here, we tested the hypothesis that treatment with thiamine (vitamin B1) can counter the development of hepatic steatosis driven by overnutrition. Remarkably, the thiamine-treated animals presented with completely normal levels of intrahepatic fat, despite consuming the same amount of liver-fattening diet. Thiamine treatment also decreased hyperglycemia and increased the glycogen content of the liver, but it did not improve insulin sensitivity, suggesting that steatosis can be addressed independently of targeting insulin resistance. Thiamine increased the catalytic capacity for hepatic oxidation of carbohydrates and fatty acids. However, at gene-expression levels, more-pronounced effects were observed on lipid-droplet formation and lipidation of very-low-density lipoprotein, suggesting that thiamine affects lipid metabolism not only through its known classic coenzyme roles. This discovery of the potent anti-steatotic effect of thiamine may prove clinically useful in managing fatty liver-related disorders.This article has an associated First Person interview with the joint first authors of the paper.

Topics: Adiposity; Animals; Blood Glucose; Cytokines; Diet, High-Fat; Dose-Response Relationship, Drug; Fatty Acids; Fatty Liver; Gene Expression Regulation; Glycogen; Inflammation Mediators; Ketoglutarate Dehydrogenase Complex; Lipid Metabolism; Liver; Male; Mitochondria; Overnutrition; RNA, Messenger; Sheep; Thiamine; Thiamine Pyrophosphate; Weight Gain

Constitutional thinness (CT) is a nonpathological state of underweight. The current study aimed to explore skeletal muscle energy storage in individuals with CT and to further characterize muscle phenotype at baseline and in response to overfeeding. Thirty subjects with CT (15 females, 15 males) and 31 normal-weight control subjects (16 females, 15 males) participated in the study. Histological and enzymological analyses were performed on muscle biopsy specimens before and after overfeeding. In the skeletal muscle of CT participants compared with controls, we observed a lower content of intramuscular triglycerides for type I (-17%,

Topics: Adaptation, Physiological; Adult; Body Weight; Dietary Supplements; Energy Intake; Female; Glycogen; Humans; Hyperphagia; Male; Muscle Fibers, Skeletal; Muscle, Skeletal; Thinness; Triglycerides; Weight Gain; Young Adult

The short-chain fatty acid propionate is a potent inhibitor of molds that is widely used as a food preservative and endogenously produced by gut microbiota. Although generally recognized as safe by the U.S. Food and Drug Administration, the metabolic effects of propionate consumption in humans are unclear. Here, we report that propionate stimulates glycogenolysis and hyperglycemia in mice by increasing plasma concentrations of glucagon and fatty acid-binding protein 4 (FABP4).

Topics: Animals; Fatty Acid-Binding Proteins; Female; Glucagon; Glycogen; Humans; Insulin Resistance; Male; Mice; Mice, Inbred C57BL; Propionates; Weight Gain

Benzo(a)pyrene (BaP) is a highly toxic polycyclic aromatic hydrocarbon and has strong affinity to suspended materials and sediments in the aquatic environment. Most crustaceans are benthic species and are easily affected by the pollution in the sediments, but there is little information on the response mechanism of crustaceans to BaP exposure. This study compared the growth and hepatopancreas transcriptomic responses of the Chinse mitten crab (Eriocheir sinensis) exposed to 0, 0.15 (BaP1) and 0.45 μg /L (BaP2) for 28 days. Crab survival and weight gain were reduced in the water born BaP in a dose-dependent way. The contents of hepatopancreas glycogen, triglyceride, total amino acids and lactic acid were all decreased after BaP exposure, indicating possible more energy consumption during detoxification. In the transcriptome analysis, a total of 106.65 million clean reads were obtained and assembled into 81,714 unigenes with an average length of 594 bp and N50 of 808 bp. Under 0.15 or 0.45 μg /L BaP exposure, 922 and 1129 unigenes in crabs were significantly expressed, annotated to 676 and 802 Gene Ontology (GO) terms respectively. The "cellular process" was the leading category for both concentrations. Thirteen significantly changed pathways were identified in both Control vs BaP1 and Control vs BaP2 groups. These pathways were divided into four different parts according to their reported functions, including metabolism, environmental information processing, organismal systems and cellular processes. Nice out of thirteen pathways in BaP1 were related to metabolism, containing amino acid metabolism, phenylpropanoid biosynthesis, monobactam biosynthesis and styrene degradation. Almost all the pathways related with the biosynthesis processes were down-regulated, while the degradation pathways were up-regulated. Seven out of thirteen pathways were classified into metabolism category in BaP2. These pathways were mostly associated with stress resistance rather than supplying energy. This study indicates that both concentrations of BaP disturbed nutrient metabolism, immune response and defense system in the crabs, while exposure to a higher concentration had a greater impact on immunity system than on metabolism. This study provides a better understanding of the underlying molecular and regulatory mechanisms in crustaceans coping with BaP toxicity.

Topics: Amino Acids; Animals; Benzo(a)pyrene; Brachyura; Energy Metabolism; Gene Expression Profiling; Gene Expression Regulation, Developmental; Gene Ontology; Glycogen; Hepatopancreas; Lactic Acid; Molecular Sequence Annotation; Reproducibility of Results; Survival Analysis; Transcriptome; Triglycerides; Water Pollutants, Chemical; Weight Gain

Processes involved in regulation of energy balance and intermediary metabolism are aligned to the light-dark cycle. Shift-work and high-fat diet (HFD)-induced obesity disrupt circadian rhythmicity and are associated with increased risk of nonalcoholic fatty liver disease. This study aimed to determine the effect of simulating shift work on hepatic lipid accumulation in lean and HFD mice. C57BL/6 mice fed a standard laboratory diet (SLD) or HFD for 4 wk were further allocated to a normal light (NL) cycle (lights on: 0600-1800) or rotating light (RL) cycle [3 days NL and 4 days reversed (lights on: 1800-0600) repeated] for 8 wk. Tissue was collected every 3 h beginning at 0600. HFD mice gained more weight than SLD mice, and RL mice gained more weight than NL mice. SLD-NL and HFD-NL mice, but not RL mice, were more active, had higher respiratory quotients, and consumed/expended more energy during the dark phase compared with the light phase. Blood glucose and plasma cholesterol and triglyceride concentrations were elevated in HFD and SLD-RL compared with SLD-NL mice. Hepatic glycogen was elevated in HFD compared with SLD mice. Hepatic triglycerides were elevated in SLD-RL and HFD mice compared with SLD-NL. Circadian rhythmicity of hepatic acetyl-CoA carboxylase (ACACA) mRNA was phase shifted in SLD-RL and HFD-NL and lost in HFD-RL mice. Hepatic ACACA protein was reduced in SLD-RL and HFD mice compared with SLD-NL mice. Hepatic adipose triglyceride lipase was elevated in HFD-NL compared with SLD-NL but lower in RL mice compared with NL mice irrespective of diet. In conclusion, an RL cycle model of shift work promotes weight gain and hepatic lipid storage even in lean conditions. NEW & NOTEWORTHY In this publication we describe the effects of a rotating light cycle model of shift work in lean and high-fat diet-induced obese mice on body mass, diurnal patterns of energy intake and expenditure, and hepatic lipid storage. The data indicate that modeling shift work, via a rotating light cycle, promotes weight gain and hepatic lipid accumulation even in mice on a standard laboratory diet.

Topics: Acetyl-CoA Carboxylase; Animals; Circadian Rhythm; Diet, High-Fat; Glycogen; Lipid Metabolism; Liver; Male; Mice; Mice, Inbred BALB C; Photoperiod; Triglycerides; Weight Gain

The present study aimed to analyze the effects of sleep restriction (SR) during pregnancy in rats. The following three groups were studied: home cage (HC pregnant females remained in their home cage), Sham (females were placed in tanks similar to the SR group but with sawdust) and SR (females were submitted to the multiple platform method for 20 h per day from gestational days (GD) 14 to 20). Plasma corticosterone after 6 days of SR was not different among the groups. However, the relative adrenal weight was higher in the SR group compared with the HC group, which suggests possible stress impact. SR during pregnancy reduces the body weight of the female but no changes in liver glycogen, cholesterol and triglycerides, and muscle glycogen were detected. On GD 20, the fetuses of the females submitted to SR exhibited increased brain derived neurotrophic factor (BDNF) in the hippocampus, which indicates that sleep restriction of mothers during the final week of gestation may affect neuronal growth factors in a fetal brain structure, in which active neurogenesis occurs during the deprivation period. However, no changes in the total reactive oxygen species (ROS) in the cortex, hippocampus, or cerebellum of the fetuses were detected. SR females showed no major change in the maternal behavior, and the pups' preference for the mother's odor on postpartum day (PPD) 7 was not altered. On GD 20, the SR females exhibited increased plasma prolactin (PRL) and oxytocin (OT) compared with the HC and Sham groups. The negative outcomes of sleep restriction during delivery could be related, in part, to this hormonal imbalance. Sleep restriction during pregnancy induces different changes compared with the changes described in males and affects both the mother and offspring.

Topics: Animals; Brain; Brain-Derived Neurotrophic Factor; Cholesterol; Corticosterone; Female; Glycogen; Liver; Maternal Behavior; Muscles; Olfactory Perception; Oxytocin; Pregnancy; Pregnancy Complications; Prolactin; Random Allocation; Rats; Reactive Oxygen Species; Sleep Deprivation; Triglycerides; Weight Gain

Nicotine is known to promote body weight loss and to disturb glucose homeostasis and lipoprotein metabolism. Electronic cigarettes, as a substitute to nicotine, are becoming increasingly popular, although there is no evidence regarding their safety. Considering the dearth of information about e-cigarette toxicity, the present study was designed to compare nicotine alone to e-liquid with or without nicotine on metabolic parameters in Wistar rats.. For this purpose, e-liquid with or without nicotine and nicotine alone (0.5mg/kg of body weight) were administered intra-peritoneally during 28 days.. Our results show a significant decrease in food and energy intake after nicotine or e-liquid with nicotine exposure, when compared to control or e-liquid without nicotine. Analysis of lipid status identified a significant decrease in cholesterol and LDL levels in e-cigarette groups, suggesting an improvement in lipid profile. Interestingly, e-liquid without nicotine induced hyperglycemia which is negatively correlated to hepatic glycogen level, acting like nicotine alone. Furthermore, an increase in liver biomarkers was observed in all treated groups. qRT-PCR analysis showed GSK3β up-regulation in e-liquid with nicotine as well as, surprisingly, in e-liquid without nicotine exposure. In contrast, PEPCK genes were only up-regulated in e-liquid with nicotine.. While some features observed in rats may not be observed in human smokers, most of our data are consistent with, e-liquid per se i.e. without nicotine, not being neutral from a metabolic stand point since disrupting glucose homeostasis in rats.

Topics: Animals; Biomarkers; Cholesterol; Cholesterol, LDL; Electronic Nicotine Delivery Systems; Glycogen; Injections, Intraperitoneal; Lipid Metabolism; Liver; Liver Function Tests; Nicotine; Nicotinic Agonists; Rats; Rats, Wistar; Weight Gain

The present study analyzes the effect of the replacement of dietary casein by soy protein on the mechanisms underlying dyslipidemia, liver steatosis and altered glucose and lipid metabolism in the skeletal muscle which developed in rats fed long-term a sucrose-rich diet (SRD).. Wistar rats were fed a SRD for 4 months. From months 4 to 8, half the animals continued with the SRD, and the other half were fed a SRD in which the source of protein casein was replaced by soy. The control group received a diet with cornstarch as source of carbohydrate.. Compared to SRD-fed animals, the rats fed soy showed: A--in the liver: reduction of triglyceride and cholesterol storage and decreased steatosis; normalization of mature forms of the protein mass levels of SREBP-1 and the activities of lipogenic enzymes, while the protein mass level of PPAR-α and fatty acid oxidase activity increased. B-in the gastrocnemius muscle: normalization of the enhanced lipid storage and the altered glucose oxidation, improving glucose phosphorylation; decreasing protein mass level of nPKCθ in the membrane fraction; reversion of the impaired insulin-stimulated glucose transporter Glut-4, and glucose-6-phosphate and glycogen concentrations. Besides, dyslipidemia and glucose homeostasis returned to control values.. This study provides new information concerning some key mechanisms related to the effect of dietary soy on hepatic lipid metabolism and insulin action in the skeletal muscle in the presence of pre-existing dyslipidemia and insulin resistance induced by a SRD.

Topics: Animals; Blood Glucose; Cholesterol; Dietary Sucrose; Dyslipidemias; Fatty Acids, Nonesterified; Fatty Liver; Glucose Transporter Type 4; Glucose-6-Phosphate; Glycogen; Insulin; Insulin Resistance; Lipid Metabolism; Liver; Male; Muscle, Skeletal; PPAR alpha; Rats; Rats, Wistar; Soybean Proteins; Sterol Regulatory Element Binding Protein 1; Triglycerides; Weight Gain

The effects of slaughter age (8 vs 12 months) were investigated on meat and carcass quality obtained from Martina Franca donkey foals. Sixteen male foals were used, eight were slaughtered at 8 months of age with a mean (±s.e.) final body weight of 101±18kg and the remaining 8 foals slaughtered at 12 months of age with a mean final body weight of 122±13kg. Carcass weight and dressing percentage were higher (P<0.05) in older foals. Shear force value was lower (P<0.05) in donkeys slaughtered at 8 months of age (54.03N) compared to the same muscle Longissimus Thoracis et Lumborum (LTL) collected in older animals (62.66N). Muscle glycogen content was higher (P<0.05) in foals slaughtered at 12months of age. Donkey foal meat showed an interesting content of essential amino acids and a notable percentage of unsaturated fatty acids in both groups of animals, giving a high nutritional value to this alternative red meat.

Topics: Amino Acids; Amino Acids, Essential; Animals; Animals, Inbred Strains; Chemical Phenomena; Dietary Fats, Unsaturated; Equidae; Fatty Acids; Food Quality; Glycogen; Humans; Italy; Male; Meat; Mechanical Phenomena; Muscle Development; Muscle, Skeletal; Nutritive Value; Shear Strength; Weight Gain

Obese leptin deficient (ob/ob) mice are a model of adiposity that displays increased levels of fat, glucose, and liver lipids. Our hypothesis is that HO-1 overexpression ameliorates fatty liver development.. Obese mice were administered cobalt protoporphyrin (CoPP) and stannic mesoporphyrin (SnMP) for 6 weeks. Heme, HO-1, HO activity, PGC1α, FGF21, glycogen content, and lipogenesis were assessed.. CoPP administration increased hepatic HO-1 protein levels and HO activity, decreased hepatic heme, body weight gain, glucose levels, and resulted in decreased steatosis. Increased levels of HO-1 produced a decrease in lipid droplet size, Fatty acid synthase (FAS) levels involving recruitment of FGF21, PPARα, and Glut 1. These beneficial effects were reversed by inhibition of HO activity.. Increased levels of HO-1 and HO activity reduced the levels of obesity by reducing hepatic heme and lipid accumulation. These changes were manifested by decreases in cellular heme, increases in FGF21, glycogen content, and fatty liver. The beneficial effect of HO-1 induction results from an increase in PPARα and FGF21 levels and a decrease in PGC1α, levels they were reversed by SnMP. Low levels of HO-1 and HO activity are responsible for fatty liver.

Topics: Adiposity; Animals; Fatty Liver; Fibroblast Growth Factors; Glucose Transporter Type 1; Glycogen; Heme; Heme Oxygenase-1; Leptin; Liver; Male; Membrane Proteins; Mesoporphyrins; Mice; Mice, Obese; Obesity; PPAR alpha; Protoporphyrins; Tin Compounds; Transcription Factors; Weight Gain

As previously reported, high temperature- and high pressure-treated red ginseng (HRG) contain higher contents of phenolic compounds and protect C2C12 muscle cells and 3T3-L1 adipocytes against oxidative stress. This study investigated the effect of HRG on oxidative stress using a mouse model. Our results show that the levels of glutamic oxaloacetic transaminase and glutamic pyruvic transaminase, hepatic malondialdehyde in the HRG group were significantly lower than those of the exercise groups supplemented with commercial red ginseng (CRG) or not supplemented. The muscular glycogen level, glucose-6-phosphate dehydrogenase and lactate dehydrogenase activities of the HGR group were higher than that of the CGR group. Furthermore, the HRG treatment group displayed upregulated mRNA expression of Cu/Zn-SOD and muscle regulatory factor 4. These results indicate that HRG may protect oxidative stress induced by exercise as well as improve exercise performance capacity.

Topics: Alanine Transaminase; Animals; Aspartate Aminotransferases; Dietary Supplements; Glycogen; Hot Temperature; Liver; Malondialdehyde; Mice; Mice, Inbred ICR; Myogenic Regulatory Factors; Oxidative Stress; Panax; Physical Conditioning, Animal; Plant Extracts; Plants, Medicinal; Pressure; RNA, Messenger; Superoxide Dismutase; Weight Gain

The aim of this study was to investigate the mechanisms underlying the involvement of gut microbes in body weight gain of high-fat diet-fed obesity-prone (obese) and obesity-resistant (lean) mice. C57BL/6 mice were grouped into an obese group, a lean group and a normal control group. Both obese and lean mice were fed a high-fat diet while normal control mice were fed a normal diet; they were observed for six weeks. The results showed that lean mice had lower serum lipid levels, body fat and weight gain than obese mice. The ATPase, succinate dehydrogenase and malate dehydrogenase activities in liver as well as oxygen expenditure and rectal temperature of lean mice were significantly lower than in obese mice. As compared with obese mice, the absorption of intestinal carbohydrates but not of fats or proteins was significantly attenuated in lean mice. Furthermore, 16S rRNA abundances of faecal Firmicutes and Bacteroidetes were significantly reduced in lean mice. In addition, faecal β-D-galactosidase activity and short chain fatty acid levels were significantly decreased in lean mice. Expressions of peroxisome proliferator-activated receptor gamma 2 and CCAAT/enhancer binding protein-β in visceral adipose tissues were significantly downregulated in lean mice as compared with obese mice. Resistance to dyslipidaemia and high-fat diet-induced obesity was mediated by ineffective absorption of intestinal carbohydrates but not of fats or proteins, probably through reducing gut Bacteroidetes and Firmicutes contents and lowering of gut carbohydrate metabolism. The regulation of intestinal carbohydrates instead of fat absorption by gut microbes might be a potential treatment strategy for high-fat diet-induced obesity.

Topics: Adenosine Triphosphatases; Adipose Tissue; Animals; Bacteroidetes; beta-Galactosidase; Body Weight; Carbohydrate Metabolism; CCAAT-Enhancer-Binding Protein-beta; Diet, High-Fat; Dyslipidemias; Fatty Acids, Volatile; Feces; Glucose Tolerance Test; Glycogen; Insulin Resistance; Intestinal Mucosa; Intestines; Lipid Metabolism; Lipids; Liver; Malate Dehydrogenase; Male; Mice; Mice, Inbred C57BL; Mice, Obese; Obesity; Oxygen Consumption; PPAR gamma; Random Allocation; RNA, Ribosomal, 16S; Succinate Dehydrogenase; Weight Gain

This study investigated the effects of fucosylated chondroitin sulfate (CHS) isolated from sea cucumber on glucose metabolism and insulin signaling in the liver of insulin-resistant C57BL/6 mice fed a high-fat, high-sucrose diet (HFSD). Male C57BL/6J mice were randomly assigned into six groups: control; HFSD; 1 mg RSG/kg·body weight (RSG); 80 mg CHS/kg · body weight (CHS); 20 mg CHS+1 mg RSG/kg · body weight (20 CHS+RSG); and 80 mg CHS+1 mg RSG/kg · body weight (80 CHS+RSG). Blood glucose, insulin parameters, glucose metabolism-related enzymes activities and insulin-signaling transducers in the liver were analyzed at 19 weeks. Results showed that CHS significantly decreased body weight gain, adipose tissue weight, and fasting blood glucose and serum insulin levels in insulin-resistant mice. Rosiglitazone (RSG) is an effective thiazolidinedione hypoglycemic agent, and CHS synergistically enhanced the effect of RSG. CHS feeding normalized the activities of hexokinase, pyruvate kinase, glycogen phosphorylase, glucose-6-phosphatase, and increased glycogen reserves in the liver. Quantitative real-time polymerase chain reaction (qRT-PCR) analysis showed that CHS promoted the mRNA expression of insulin receptors (IR), insulin receptor substrate 2 (IRS-2), phosphatidylinositol 3 kinase (PI3K), protein kinase B (PKB), and glycogen synthase (GS) in the liver of insulin resistant mice, and inhibited glycogen synthase kinase-3 (GSK-3β) mRNA expression. The results suggested that CHS treatment improved glucose metabolism by modulating metabolic enzymes and promoting the PI3K/PKB/GSK-3β signaling pathway mediated by insulin at the transcriptional level. These results provided strong justification for the development of CHS as a functional food.

Topics: Adipose Tissue; Animals; Blood Glucose; Carbohydrate Metabolism; Chondroitin Sulfates; Diet, High-Fat; Dietary Sucrose; Drug Synergism; Glycogen; Glycogen Synthase; Hypoglycemic Agents; Insulin; Insulin Receptor Substrate Proteins; Liver; Male; Mice; Mice, Inbred C57BL; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Real-Time Polymerase Chain Reaction; Rosiglitazone; Sea Cucumbers; Signal Transduction; Thiazolidinediones; Weight Gain

To analyze Paraoxonase1 (PON1) impact on GLUT4 expression, glucose metabolism, and the insulin signaling pathway in skeletal muscle cells.. We analyzed the effect of PON1 in high-fat-diet-induced insulin resistance in C57BL/6J and in PON1KO mice. Mice were fed normal diet (ND) or high Fat Diet (HFD) for 8 weeks. PON1 deficiency caused enhanced insulin resistance in both ND and HFD mice. PON1 deficiency was associated with increased oxidative stress (OS), increased p38MAPK activity and attenuated insulin-mediated tyrosine phosphorylation of muscle insulin receptor substrate-1 (IRS-1), with a corresponding increase in serine phosphorylation. These effects resulted in decreased glucose uptake in whole-body level, as reflected by glucose tolerance test (GTT), by insulin tolerance test (ITT) and by cellular glycogen accumulation in the liver and in the muscles. PON1 addition to cultured C2 muscle cells enhanced GLUT4 mRNA expression, in a time and concentration dependent manner, increased GLUT4 protein and cellular glycogen accumulation. These effects were mediated via inhibition of p38MAPK activity, resulting in reduced IRS-1 serine phosphorylation and in enhanced IRS-1 tyrosine phosphorylation. The ability of PON1 to increase myocytes GLUT4 expression was partially inhibited upon blocking PON1 SH group, and completely abolished upon PON1 mutation in HIS115 of its catalytic site.. PON1 plays a beneficial role in glucose regulation and metabolism and may serve as an important tool in diabetes control.

Topics: Animals; Aryldialkylphosphatase; Diet, High-Fat; Dietary Fats; Glucose Intolerance; Glucose Transporter Type 4; Glycogen; Insulin Receptor Substrate Proteins; Insulin Resistance; Liver; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Muscle Fibers, Skeletal; Muscle, Skeletal; Proto-Oncogene Proteins c-akt; Signal Transduction; Weight Gain

Ketamine can induce hepatotoxicity which has been suggested to be dependent on mitochondrial impairment. This study investigated the long-term effects of chronic low-dose ketamine on liver mitochondrial function, oxidative stress parameters, liver histology and glycogen content.. Adult rats were administered with saline or ketamine (5 or 10mg/kg) twice a day for a fourteen-day period in order to mimic chronic treatments. Effects between groups were compared ten days after the treatment had ended. Liver mitochondrial function was monitored in isolated mitochondrial extracts through evaluation of respiration parameters and activity of respiratory complexes, as well as oxidative stress, through lipid peroxidation, protein oxidation and superoxide dismutase activity. The hepatic histology and liver glycogen content were also evaluated.. Ketamine groups showed a decreased evolution in body weight gains during the treatment period. Ketamine had no effect either on serum liver enzymes or on the oxidative stress parameters of liver mitochondria. Ketamine decreased the hepatic glycogen content, inhibited mitochondrial complex I and oxygen consumption when glutamate-malate substrate was used.. These findings reflect a long-term mitochondrial bioenergetic deterioration induced by ketamine, which may explain the increased susceptibility of some patients to its prolonged or repeated use.

Topics: Analgesics; Animals; Electron Transport Complex I; Glycogen; Ketamine; Liver; Male; Mitochondria, Liver; Oxidative Stress; Oxygen Consumption; Rats; Rats, Wistar; Weight Gain

Diabetes in humans induces chronic complications such as cardiovascular damage, cataracts and retinopathy, nephropathy and polyneuropathy. The most common animal model of human diabetes is streptozotocin (STZ)-induced diabetes in the rat. The present study investigated the effects of Nigella sativa hydroalcholic extract on glucose concentrations in streptozotocin (STZ) diabetic rats.. In this study Twenty-five Wister-Albino rats (aged 8-9 weeks and weighing 200-250 g) were tested. Rats were divided into five experimental groups (control, untreated STZ-diabetic (60 mg/kg B.W., IP), treated STZ-diabetic with hydroalcholic extract of Nigella Sativa (NS) (5 mg/kg B.W, IP), treated STZ-diabetic with hydroalcholic extract of NS (10 mg/kg B.W., IP) and treated STZ-diabetic with hydroalcholic extract of NS (20 mg/kg B.W., IP and 32 days were evaluated to assess its effect on fasting blood glucose (FBG), and in different groups fasting blood glucose (FBG) and body weight (BW) were measured in the particular days (1, 16 and 32). At the end of the study, the animals were fasted overnight, anaesthetized with an intraperitoneal injection of sodium pentobarbital (60 mg/kg), and sacrificed for obtaining tissues samples (liver, pancreases). The number of islets and cells were counted and the islet diameters were determined by calibrated micrometer. The glycogen content in the liver was examined by Periodic Acid-Schiff (PAS) staining.. Treatment with NS (5 mg/kg b.w.) markedly increased BW gain and the FBG level was significantly (p<0.001) reduced when compared to the control. Histopathological examination showed that the NS (5 mg/kg b.w.) partially recovered hepatic glycogen content and protected the great deal of the pancreatic islet cells. The number of islets, cells and islets diameter were found statistically significant when compared to the control (p<0.01, p<0.05).. Higher doses of NS did not exhibit any therapeutic effect. These results showed that hydroalcholic extract of NS at low doses has hypoglycemic effect and ameliorative effect on regeneration of pancreatic islets and may be used as a therapeutic agent in the management of diabetes mellitus. The hypoglycemic effect observed could be due to amelioration of β-cell, thus leading to increased insulin levels. Consequently, N. sativa may prove clinically useful in the treatment of diabetics and in the protection of β-cells against streptozotocin.. The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1845133011104231.

Topics: Animals; Biomarkers; Blood Glucose; Cytoprotection; Diabetes Mellitus, Experimental; Dose-Response Relationship, Drug; Female; Glycogen; Hypoglycemic Agents; Islets of Langerhans; Liver; Male; Nigella sativa; Phytotherapy; Plant Extracts; Plants, Medicinal; Rats; Rats, Wistar; Seeds; Streptozocin; Time Factors; Weight Gain

Insulin resistance in Type 2 diabetes leads to hepatic steatosis that can accompanied by progressive inflammation of the liver. Citrus unshiu peel is a rich source of citrus flavonoids that possess anti-inflammatory, anti-diabetic and lipid-lowering effects. However, the ability of citrus unshiu peel ethanol extract (CPE) to improve hyperglycemia, adiposity and hepatic steatosis in Type 2 diabetes is unknown. Thus, we evaluated the effects of CPE on markers for glucose, lipid metabolism and inflammation in Type 2 diabetic mice. Male C57BL/KsJ-db/db mice were fed a normal diet with CPE (2 g/100 g diet) or rosiglitazone (0.001 g/100 g diet) for 6 weeks. Mice supplemented with the CPE showed a significant decrease in body weight gain, body fat mass and blood glucose level. The antihyperglycemic effect of CPE appeared to be partially mediated through the inhibition of hepatic gluconeogenic phosphoenolpyruvate carboxykinase mRNA expression and its activity and through the induction of insulin/glucagon secretion. CPE also ameliorated hepatic steatosis and hypertriglyceridemia via the inhibition of gene expression and activities of the lipogenic enzymes and the activation of fatty acid oxidation in the liver. These beneficial effects of CPE may be related to increased levels of anti-inflammatory adiponectin and interleukin (IL)-10, and decreased levels of pro-inflammatory markers (IL-6, monocyte chemotactic protein-1, interferon-γ and tumor necrosis factor-α) in the plasma or liver. Taken together, we suggest that CPE has the potential to improve both hyperglycemia and hepatic steatosis in Type 2 diabetes.

Topics: Adipose Tissue; Animals; Blood Glucose; Citrus; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 2; Enzymes; Fatty Liver; Gene Expression Regulation; Glycogen; Hyperglycemia; Inflammation; Lipid Metabolism; Male; Mice; Mice, Inbred C57BL; Mice, Mutant Strains; Phosphoenolpyruvate Carboxykinase (ATP); Plant Extracts; Weight Gain

The liver plays an important role in maintaining glucose homeostasis in the body. In the prandial state, some of the glucose which is absorbed by the gastrointestinal tract is converted into glycogen and stored in the liver. In contrast, the liver produces glucose by glycogenolysis and gluconeogenesis while fasting. Thus, the liver contributes to maintaining blood glucose level within normoglycemic range. Glycogenesis and glycogenolysis are regulated by various mechanisms including hormones, the sympathetic and parasympathetic nervous systems and the hepatic glucose content. In this study, we examined a rat model in which the celiac superior mesenteric ganglion (CSMG) was resected. We attempted to elucidate how the celiac sympathetic nervous system is involved in regulating glucose homeostasis by assessing the effects of CSMG resection on glucose excursion during an oral glucose tolerance test, and by examining hepatic glycogen content and hepatic glycogen phosphorylase (GP) activity. On the oral glucose tolerance test, CSMG-resected rats demonstrated improved glucose tolerance and significantly increased GP activity compared with sham-operated rats, whereas there were no significant differences in insulin, glucagon or catecholamine levels between the 2 groups. These results suggest that the celiac sympathetic nervous system is involved in regulating the rate of glycogen consumption through GP activity. In conclusion, the examined rat model showed that the celiac sympathetic nervous system regulates hepatic glucose metabolism in conjunction with vagal nerve innervations and is a critical component in the maintenance of blood glucose homeostasis.

Topics: Animals; Blood Glucose; Catecholamines; Down-Regulation; Ganglia, Sympathetic; Ganglionectomy; Glucagon; Glucose Tolerance Test; Glycogen; Glycogen Phosphorylase, Liver Form; Glycogenolysis; Homeostasis; Insulin; Liver; Male; Random Allocation; Rats; Rats, Sprague-Dawley; Splanchnic Circulation; Weight Gain

The gastrointestinal tract of neonates is sensitive to dietary manipulations. When nursing mothers use Aloe vera, their babies are at risk of indirect exposure to Aloe vera via breast feeding or directly as health supplements. The effects of orally administered extracts of Aloe vera in unweaned rats were investigated. Six day old Sprague-Dawley rats were gavaged with aqueous or alcohol extracts of Aloe vera (low dose 50mg. kg⁻¹ or high dose 500mg. kg⁻¹) daily for eight days. All data were expressed as mean ± SD and analyzed by one way ANOVA. Pups receiving high doses of either extract had a significantly higher body mass gain than the group receiving lower dose (p < 0.05). Tibial length was significantly increased in the high dose aqueous extract group (15-26%). The differences in growth could not be attributed to circulating insulin-like growth factor-1 as the levels were not significantly different. The caecum was significantly enlarged in the rats that received the high doses of both extracts. Although, there was no significant difference in the non-fasting plasma concentration of glucose and triglycerides, the hepatic lipid and glycogen content were significantly higher (p < 0.001) for the high dose aqueous extract group. The plasma alanine transaminase was not affected by the treatments, however the high doses of the extracts significantly increased plasma alkaline phosphatase activity. Short term administration of Aloe vera extracts resulted in growth promotion, enhanced hepatic storage of metabolic substrates, increased ALP possibly in relation to bone growth and caused hypertrophy of the caecum of neonatal rats. These effects need to be explored further to enhance animal production and health.

Topics: Abdomen; Administration, Oral; Alanine Transaminase; Alkaline Phosphatase; Aloe; Analysis of Variance; Animals; Cecum; Female; Glycogen; Hypertrophy; Lipid Metabolism; Liver; Male; Plant Extracts; Rats; Rats, Sprague-Dawley; Tibia; Weight Gain

The effect of dietary feeding of hydroxyethyl methylcellulose (HEMC) and hydroxypropyl methylcellulose (HPMC) on the glucose metabolism and antioxidative status in mice under high fat diet conditions was investigated. The mice were randomly divided and given experimental diets for six weeks: normal control (NC group), high fat (HF group), and high fat supplemented with either HEMC (HF+HEMC group) or HPMC (HF+HPMC group). At the end of the experimental period, the HF group exhibited markedly higher blood glucose and insulin levels as well as a higher erythrocyte lipid peroxidation rate relative to the control group. However, diet supplementation of HEMC and HPMC was found to counteract the high fat-induced hyperglycemia and oxidative stress via regulation of antioxidant and hepatic glucose-regulating enzyme activities. These findings illustrate that HEMC and HPMC were similarly effective in improving the glucose metabolism and antioxidant defense system in high fat-fed mice and they may be beneficial as functional biomaterials in the development of therapeutic agents against high fat dietinduced hyperglycemia and oxidative stress.

Topics: Animals; Antioxidants; Blood Glucose; Diet, High-Fat; Dietary Supplements; Glucose; Glycogen; Hypoglycemic Agents; Hypromellose Derivatives; Insulin; Insulin Resistance; Lipid Metabolism; Lipid Peroxidation; Liver; Male; Methylcellulose; Mice; Mice, Inbred C57BL; Oxidative Stress; Weight Gain

Considering the explosive increase in obesity worldwide, there must be an unknown mechanism(s) promoting energy accumulation under conditions of overnutrition. We identified a feed-forward mechanism favoring energy storage, originating in hepatic glucokinase (GK) upregulation. High-fat feeding induced hepatic GK upregulation, and hepatic GK overexpression dose-dependently decreased adaptive thermogenesis by downregulating thermogenesis-related genes in brown adipose tissue (BAT). This intertissue (liver-to-BAT) system consists of the afferent vagus from the liver and sympathetic efferents from the medulla and antagonizes anti-obesity effects of leptin on thermogenesis. Furthermore, upregulation of endogenous GK in the liver by high-fat feeding was more marked in obesity-prone than in obesity-resistant strains and was inversely associated with BAT thermogenesis. Hepatic GK overexpression in obesity-resistant mice promoted weight gain, while hepatic GK knockdown in obesity-prone mice attenuated weight gain with increased adaptive thermogenesis. Thus, this intertissue energy-saving system may contribute to determining obesity predisposition.

Topics: Adipose Tissue, Brown; Animals; Diet, High-Fat; Glucokinase; Glycogen; Leptin; Liver; Mice; Mice, Inbred C57BL; Neurons; Obesity; RNA Interference; RNA, Small Interfering; Signal Transduction; Thermogenesis; Up-Regulation; Weight Gain

Resistance exercise such as weight-lifting (WL) increases oxidation products in plasma, but less is known regarding the effect of WL on oxidative damage to tissues. Dietary compounds are known to improve antioxidant defences. Whey protein (WP) is a source of protein in a variety of sport supplements and can enhance physical performance.. To evaluate the effect of WL on biomarkers of lipid and protein oxidation, on liver antioxidants and on muscle growth in the absence or presence of WP in rats.. Thirty-two male Fisher rats were randomly assigned to sedentary or exercise-trained groups and were fed with control or WP diets. The WL programme consisted of inducing the animals to perform sets of jumps with weights attached to the chest. After 8 weeks, arteriovenous blood samples, abdominal fat, liver and gastrocnemius muscle were collected for analysis.. WP precludes WL-mediated increases in muscle protein carbonyl content and maintains low levels of TBARS in exercised and sedentary animals. WL reduced liver CAT activity, whereas WP increased hepatic glutathione content. In addition, WL plus WP generated higher body and muscle weight than exercise without WP.. These data suggest that WP improves antioxidant defences, which contribute to the reduction of lipid and protein oxidation as well as body and muscle weight gain in resistance-exercised rats.

Topics: Abdominal Fat; Animals; Antioxidants; Biomarkers; Body Weight; Catalase; Diet; Glutathione; Glycogen; Lipid Metabolism; Liver; Male; Milk Proteins; Muscle, Skeletal; Oxidation-Reduction; Physical Conditioning, Animal; Rats; Resistance Training; Thiobarbituric Acid Reactive Substances; Weight Gain; Whey Proteins

Ghrelin, a hormone whose levels increase during food deprivation, plays a pivotal role in the regulation of food intake, energy metabolism and storage, as well as in insulin sensitivity. Here, we investigated the effects of acyl-ghrelin neutralization with the acyl-ghrelin-binding compound NOX-B11(2) during the fasting-refeeding cycle. Our data demonstrate that ghrelin neutralization with NOX-B11(2) impairs recuperation of lost body weight after food deprivation. Analysis of enzymes involved in glucose and lipid metabolism in liver of fed, fasted and refed rats revealed that neutralization of acyl-ghrelin resulted in minor decreases in the enzymes of glycolytic and lipogenic pathways during fasting. However, during refeeding these enzymes as well as glycogen levels recovered more slowly when acyl-ghrelin was blocked. The high levels of ghrelin in response to food deprivation may contribute to an adequate decrease in hepatic glycolytic and lipogenic enzymes and aid in the recovery of body weight and energetic reserves once food becomes available after the fasting period.

Topics: Animals; Blood Glucose; Carnitine O-Palmitoyltransferase; Eating; Energy Metabolism; Food Deprivation; Ghrelin; Glucokinase; Glucose; Glycogen; Growth Hormone; Hexokinase; Insulin; Lactic Acid; Lipogenesis; Liver; Male; Oligonucleotides; Pyruvate Kinase; Rats; Rats, Wistar; Transcription, Genetic; Triglycerides; Weight Gain

Although the umami compound monosodium glutamate (MSG) is a widely used flavor enhancer, controversy still persists regarding the effects of MSG intake on body weight. It has been claimed, in particular, that chronic MSG intake may result in excessive body weight gain and obesity. In this study we assessed the effects of chronic (16 weeks) ad libitum MSG on body weight and metabolism of C57BL6/J mice. Adult male mice were divided in four experimental groups and fed with either a low-fat (LF) or high-fat (HF) diet and with either two bottles of plain water or one bottle containing 1% MSG and another one containing water according to a factorial design. Mice were monitored weekly for body weight and food/fluid intake for 15 weeks. At the end of the experiments, the circulating levels of leptin, insulin, total protein, total cholesterol, triglyceride, blood urea nitrogen, and non-esterified fatty acids were also analyzed. Our results show that MSG intake did not influence body weight in either LF or HF groups. Interestingly, although animals overall displayed strong preferences for MSG against water, preferences were relatively higher in LF compared to HF group. Consistent with the body weight data, while significant differences in leptin, insulin, total cholesterol, and non-esterified fatty acids were found between HF and LF groups, such an effect was not influenced by MSG intake. Finally, indirect calorimetry measurements revealed similar energy expenditure levels between animals being presented water only and MSG only. In summary, our data does not support the notion that ad libitum MSG intake should trigger the development of obesity or other metabolic abnormalities.

Topics: Analysis of Variance; Animals; Basal Metabolism; Blood Glucose; Blood Proteins; Blood Urea Nitrogen; Calorimetry, Indirect; Cholesterol; Diet; Drinking; Eating; Fatty Acids, Nonesterified; Glycogen; Insulin; Leptin; Liver; Male; Mice; Mice, Inbred C57BL; Sodium Glutamate; Triglycerides; Weight Gain

1. This study examined responses of male broilers during a 42-d production cycle to two different rearing and feeding methods. 2. A total of 400 Chinese Yellow male broilers were allotted randomly at 21 d into two groups; the control was a typical indoor commercial rearing method and the treatment had outdoor access with scattered feeding (OS). Each group had 5 replicates with 40 birds per replicate. 3. Growth performance was similar for both groups from 21 to 63 d of age. OS birds had significantly lower abdominal fat percentage, meat shear force, drip loss, breast meat colour b* value and significantly higher pH value compared with the controls. OS birds had significantly lower muscle fibre diameter and greater muscle fibre density. Serum glutathione peroxidase and catalase activities were significantly higher and the contents of cholesterol, lactic acid, glycogen and malondialdehyde of breast muscle were significantly lower in OS birds than controls. 4. The results suggest that the OS feeding method had no negative effects on performance (weight, gain, feed conversion rate, carcase traits) compared with controls, and appeared to be beneficial for meat quality indices and oxidative stability.

Topics: Abdominal Fat; Animal Feed; Animal Husbandry; Animal Nutritional Physiological Phenomena; Animals; Antioxidants; Catalase; Chickens; Cholesterol; Diet; Dietary Supplements; Glutathione Peroxidase; Glycogen; Lactic Acid; Male; Malondialdehyde; Meat; Random Allocation; Superoxide Dismutase; Weight Gain

Consumption of energy-dense/high-fat diets is strongly and positively associated with overweight and obesity, which are associated with increase in the prevalence of certain chronic diseases. We evaluated the effect of hypercaloric/fat or normocaloric diets on some biochemical parameters in rats. Seventy-two rats were divided into four groups that were fed for 16 weeks with diets: normocaloric [9.12% soy oil, normocaloric soy oil (NSO)], hypercaloric olive oil [43.8% olive oil, hypercaloric olive oil (HOO)], hypercaloric saturated fat [43.8% saturated fat, hypercaloric saturated fat (HSF)] and normocaloric saturated fat [43.8% saturated fat, normocaloric saturated fat (NSF)]. HSF rats consumed more calories daily than the others and gained more retroperitoneal fat, although HSF and HOO rats had higher body weight. In liver, glycogen synthesis and concentration were higher in rats HSF and NSF. In plasma, total cholesterol (TC) levels were higher in HSF rats than in the others, and triacylglycerol (TAG) levels were lower in HOO and higher in HSF rats in relation to the others. In liver, TC and TAG were elevated in HSF, NSF and HOO rats. Paraoxonase 1 activity, which is related to high-density lipoprotein cholesterol and has anti-atherogenic role was lower in rats HSF. In HOO rats, glucose tolerance test was altered, but insulin tolerance test was normal. These results suggest that consumption of energy-dense/high-fat diets, both saturated or monounsaturated, causes damaging effects. However, more studies are necessary to understand the mechanisms by which these diets cause the metabolic alterations observed.

Topics: Adipose Tissue; Animals; Aryldialkylphosphatase; Blood Glucose; Cholesterol; Diet, High-Fat; Dietary Fats; Energy Intake; Fatty Acids; Feces; Glucose Tolerance Test; Glycogen; Homeostasis; Liver; Male; Muscle, Skeletal; Olive Oil; Plant Oils; Rats; Rats, Wistar; Soybean Oil; Triglycerides; Weight Gain

Malnutrition in utero can "program" the fetal tissues, making them more vulnerable to metabolic disturbances. Also there is association between excessive consumption of fructose and the development of metabolic syndrome. However, there is little information regarding the acute effect of physical exercise on subjects recovered from malnutrition and/or fed with a fructose-rich diet. The objective of this study was to evaluate the metabolic aspects and the response to acute physical exercise in rats recovered from fetal protein malnutrition with a fructose-rich diet.. Pregnant Wistar rats were fed with a balanced (B) diet or a low-protein (L) diet. After birth and until 60 days of age, the offspring were distributed into four groups according to the diet received: B: B diet during the whole experiment; balanced/fructose (BF): B diet until birth and fructose-rich (F) diet afterwards; low protein/balanced (LB): L diet until birth and B diet afterwards; low protein/fructose (LF): L diet until birth and F diet afterwards.. The excess fructose intake reduced the body weight gain, especially in the BF group. Furthermore, the serum total cholesterol and the LDL cholesterol were elevated in this group. In the LF group, the serum total cholesterol and the muscle glycogen increased. Acute physical exercise increased the serum concentrations of glucose, triglycerides, HDL cholesterol and liver lipids and reduced the concentrations of muscle glycogen in all groups.. An excess fructose intake induced some signs of metabolic syndrome. However, protein malnutrition appeared to protect against the short term effects of fructose. In other hand, most responses to acute physical exercise were not influenced by early malnutrition and/or by the fructose overload.

Topics: Animals; Animals, Newborn; Female; Fructose; Glycogen; Hyperglycemia; Hyperlipidemias; Lactation; Lipid Metabolism; Liver; Male; Maternal Nutritional Physiological Phenomena; Metabolic Syndrome; Motor Activity; Muscle, Skeletal; Pregnancy; Protein Deficiency; Rats; Rats, Wistar; Weight Gain

The purpose of the present study was to determine calorimetric parameters to predict obesity adverse effects on oxidative stress and cardiac energy metabolism. Male Wistar 24 rats were divided into three groups (n = 8): given standard chow and water (C), receiving standard chow and 30% sucrose in its drinking water (S), and given sucrose-rich diet and water (SRD). After 45 days, both S and SRD rats had obesity, serum oxidative stress, and dyslipidemic profile, but the body weight gain and feed efficiency (FE) were higher in SRD than in S, whereas the obesity-related oxidative stress, myocardial triacylglycerol accumulation, and enhanced cardiac lactate dehydrogenase (LDH) activity were higher in S than in SRD rats. Myocardial beta-hydroxyacyl coenzyme-A-dehydrogenase was lower in SRD and in S than in C, whereas glycogen was only depleted in S rats. Myocardial pyruvate dehydrogenase (PDH) was lowest in S rats indicating depressed glucose oxidation. There was higher myocardial LDH/citrate synthase (CS) ratio and lower adenosine triphosphate (ATP)-synthetase indicating delayed aerobic metabolism in S rats than in the others. Cardiac ATP-synthetase was positively correlated with energy expenditure, namely resting metabolic rate (RMR), and with oxygen consumption per body weight (VO(2)/body weight). Myocardial lipid hydroperoxide (LH)/ total antioxidant substances (TAS) ratio and triacylglycerol accumulation were negatively correlated with RMR and with VO(2)/body weight. In conclusion, the present study brought new insights into obesity because the study demonstrated for the first time that reduced energy expenditure and oxygen consumption may provide novel risk factors of obesity-induced reduced energy generation for myocardial contractile function. The results serve to highlight the role of calorimetric changes as novel biomarkers of risk to obesity-induced cardiac effects.

Topics: Animals; Antioxidants; ATP Synthetase Complexes; Basal Metabolism; Biomarkers; Blood Glucose; Citrate (si)-Synthase; Dietary Sucrose; Energy Metabolism; Enzymes; Glycogen; Heart; Heart Diseases; Lipid Peroxides; Male; Myocardium; Obesity; Oxidation-Reduction; Oxidative Stress; Oxidoreductases; Oxygen Consumption; Rats; Rats, Wistar; Triglycerides; Weight Gain

The present study was aimed to investigate the possible effects of beta-casomorphin-7, against hyperglycemia and free radical-mediated oxidative stress in streptozotocin-induced diabetic rats by assaying the blood glucose level and the activity of plasma enzymatic antioxidants, such as superoxide dismutase (SOD), catalase and glutathione peroxidase (GSH-Px). A significant increase in the levels of both blood glucose and oxidative stress with a predominant decrease in antioxidant status was observed in the diabetic rats when compared to control rats. After 15 days oral administration of beta-casomorphin-7 (7.5 x 10(-8) mol/day), the elevated blood glucose level was reduced. Oral administration of beta-CM-7 to diabetic rats showed an increase in the level of plasma insulin, the elevated plasma glucagon level was markedly reduced by the oral administration of beta-CM-7. Oral administration of beta-CM-7 to the diabetic group of rats also showed a significant elevation in the activity of SOD and catalase. Thus, the results of the present study suggest that beta-casomorphin-7 can protect rats from hyperglycemia and free radical-mediated oxidative stress in diabetic rats.

Topics: Animals; Antioxidants; Blood Glucose; Diabetes Mellitus, Type 1; Endorphins; Glucagon; Glycogen; Hyperglycemia; Hypoglycemic Agents; Insulin; Male; Malondialdehyde; Oxidative Stress; Oxidoreductases; Peptide Fragments; Random Allocation; Rats; Rats, Sprague-Dawley; Streptozocin; Time Factors; Weight Gain

Insufficient maternal protein intake has been postulated to cause impaired fuel metabolism and diabetes mellitus in adult mammalian progeny, but the mechanism remains unclear.. To investigate the effect of a maternal low protein whey-based diet during pregnancy and lactation on pancreatic function and skeletal muscle glucose metabolism in the offspring.. Sprague-Dawley rats: 8 mothers and 46 offspring.. Female rats were fed throughout pregnancy and lactation with otherwise-complete isoenergetic diets sufficient (20% whey protein; control: n=3) or insufficient (5% whey protein; low-protein: n=5) in whey protein. From weaning all offspring ate control diet.. Food intake and weight gain were measured for both mothers and offspring, and in vitro functional studies of endocrine pancreas and skeletal muscle were performed on offspring at 40 and 50 days of age, respectively.. Food intake (P=0.004) and weight gain (P=0.006) were lower in low protein than control mothers during early gestation. Offspring of low protein mothers had significant lower body weight from 5 to 15 days of age, although there was no significant difference in food consumption. Glucose, arginine- and glucose/arginine-stimulated insulin secretion from perfused pancreases isolated from low protein offspring were decreased by between 55 and 65% compared with control values. Studies in skeletal muscle demonstrated no difference in insulin sensitivity between the two groups.. Dietary whey protein insufficiency in female rats during pregnancy and lactation can evoke major changes in insulin secretion in progeny, and these changes represent a persistent functional abnormality in the endocrine pancreas.

Topics: Animals; Animals, Newborn; Blood Glucose; Body Weight; Diet, Protein-Restricted; Eating; Female; Glucose; Glycogen; Insulin; Insulin Secretion; Lactation; Male; Milk Proteins; Mothers; Muscle, Skeletal; Organ Culture Techniques; Pancreas; Pregnancy; Prenatal Exposure Delayed Effects; Rats; Rats, Sprague-Dawley; Weight Gain; Whey Proteins

This study evaluated the effects of Prunus mume extract on exercise-induced fatigue recovery in a trained rat model. Male Sprague-Dawley rats were raised either on a control diet (EC) or on diets supplemented with 0.15% (0.15EP), 0.3% (0.3EP), or 0.9% (0.9EP) Prunus mume extract for 4 weeks (n = 18). Each dietary group was divided into two subgroups; at the end of the experimental period, one subgroup was sacrificed immediately after a 1-hour exercise, and the other subgroup was sacrificed after a 30-minute rest following the exercise (n = 9). Compared to the values for EC rats, serum ammonia concentration was significantly lower in 0.3EP and 0.9EP rats that were sacrificed immediately after the exercise-loading and in 0.15EP, 0.3EP and 0.9EP rats that were sacrificed after a 30-minute rest following the exercise. Compared to that in EC rats, serum lactate levels were significantly lower in rats fed 0.15% or higher levels of P. mume extract when they were sacrificed after a 30-minute rest following the exercise. Dietary supplementation with the P. mume extract significantly elevated hepatic and muscle glycogen concentrations of the rats sacrificed immediately after the exercise. P. mume extract significantly reduced lactate dehydrogenase activity and increased citrate synthase activity in the skeletal muscles of the rats sacrificed immediately after the exercise-loading. Taken together, these results indicate that the P. mume extract administered during endurance exercise training may enhance the oxidative capacity of exercising skeletal muscle and may induce the muscle to prefer fatty acids for its fuel use rather than amino acids or carbohydrates.

Topics: Animals; Biomarkers; Dietary Supplements; Enzymes; Fatigue; Glycogen; Male; Muscle, Skeletal; Physical Conditioning, Animal; Phytotherapy; Plant Extracts; Prunus; Rats; Rats, Sprague-Dawley; Weight Gain

A dual-tracer approach (dietary 14C-palmitate and intraperitoneal 3H-H2O) was used to assess the trafficking of dietary fat and net retention of carbon in triglyceride depots during the first 24 h of weight regain. Obesity-prone male Wistar rats were allowed to mature under obesogenic conditions for 16 wk. One group was switched to ad libitum feeding of a low-fat diet for 10 wk (Obese group). The remaining rats were switched to an energy-restricted, low-fat diet for 10 wk that reduced body weight by 14% and were then assessed in energy balance (Reduced group), with free access to the low-fat diet (Relapse-Day1 group), or with a provision that induced a minor imbalance (+10 kcal) equivalent to that observed in obese rats (Gap-Matched group). Fat oxidation remained at a high, steady rate throughout the day in Obese rats, but was suppressed in Reduced, Gap-Matched, and Relapse-Day1 rats though 9, 18, and 24 h, respectively. The same caloric excess in Obese and Gap-Matched rats led to less fat oxidation over the day and greater trafficking of dietary fat to visceral depots in the latter. In addition to trafficking nutrients to storage, Relapse-Day1 rats had more small, presumably new, adipocytes at the end of 24 h. Dietary fat oxidation at 24 h was related to the phosphorylation of skeletal muscle acetyl-CoA carboxylase and fatty acid availability. These observations provide evidence of adaptations in the oxidation and trafficking of dietary fat that extend beyond the energy imbalance, which facilitate rapid, efficient regain during the relapse to obesity.

Topics: Acetyl-CoA Carboxylase; Adaptation, Physiological; Adipocytes; Animals; Body Composition; Cell Proliferation; Diet, Fat-Restricted; Dietary Fats; Disease Models, Animal; Down-Regulation; Energy Intake; Energy Metabolism; Fatty Acids; Glycogen; Hyperplasia; Intra-Abdominal Fat; Male; Muscle, Skeletal; Obesity; Oxidation-Reduction; Phosphorylation; Rats; Rats, Wistar; Recurrence; Time Factors; Triglycerides; Weight Gain; Weight Loss

The action of orally administered dexamethasone (0.2 mg kg(-1) day(-1)) on metabolic parameters of adjuvant-induced arthritic rats was investigated. The body weight gain and the progression of the disease were also monitored. Dexamethasone was very effective in suppressing the Freund's adjuvant-induced paw edema and the appearance of secondary lesions. In contrast, the body weight loss of dexamethasone-treated arthritic rats was more accentuated than that of untreated arthritic or normal rats treated with dexamethasone, indicating additive harmful effects. The perfused livers from dexamethasone-treated arthritic rats presented high content of glycogen in both fed and fasted conditions, as indicated by the higher rates of glucose release in the absence of exogenous substrate. The metabolization of exogenous L: -alanine was increased in livers from dexamethasone-treated arthritic rats in comparison with untreated arthritic rats, but there was a diversion of carbon flux from glucose to L: -lactate and pyruvate. Plasmatic levels of insulin and glucose were significantly higher in arthritic rats following dexamethasone administration. Most of these changes were also found in livers from normal rats treated with dexamethasone. The observed changes in L: -alanine metabolism and glycogen synthesis indicate that insulin was the dominant hormone in the regulation of the liver glucose metabolism even in the fasting condition. The prevalence of the metabolic effects of dexamethasone over those ones induced by the arthritis disease suggests that dexamethasone administration was able to suppress the mechanisms implicated in the development of the arthritis-induced hepatic metabolic changes. It seems thus plausible to assume that those factors responsible for the inflammatory responses in the paws and for the secondary lesions may be also implicated in the liver metabolic changes, but not in the body weight loss of arthritic rats.

Topics: Alanine; Ammonia; Animals; Arthritis, Experimental; Blood Glucose; Body Weight; Dexamethasone; Fasting; Feeding Behavior; Freund's Adjuvant; Glycogen; Inflammation; Insulin; Lactates; Male; Oxygen; Perfusion; Pyruvates; Rats; Urea; Weight Gain

The liver X receptors (LXRalpha and beta) are nuclear receptors that coordinate carbohydrate and lipid metabolism. Treatment of insulin-resistant mice with synthetic LXR ligands enhances glucose tolerance, inducing changes in gene expression expected to decrease hepatic gluconeogenesis (via indirect suppression of gluconeogenic enzymes) and increase peripheral glucose disposal (via direct up-regulation of glut4 in fat). To evaluate the relative contribution of each of these effects on whole-body insulin sensitivity, we performed hyperinsulinemic-euglycemic clamps in high-fat-fed insulin-resistant rats treated with an LXR agonist or a peroxisome proliferator-activated receptor gamma ligand. Both groups showed significant improvement in insulin action. Interestingly, rats treated with LXR ligand had lower body weight and smaller fat cells than controls. Insulin-stimulated suppression of the rate of glucose appearance (Ra) was pronounced in LXR-treated rats, but treatment failed to enhance peripheral glucose uptake (R'g), despite increased expression of glut4 in epididymal fat. To ascertain whether LXR ligands suppress hepatic gluconeogenesis directly, mice lacking LXRalpha (the primary isotype in liver) were treated with LXR ligand, and gluconeogenic gene expression was assessed. LXR activation decreased expression of gluconeogenic genes in wild-type and LXRbeta null mice, but failed to do so in animals lacking LXRalpha. Our observations indicate that despite inducing suggestive gene expression changes in adipose tissue in this model of diet-induced insulin resistance, the antidiabetic effect of LXR ligands is primarily due to effects in the liver that appear to require LXRalpha. These findings have important implications for clinical development of LXR agonists as insulin sensitizers.

Topics: Animal Feed; Animals; DNA-Binding Proteins; Energy Metabolism; Fats; Gene Expression Regulation; Glucose Tolerance Test; Glycogen; Insulin; Ligands; Liver; Liver X Receptors; Male; Mice; Oligopeptides; Orphan Nuclear Receptors; Oxygen; Rats; Receptors, Cytoplasmic and Nuclear; Weight Gain

Hypothyroid heart displays a phenotype of cardioprotection against ischemia and this study investigated whether administration of dronedarone, an amiodarone-like compound that has been shown to preferentially antagonize thyroid hormone binding to thyroid hormone receptor alpha1 (TRalpha1), results in a similar effect. Dronedarone was given in Wistar rats (90 mg/kg, once daily (od) for 2 weeks) (DRON), while untreated animals served as controls (CONT). Hypothyroidism (HYPO) was induced by propylthiouracil administration. Isolated rat hearts were perfused in Langendorff mode and subjected to 20 minutes of zero-flow global ischemia (I) followed by 45 minutes of reperfusion (R). 3,5,3' Triiodothyronine remained unchanged while body weight and food intake were reduced. alpha-Myosin heavy chain (alpha-MHC) decreased in DRON while beta-myosin heavy chain (beta-MHC) and sarcoplasmic reticulum Ca2+ adenosine triphosphatase (ATPase) expression (SERCA) was similar to CONT. In HYPO, alpha-MHC and SERCA were decreased while beta-MHC was increased. Myocardial glycogen content was increased in both DRON and HYPO. In DRON, resting heart rate and contractility were reduced and ischemic contracture was significantly suppressed while postischemic left ventricular end-diastolic pressure and lactate dehydrogenase release (IU/L min) after I/R were significantly decreased. In conclusion, dronedarone treatment results in cardioprotection by selectively mimicking hypothyroidism. This is accompanied by a reduction in body weight because of the suppression of food intake. TRs might prove novel pharmacologic targets for the treatment of cardiovascular illnesses.

Topics: Adaptation, Physiological; Amiodarone; Animals; Calcium-Transporting ATPases; Dronedarone; Eating; Glycogen; Heart; Heart Rate; Hypothyroidism; In Vitro Techniques; Isomerism; L-Lactate Dehydrogenase; Male; Myocardial Contraction; Myocardial Ischemia; Myocardial Reperfusion Injury; Myocardium; Myosins; Rats; Rats, Wistar; Sarcoplasmic Reticulum; Thyroid Hormone Receptors alpha; Thyroid Hormones; Weight Gain

Previous studies demonstrated that young mice exposed chronically to industrial surfactant (IS) do not exhibit obvious adverse health effects, but do have persistently reduced body weights and compromised hepatic energy metabolism. The present study examined the time course of effects of two formulations of the Toximul (Tox) class of anionic/nonionic IS on body weights and liver glycogen (+/-virus) during early development. Results showed that effects differed in two commonly used strains of mice. In CFW mice, 12 days' exposure to Tox resulted in retardation of weight gain that was most obvious several days after exposure ceased. In this strain effects were greater with Tox 3409F than with Tox MP-A and appeared to be reversible except when the mice were treated with both Tox 3409F and FluB. Weights of the CD-1 mice were not affected by either Tox treatment alone, but were significantly reduced on postnatal day 20 when Tox exposure had been combined with FluB infection. Postnatal replenishment of hepatic glycogen stores during the first three weeks also occurred at different rates in CFW and CD-1 mice. The effects of Tox (+/-FluB) on glycogen also varied with mouse strain and Tox formulation. In CFW mice, exposure to either formulation resulted in significant (55-59%) reductions in glycogen, although reductions were not evident until nine days after Tox exposure stopped. By contrast, hepatic glycogen in CD-1 mice was reduced both during and after dermal exposure to Tox 3409F, whereas no effect was observed with Tox MP-A. Notably, the 3409F effect was reversible in the CD-1 mice, but reversal did not occur in mice also infected with FluB. Tox MP-A+FluB-treated mice exhibited only a transient glycogen reduction. These results illustrate the importance of mouse strain and formulation specificities in assessing biological effects of xenobiotic surfactants. As well, they emphasize that chronic IS exposure can induce changes in growth and energy substrate availability in young mice that may not be evident unless there is a precipitating cofactor such as a viral infection.

Topics: Animals; Female; Glycogen; Influenza B virus; Liver; Male; Mice; Surface-Active Agents; Weight Gain

We investigated the effect of different types of dietary protein on glycogen content in liver and skeletal muscle of exercise-trained rats. Twenty-four male Sprague-Dawley rats (approximately 100 g; n 6 per group) were divided into sedentary or exercise-trained groups with each group being fed either casein or whey protein as the source of dietary protein. Rats in the exercised groups were trained during 2 weeks using swimming exercise for 120 min/d, 6 d/week. Exercise training resulted in an increase in the skeletal muscle glycogen content. Furthermore, the whey protein group significantly increased the skeletal muscle glycogen content compared with the casein group. The increase in glycogen content in liver was significantly greater in rats fed the whey protein diet compared with those fed the casein diet. We also found that the whey protein diet increased the activity of liver glucokinase, whereas it decreased the activities of 6-phosphofructokinase and pyruvate kinase compared with the casein diet. However, hepatic total glycogen synthase activity and mRNA expression were similar with the two diets. In the skeletal muscle, whey protein decreased only 6-phosphofructokinase activity compared with casein. Total glycogen synthase activity in the skeletal muscle in the whey protein group was significantly higher than that in the casein group. The present study is the first to demonstrate that a diet based on whey protein may increase glycogen content in liver and skeletal muscle of exercise-trained rats. We also observed that whey protein regulated glycogen metabolism in these two tissues by different mechanisms.

Topics: Animals; Blood Glucose; Caseins; Dietary Proteins; Glycogen; Liver; Liver Glycogen; Male; Milk Proteins; Muscle, Skeletal; Physical Conditioning, Animal; Proteins; Rats; Rats, Sprague-Dawley; RNA, Messenger; Weight Gain; Whey Proteins

Topics: Glycogen; Humans; Hyponatremia; Running; Sodium; Water; Weight Gain

Physical exercises have been recommended in the prevention of non-insulin dependent diabetes mellitus (NIDDM), but the mechanisms involved in this intervention are not yet fully understood. Experimental models offer the opportunity for the study of this matter. The present study was designed to analyze the diabetes evolution in rats submitted to neonatal treatment with alloxan with the objective of verifying the suitability of the model to future studies with exercises. For this, newly born rats (6 days old) received intraperitoneal alloxan (A=200 mg/kg of body weight). Rats injected with vehicle (citrate buffer) were used as controls (C). The fasting blood glucose level (mg/dL) was higher in the alloxan group at the day 28 (C=47.25 +/- 5.08; A=54.51 +/- 7.03) but not at the 60 day of age (C=69.18 +/- 8.31; A=66.81 +/- 6.08). The alloxan group presented higher blood glucose level during glucose tolerance test (GTT) (mg/dL. 120 min) in relation to the control group both at day 28 (C=16908.9 +/- 1078.8; A=21737.7 +/- 1106.4) and at day 60 (C=11463.45 +/- 655.30; A=15282.21 +/- 1221.84). Insulinaemia during GTT (ng/mL. 120 min) was lower at day 28 (C=158.67 +/- 33.34; A=123.90 +/- 19.80), but presented no difference at day 60 (C=118.83 +/- 26.02; A=97.88 +/- 10.88). At day 60, the glycogen concentration in the soleus muscle (mg/100 mg) was lower in the alloxan group (0.3 +/- 0.13) in relation to the control group (0.5 +/- 0.07). No difference was observed between groups in relation to (micromol/g.h): Glucose Uptake (C=5.8 +/- 0.63; A=5.2 +/- 0.73); Glucose Oxidation (C=4.3 +/- 1.13; A=3.9 +/- 0.44); Glycogen Synthesis (C=0.8 +/- 0.18; A=0.7 +/- 0.18) and Lactate Production (C=3.8 +/- 0.8; A=3.8 +/- 0.7) by the isolated soleus muscle. The glucose-stimulated insulin secretion (16.7mM) by the isolated islets (ng/5 islets. h) of the alloxan group was lower (14.3 +/- 4.7) than the control group (32.0 +/- 7.9). Thus, we may conclude that this neonatal diabetes induction model gathers interesting characteristics and may be useful for further studies on the role of the exercise in the diabetes mellitus appearance.

Topics: Animals; Animals, Newborn; Diabetes Mellitus, Experimental; Disease Progression; Female; Glucose; Glucose Tolerance Test; Glycogen; Insulin; Insulin Resistance; Islets of Langerhans; Male; Muscle, Skeletal; Rats; Rats, Wistar; Weight Gain

Disruption of the PPP1R3A gene encoding the glycogen targeting subunit (G(M)/R(GL)) of protein phosphatase 1 (PP1) causes substantial lowering of the glycogen synthase activity and a 10-fold decrease in the glycogen levels in skeletal muscle. Homozygous G(M)(-/-) mice show increased weight gain after 3 months of age and become obese, weighing approximately 20% more than their wild-type (WT) littermates after 12 months of age. Glucose tolerance is impaired in 11-month-old G(M)(-/-) mice, and their skeletal muscle is insulin-resistant at > or =12 months of age. The massive abdominal and other fat depositions observed at this age are likely to be a consequence of impaired blood glucose utilization in skeletal muscle. PP1-G(M) activity, assayed after specific immunoadsorption, was absent from G(M)(-/-) mice and stimulated in the hind limb muscles of WT mice by intravenous infusion of insulin. PP1-R5/PTG, another glycogen targeted form of PP1, was not significantly stimulated by insulin in the skeletal muscle of WT mice but showed compensatory stimulation by insulin in G(M)(-/-) mice. Our results suggest that dysfunction of PP1-G(M) may contribute to the pathophysiology of human type 2 diabetes.

Topics: Adipose Tissue; Animals; Blood Glucose; Body Composition; Carrier Proteins; Glucose Intolerance; Glycogen; Glycogen Synthase; Insulin; Insulin Resistance; Intracellular Signaling Peptides and Proteins; Mice; Mice, Knockout; Muscle, Skeletal; Obesity; Phosphoprotein Phosphatases; Protein Phosphatase 1; Weight Gain

High-fat (HF) diets cause glucose intolerance. Fibrates improve glucose tolerance. We have tried to obtain information on possible hepatic mechanisms contributing to this effect.. Rats were fed a HF diet, isocaloric with the control diet, for 3 weeks without or with clofibrate. Several parameters related to liver glucose and glycogen metabolism were measured.. Clofibrate prevented the induction of glucose intolerance by 3 weeks HF feeding. Improved glucose tolerance by clofibrate was not due to increases in glucose phosphorylation or glycolysis in the liver, since both the HF diet and clofibrate suppressed glucokinase and pyruvate kinase activities with no effect on glucose 6-phosphatase. Clofibrate decreased glycogen storage in both control and HF rats. Clofibrate, with and without HF feeding, inhibited weight gain during the experimental period. Body temperature was significantly elevated by clofibrate, indicative of an increased basal metabolic rate. The capacity of liver mitochondria to oxidize long-chain fatty acids increased by clofibrate treatment. Mitochondria did not show uncoupling.. Clofibrate does not improve glucose tolerance by improving hepatic glucose or glycogen metabolism. Peripheral glucose oxidation may be facilitated by increased energy dissipation.

Topics: Animal Feed; Animals; Blood Glucose; Body Temperature; Clofibrate; Dietary Fats; Eating; Fatty Acids, Nonesterified; Glucagon; Glucokinase; Glucose Intolerance; Glucose-6-Phosphatase; Glycogen; Hypolipidemic Agents; Insulin; Liver; Male; Rats; Rats, Wistar; Receptors, Cytoplasmic and Nuclear; Transcription Factors; Weight Gain

Although lipid excess can impair beta-cell function in vitro, short-term high-fat feeding in normal rats produces insulin resistance but not hyperglycemia. This study examines the effect of long-term (10-mo) high polyunsaturated fat feeding on glucose tolerance in Wistar rats. The high fat-fed compared with the chow-fed group was 30% heavier and 60% fatter, with approximately doubled fasting hyperinsulinemia (P < 0.001) but only marginal fasting hyperglycemia (7.5 +/- 0.1 vs. 7.2 +/- 0.1 mmol/l, P < 0.01). Insulin sensitivity was approximately 67% lower in the high-fat group (P < 0.01). The acute insulin response to intravenous arginine was approximately double in the insulin-resistant high-fat group (P < 0.001), but that to intravenous glucose was similar in the two groups. After the intravenous glucose bolus, plasma glucose decline was slower in the high fat-fed group, confirming mild glucose intolerance. Therefore, despite severe insulin resistance, there was only a mildly elevated fasting glucose level and a relative deficiency in glucose-stimulated insulin secretion; this suggests that a genetic or congenital susceptibility to beta-cell impairment is required for overt hyperglycemia to develop in the presence of severe insulin resistance.

Topics: Acyl Coenzyme A; Aging; Animals; Arginine; Blood Glucose; Body Composition; Diabetes Mellitus; Dietary Fats; Fasting; Genetic Predisposition to Disease; Glucose Clamp Technique; Glucose Intolerance; Glucose Tolerance Test; Glycogen; Insulin; Insulin Resistance; Liver; Male; Muscle, Skeletal; Rats; Rats, Wistar; Time Factors; Triglycerides; Weight Gain

The effect of insulin-like growth factor I (IGF-I) on insulin-stimulated glucose uptake was studied in adipose and muscle tissues of hypophysectomized female rats. IGF-I was given as a subcutaneous infusion via osmotic minipumps for 6 or 20 days. All hypophysectomized rats received L-thyroxine and cortisol replacement therapy. IGF-I treatment increased body weight gain but had no effect on serum glucose or free fatty acid levels. Serum insulin and C-peptide concentrations decreased. Basal and insulin-stimulated glucose incorporation into lipids was reduced in adipose tissue segments and isolated adipocytes from the IGF-I-treated rats. In contrast, insulin treatment of hypophysectomized rats for 7 days increased basal and insulin-stimulated glucose incorporation into lipids in isolated adipocytes. Pretreatment of isolated adipocytes in vitro with IGF-I increased basal and insulin-stimulated glucose incorporation into lipids. These results indicate that the effect of IGF-I on lipogenesis in adipose tissue is not direct but via decreased serum insulin levels, which reduce the capacity of adipocytes to metabolize glucose. Isoproterenol-stimulated lipolysis, but not basal lipolysis, was enhanced in adipocytes from IGF-I-treated animals. In the soleus muscle, the glycogen content and insulin-stimulated glucose incorporation into glycogen were increased in IGF-I-treated rats. In summary, IGF-I has opposite effects on glucose uptake in adipose tissue and skeletal muscle, findings which at least partly explain previous reports of reduced body fat mass, increased body cell mass, and increased insulin responsiveness after IGF-I treatment.

Topics: Adipocytes; Adipose Tissue; Animals; Blood Glucose; C-Peptide; Female; Glucose; Glycogen; Hypoglycemic Agents; Hypophysectomy; Insulin; Insulin-Like Growth Factor I; Lipid Metabolism; Lipolysis; Muscle, Skeletal; Organ Size; Rats; Rats, Sprague-Dawley; Spleen; Weight Gain

The purpose of this study was to compare the hepatic enzyme activities of gluconeogenesis between control cows and experimental cows that had been overfed during the dry period to induce fatty liver postpartum. Blood and liver samples were collected 1 wk before and 0.5, 1, 2, and 3 wk after parturition. Before parturition, neither the serum nonesterified fatty acid nor the liver triacylglycerol concentration differed between the two groups. After parturition, these variables were higher in experimental cows than in control cows. Liver glycogen was higher at 1 wk before parturition in experimental cows; sharply decreased after parturition in both groups; and, at 1 wk after parturition, was lower in experimental cows than in control cows. In the liver, activities of phosphoenolpyruvate carboxykinase were significantly lower at 1 wk before and at 0.5 and 2 wk after parturition in experimental cows; in addition, the activities tended to be lower at 1 wk after parturition. Activities of fructose 1,6-bisphosphatase tended to be lower, but activities of glucose 6-phosphatase tended to be higher, at 0.5 wk after parturition in experimental cows than in control cows. Our results suggest that, in fatty infiltrated liver, the rate of gluconeogenesis is not optimal, which results in prolongation of lipolysis, particularly during the first weeks after parturition.

Topics: Animals; Cattle; Cattle Diseases; Energy Intake; Fatty Acids, Nonesterified; Fatty Liver; Female; Fructose-Bisphosphatase; Gluconeogenesis; Glucose-6-Phosphatase; Glycogen; Labor, Obstetric; Liver; Phosphoenolpyruvate Carboxykinase (GTP); Pregnancy; Triglycerides; Weight Gain

BRL 26830A, a beta adrenoceptor agonist, has been shown to have antiobesity and antidiabetic properties in rodents. The aim of this study was to study the effects of chronic BRL 26830A treatment (20 mg/kg/day for 9 weeks) on weight gain and the development of insulin resistance in gold-thioglucose-injected mice (GTG). BRL 26830A slowed the rate of weight gain in GTG such that mice weighed significantly less between 2 w and 7 w of treatment. However, at the time of sacrifice (9 w), there was no difference in body weight between treated and untreated GTG. The obesity-induced reduction in lipogenesis in brown adipose tissue (BAT) was increased 9 fold to greater than CON levels. However, weight and fatty acid (FA) content of BAT were reduced, suggesting increased lipid turnover and thermogenesis. Lipogenesis, FA content and fat pad weight were unchanged in white adipose tissue (WAT) and decreased in liver of GTG. Glucose tolerance was improved in both CON and GTG. Hyperglycemia, hyperinsulinemia and changes in cardiac and hepatic glucose oxidation as indicated by PDHC activity were normalized. Serum triglycerides and non-esterified fatty acids were reduced. Thus, chronic BRL 26830A treatment prevented the development of insulin resistance and attenuated weight gain, but did not prevent the development of obesity in this model.

Topics: Adipose Tissue; Adipose Tissue, Brown; Adrenergic beta-Agonists; Animals; Aurothioglucose; Blood Glucose; Body Composition; Ethanolamines; Fatty Acids; Glycogen; Insulin; Insulin Resistance; Lipid Metabolism; Lipids; Male; Mice; Mice, Inbred CBA; Obesity; Pyruvate Dehydrogenase Complex; Weight Gain

Tumor-bearing rats have a high rate of postprandial hepatic glycogen synthesis by the indirect pathway that involves gluconeogenesis. This study was designed to investigate the role of glycerol as a precursor for postprandial glycogen synthesis in tumor-bearing rats. Rats bearing a Leydig cell tumor and freely fed controls were fasted overnight, then fed a 16-kJ meal with or without 50 mg of glycerol by gavage. [U-14C]glycerol (1 microCi) was also administered intragastrically, and 7 mCi of 3H2O were injected intraperitoneally. The rats were killed one hour later, and the specific activities at different positions within the glycogen glucose residues in the liver were measured. Increasing the glycerol content of the meal had no significant effect on the overall incorporation of 3H into liver glycogen or on the proportion of glycogen synthesized via pyruvate in tumor-bearing or control rats. There was no difference between tumor-bearing and control rats in the amount of glycerol incorporated into glycogen, although this was increased by the high-glycerol meal. Thus glycerol appeared to make a small contribution to postprandial glycogen synthesis in tumor-bearing and control rats.

Topics: Animals; Eating; Fatty Acids; Glycerol; Glycogen; Leydig Cell Tumor; Liver; Male; Organ Size; Rats; Rats, Inbred F344; Testicular Neoplasms; Tritium; Weight Gain

This study presents the use of physiological principles and assessment techniques in addressing four objectives that can enhance a swimmer's likelihood of successfully swimming the English Channel. The four objective were: (1) to prescribe training intensities and determine ideal swimming pace; (2) to determine the amount of insulation needed, relative to heat produced, to diminish the likelihood of the swimmer suffering from hypothermia; (3) to calculate the caloric expenditure for the swim and the necessary glucose replacement required to prevent glycogen depletion; and (4) to determine the rate of acclimatization to cold water (15.56 C/60 F).. The subject participated in several pool swimming data collection sessions including a tethered swim incremental protocol to determine peak oxygen consumption and onset of lactate accumulation and several steady state swims to determine ideal swimming pace at 4.0 mM/L of lactate. Additionally, these swims provided information on oxygen consumption, which in combination with ultrasound assessment of subcutaneous fat was used to assess heat production and insulation capabilities. Finally, the subject participated in 18 cold water immersions to document acclimatization rate.. The data demonstrated the high fitness level of this subject and indicated that at a stroke rate of 63 stokes/min, HR was 130 heats/min and lactate was 4 mM/L. At this swimming pace the swimmer would need to consume 470 kcal of glucose/hr. In addition, the energy produced at this swim pace was 13.25 kcal/min while the energy lost at the present subcutaneous fat quantity was 13.40 kcal/min, requiring a fat weight gain of 6,363.03 g (13.88 lbs) to resist heat loss.. Finally, the data from the cold water immersions suggested that acclimatization occurred following two weeks of immersions. There results were provided to the swimmer and utilized in making decisions in preparation for the swim.

Topics: Acclimatization; Adipose Tissue; Adult; Anaerobic Threshold; Body Mass Index; Body Temperature; Cold Temperature; Dietary Carbohydrates; Energy Intake; Energy Metabolism; Glucose; Glycogen; Humans; Hypothermia; Lactates; Male; Motor Activity; Oceans and Seas; Oxygen Consumption; Physical Endurance; Physical Fitness; Swimming; Weight Gain

By immunocytochemistry we have studied the effect of recombinant human insulin-like growth factor I (rhIGF-I) on expression of renal GLUT-1, -2, and -5 in rats with streptozotocin (STZ)-induced diabetes. In the renal tubules of these rats, expression of GLUT-1 was reduced and that of GLUT-2 was increased. GLUT-1 expression was restored, and GLUT-2 expression was normalized by 2-wk administration of rhIGF-I. We have shown that GLUT-5 was expressed at the brush-border membrane of the proximal convoluted tubules (PCT) of the cortex and at the glomerular mesangial cells (GMC) in normal rat kidney. In the diabetic rats, GLUT-5 expression was increased at both sites, along with an increase of GLUT-2 expression at the basolateral membrane of PCT, and was decreased to normal level at both sites by treatment with rhIGF-I. Thus, like GLUT-2, GLUT-5 is suggested to regulate glucose reabsorption in PCT. The relationship between overexpression of GLUT-5 in GMC and accumulation of sorbitol and advanced glycosylation end products are discussed. Regulation of GLUT expression may play an important role on renal glucose homeostasis.

Topics: Analysis of Variance; Animals; Body Weight; Cell Membrane; Diabetes Mellitus, Experimental; Diabetic Nephropathies; Gene Expression; Glomerular Mesangium; Glucose Transporter Type 1; Glucose Transporter Type 2; Glucose Transporter Type 4; Glycogen; Humans; Immunohistochemistry; Insulin; Insulin-Like Growth Factor I; Kidney; Kidney Cortex; Kidney Tubules, Proximal; Male; Microvilli; Models, Biological; Monosaccharide Transport Proteins; Muscle Proteins; Organ Size; Rats; Rats, Sprague-Dawley; Recombinant Proteins; Reference Values; Weight Gain

Metabolic evidence was sought to explain the reduced body fat and increased body protein observed in Atlantic salmon fed diets supplemented with L-carnitine. By stimulating fatty acid oxidation, dietary carnitine might increase flux through pyruvate carboxylase and decrease flux through the branched-chain alpha-keto acid dehydrogenase complex, by increasing regulatory ratios of acetyl CoA:free enzyme A (CoA-SH) and ATP:ADP. Such changes could conserve nitrogen by providing more carbon for amino acid biosynthesis and by blocking oxidative loss of the branched-chain amino acids. Consistent with this hypothesis, salmon fed carnitine (23 mmol/kg diet) for 9 wk exhibited greater metabolic rates than cohorts fed a carnitine-free diet (P < 0.05) for the following: 1) 1-[14C] palmitate oxidation by liver cubes (48%) and by isolated hepatocytes (151%), 2) pyruvate-dependent [14 CO2]-fixation by isolated mitochondria (81%), 3) incorporation of 1-[14C] lactate into glucose by liver cubes (120%) and by isolated hepatocytes (210%), and 4) incorporation of [35S]-methionine into the acid-insoluble fraction of liver cubes (59%) and isolated hepatocytes (89%). Hepatic concentrations of seven amino acids, including the branched-chain amino acids, were greater (7-112%), as were the plasma concentrations of three of these (45-130%). However, 230% more enzyme in the mitochondria of carnitine-fed fish, and not a difference in the ratios of acetyl CoA:CoA-SH or ATP:ADP, appeared to account for accelerated flux through pyruvate carboxylase; flux through the dehydrogenase complex was unchanged. These results implicate induction of pyruvate carboxylase (or a reduction in turnover) and enhanced protein synthesis in the mechanism for carnitine-induced changes in gluconeogenesis and nitrogen metabolism.

Topics: Amino Acids; Animals; Body Composition; Carnitine; Cell Separation; Diet; Glycogen; Lipid Metabolism; Lipids; Liver; Mitochondria, Liver; Muscle, Skeletal; Nitrogen; Oxidation-Reduction; Salmon; Weight Gain

The effect of omega-3 fatty acids derived from fish and marine mammals on subjects with normal glucose tolerance is still unclear. The aim of the present study was to test whether the hypolipidemia that follows the chronic administration of cod liver oil, rich in polyunsaturated fatty acids (omega-3), to normal rats is accompanied by changes in glucose metabolism, insulin secretion and sensitivity, and pancreatic insulin content. To achieve this goal, male Wistar rats were fed with a semisynthetic diet (w/w): 62.5% cornstarch, 7% cod liver oil plus 1% corn oil, and 17% protein (CD + CLO). Control rats were fed with the same semisynthetic diet with the only exception that the source of fat was 8% (w/w) corn oil (CD). Both diets were administered ad libitum for 1 month. At the end of the experimental period, the results obtained were as follows (mean +/- SEM): serum triacylglycerol (mM): CD + CLO 0.21 +/- 0.04 vs. CD 0.58 +/- 0.05 (p < 0.05); free fatty acids (microM): CD + CLO 257 +/- 20 vs. CD 288 +/- 22 (p = NS); total cholesterol (mM): CD + CLO 1.13 +/- 0.09 vs. CD 1.82 +/- 0.06 (p < 0.05); high-density lipoprotein cholesterol (mM): CD + CLO 0.58 +/- 0.08 vs. CD 1.07 +/- 0.04 (p < 0.05); plasma glucose (mM): CD + CLO 6.30 +/- 0.29 vs. CD 6.28 +/- 0.10 (p = NS); liver triacylglycerol (mumol/liver): CD + CLO 104.1 +/- 11.4 vs. CD 136.8 +/- 4.3 (p < 0.05); glycogen (mumol/g wet weight): CD + CLO 298.3 +/- 21.0 vs. CD 297.0 +/- 19.0 (p = NS); glucose-6-phosphate dehydrogenase (U/liver): CD + CLO 37.9 +/- 2.2 vs. CD 58.8 +/- 5.0 (p < 0.05); triacylglycerol secretion (nmol/min/100 g body weight): CD + CLO 101.0 +/- 2.0 vs. CD 166.0 +/- 9.7 (p < 0.01); removal of fat emulsion (K2% min-1): CD + CLO 15.0 x 10(-2) +/- 0.8 x 10(-2) vs. CD 8.2 x 10(-2) +/- 0.2 x 10(-2) (p < 0.01); intravenous glucose tolerance (kg 10(-2): CD + CLO 2.68 +/- 0.37 vs. CD 2.70 +/- 0.14 (p = NS); immunoreactive insulin (microU/ml/ min): with the area under the curve between 0 and 30 min CD + CLO 544 +/- 60 vs. CD 1,050 +/- 38 (p < 0.05), with the area under the curve between 0 and 60 min CD + CLO 1,188 +/- 150 vs. CD 2,160 +/- 137 (p < 0.05), and pancreas insulin content (microU/mg pancreas): CD + CLO 1.85 +/- 0.29 vs. CD 2.04 +/- 0.12 (p = NS). In conclusion, the present study shows that the strong hypolipidemic effect produced by the administration of low doses of fish oil to normal rats is accompanied by a significant reduction of plasma insulin levels without changes in glucose tole

Topics: Animals; Area Under Curve; Blood Glucose; Cholesterol; Cholesterol, HDL; Corn Oil; Dose-Response Relationship, Drug; Eating; Fatty Acids, Omega-3; Fish Oils; Glucose; Glucose Tolerance Test; Glucosephosphate Dehydrogenase; Glycogen; Insulin; Insulin Resistance; Insulin Secretion; Lipids; Liver; Male; Pancreas; Rats; Rats, Wistar; Triglycerides; Weight Gain

The role of glucagon in glucose homeostasis during chronic malnutrition was studied in weanling-littermate rats either fed ad libitum or restricted to 60% of ad libitum intake for 8 weeks. Fasting glucose and insulin levels were lower in malnourished rats, and their response to glucagon (0.02 mg/kg intravenous [IV]) after a 16-hour fast was significantly less than in control littermates for both glucose (P = .039) and insulin (P = .008). During euglycemic glucose clamp studies at identical plasma glucose (PG) levels, insulin suppression of hepatic glucose production (HGP) was impaired in malnourished rats, indicating insulin resistance (mean +/- SE HGP: 48 +/- 5 v 32 +/- 10 mumol.kg-1.min-1 for controls, P = .028). Glucose disposal was not significantly different in the two groups. However, after IV glucagon, the increase in HGP was markedly impaired in malnourished rats (P = .0004), with the total amount of glucose produced by the liver over 15 minutes being 1,397 +/- 114 mumol/kg as compared with 2,031 +/- 118 in controls (P = .0047). The impaired response was not due to defective glycogenolysis, because the release of glucose from prelabeled glycogen in response to glucagon injection contributed only 6% to 8% of the overall increase in glucose output from the liver, and was not different in the two groups. Furthermore, liver glycogen stores were virtually exhausted after the 16-hour fast, without glucagon injection. Glucagon receptor affinity and number were not affected by malnutrition. It is concluded that (1) chronic malnutrition is associated with hepatic resistance to both insulin and glucagon, (2) the glucagon resistance is not due to impaired glycogenolysis, and (3) it is mediated by a postreceptor defect.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adaptation, Physiological; Animals; Blood Glucose; Drug Resistance; Food Deprivation; Glucagon; Glucose Clamp Technique; Glycogen; Homeostasis; Insulin; Insulin Resistance; Liver; Male; Rats; Rats, Sprague-Dawley; Receptors, Glucagon; Time Factors; Weight Gain

The purpose of the present study was to compare tissue oxidative capacity, skeletal muscle fatty acid composition, and tissue fuel stores in low-fat fed (LFD, 12% of energy from corn oil) male Wistar rats, and in high-fat fed (45% of energy from corn oil) obesity-prone (OP) and obesity-resistant (OR) male Wistar rats. Designation of OP and OR rats was based on body weight gain (upper tertile for OP; lower tertile for OR) after 5 weeks on the high-fat diet. Body weight gain over the 5-week dietary period was 91 +/- 9 g in LFD, 98 +/- 4 g in OR, and 158 +/- 5 g in OP (p < 0.05 vs. LFD and OR). Energy intake over the 5-week dietary period was 3099 +/- 101 kcal in LFD, 3185 +/- 51 kcal in OR, and 3728 +/- 45 kcal in OP (p < 0.05 vs. LFD and OR). Maximal citrate synthase activity (mumol.g-1.min-1) in the gastrocnemius muscle was not significantly different among groups: 12.1 +/- 2.4 in LFD, 11.4 +/- 1.9 in OR and 13.3 +/- 2.5 in OP rats. Similarly, citrate synthase activity in the heart, 59.3 +/- 7.2, and liver, 6.6 +/- 0.4, was also not significantly different among groups. Fatty acid composition of the gastrocnemius muscle was not significantly different among groups. Fasting glycogen levels in the liver, gastrocnemius muscle, and heart were 6.4 +/- 3.7, 13.2 +/- 2.3 and 6.8 +/- 1.9 mumol/g in LFD, 21.2 +/- 5.1 (p < 0.05 vs.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adipose Tissue; Animals; Blood Glucose; Body Composition; Citrate (si)-Synthase; Dietary Fats; Energy Intake; Fatty Acids; Glycogen; Insulin; Liver; Male; Muscle, Skeletal; Myocardium; Obesity; Oxidation-Reduction; Rats; Rats, Wistar; Triglycerides; Weight Gain

Hepatic changes of mice in the subacute phase of streptozotocin (SZ)-induced diabetes were investigated biochemically and pathologically. Biochemically, the contents of serum glucose and of serum and liver lipids increased while the content of liver glycogen decreased in SZ-induced diabetic mice. Histopathologically, hypertrophy of hepatocytes due to an increase in number of intracytoplasmic acidophilic granules was common to SZ-induced diabetic mice. Electron microscopically, these hepatocytes were characterized by a prominent increase in number of mitochondria showing normal structure, a marked decrease of glycogen granules and poorly developed rough endoplasmic reticulum, which were common to so-called oncocytic cells. In some SZ-induced diabetic mice, bile duct hyperplasia with an appearance of cytomegalic hepatocytes was also observed.

Topics: Animals; Blood Glucose; Diabetes Mellitus, Experimental; Endoplasmic Reticulum; Glycogen; Hypertrophy; Lipids; Liver; Male; Mice; Mice, Inbred ICR; Microscopy, Electron; Organ Size; Streptozocin; Weight Gain

Twenty-five newborn pigs were used to evaluate the energy utilization of sow colostrum by pigs maintained for 24 h in respiratory chambers at an environmental temperature of 33 degrees C. Within a litter, five neonatal pigs were obtained before nursing and allotted on the basis of initial body weight (IBW) at 3 h of age to one of the five treatments: killed, fed intragastrically 6, 12, or 18 g of sow colostrum/kg IBW per meal, or fasted. A total of 24 meals at 60-min intervals was provided and pigs were killed 1 h after the last meal. Heat production (HP) was measured by indirect calorimetry and energy retention (ER) was calculated by metabolizable energy (ME)-HP. A balance technique was used to determine nitrogen (N) retention, and comparative slaughter technique (CST) was used to determine fat accretion and glycogen mobilization. The ME intake increased quadratically (P < .01) with the level of colostrum intake. The efficiency of ME for ER was 91 +/- 4%. Nitrogen absorbed was utilized with an efficiency of 89 +/- 3% for N retention, and the estimated energy cost of 1 kcal of protein synthesized was 1.11 +/- .11 kcal. Thermoneutral maintenance ME requirement was low (68.5 kcal.kg avg BW-1 x 24 h-1) because of the low activity of pigs. Fasting heat production (FHP) measured by calorimetry and CST amounted to 56.4 and 60.4 kcal.kg avg BW-1 x 24 h-1, respectively. Estimates of the contribution of glycogen and protein catabolism to FHP were 83.0 and 6.8%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Animals, Newborn; Blood Glucose; Body Temperature Regulation; Calorimetry, Indirect; Colostrum; Energy Metabolism; Female; Glycogen; Lipid Metabolism; Nitrogen; Swine; Weight Gain

Glycogen is stored in the liver, muscles, and fat cells in hydrated form (three to four parts water) associated with potassium (0.45 mmol K/g glycogen). Total body potassium (TBK) changes early in very-low-calorie diets (VLCDs) primarily reflect glycogen storage. Potassium released from glycogen can distort estimates of body composition during dieting. TBK changes due to glycogen mobilization were measured in 11 subjects after 4 d dieting with a VLCD. The influence of water-laden glycogen on weight fluctuations during the dieting process, the exaggerated regain if carbohydrate loading occurs, and the implications for weight control programs and overestimation of nitrogen losses with dieting are discussed.

Topics: Body Composition; Body Weight; Diet, Reducing; Energy Intake; Female; Glycogen; Humans; Obesity; Potassium; Weight Gain; Weight Loss

During studying the pathogenicity of Ascaridia galli for young Ross-Broiler chickens fed with single doses of 100, 200 and 500 infective eggs, it was found that the infected chickens showed variable decreases in body weight gain and increases in the ratio of liver weight relative to body weight when compared with the control. Both decrease and increase was proportionally related with the number of infective eggs given to the chickens. Biochemical analysis of muscle and liver tissue of the previous groups of chickens showed a decrease in both glycogen and protein content and an increase in fat content of muscle and liver of infected chickens when compared with those of normal tissues. The decrease in the glycogen content due to ascaridiasis was mostly apparent in case of 500 egg dose and that of the protein content was noted with the egg doses of 200 and 500. Each of the three egg doses showed a significant increase in the fat content of the muscle and liver of infected chickens when compared with the control. After the sixth week of infection chickens fed with 500 eggs showed emaciation, loss of colour of combs and legs and of brightness of plumage, diarrhoea, drooping wings, ruffled feathers and a gradual loss of strength manifested by leg weakness. At autopsy, the small intestine showed external macroscopic lesions of haemorrhage and congestion. Intestinal obstruction with adult Ascaridia galli was also found in the infected birds.

Topics: Animals; Ascaridiasis; Chickens; Glycogen; Lipids; Liver; Liver Diseases, Parasitic; Liver Glycogen; Muscle Proteins; Muscles; Organ Size; Poultry Diseases; Proteins; Weight Gain

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

The effects of insulin on carbohydrate metabolism in atrophied rat soleus muscle are increased after unweighting by tail-cast suspension. This work has been extended by testing the effect of unweighting on the response of carbohydrate metabolism to isoproterenol, a beta-adrenergic agonist. Isoproterenol promoted glycogen degradation more in the unweighted than in the weight-bearing soleus but showed no differences in the extensor digitorum longus, which is unresponsive to hindlimb unweighting. In soleus muscles depleted of glycogen, to avoid varied inhibitory effects of glycogen on glycogen synthesis, isoproterenol inhibited this process more in the unweighted muscle. Isoproterenol did not have a greater inhibitory effect on net uptake of 2-deoxy-D[1,2-3H]glucose by the unweighted muscle. Measurements of intracellular 2-deoxy-[3H]glucose 6-phosphate and 3-O-methyl-D-[1-3H]glucose, which cannot be phosphorylated, showed that isoproterenol inhibited glucose phosphorylation but not transport. This effect could be explained by an increase of glucose 6-phosphate, an inhibitor of hexokinase. At 100 microU insulin/ml but not at a lower amount (10 microU/ml), isoproterenol inhibited hexose phosphorylation more in the control than in the unweighted muscle. This result may be explained by greater insulin antagonism in the unweighted muscle owing to increased insulin sensitivity. However, insulin antagonism of isoproterenol stimulation of glycogenolysis or inhibition of glycogenesis was not altered by unweighting. Therefore, for some aspects of carbohydrate metabolism, the unweighted muscle has an increased response to beta-adrenergic activation, just as this muscle shows increased responses to insulin.

Topics: 3-O-Methylglucose; Animals; Atrophy; Biological Transport, Active; Deoxyglucose; Female; Glucose-6-Phosphate; Glucosephosphates; Glycogen; Insulin; Isoproterenol; Lactates; Methylglucosides; Muscles; Rats; Rats, Inbred Strains; Weight Gain; Weightlessness

The objectives of this study were to determine how long increased insulin sensitivity, elicited by exercise training, persists after the end of training and what the effect of weight gain is on this retention. Exercise-trained (ET) rats ran voluntarily in freely rotating wheel cages, and insulin sensitivity was assessed by oral glucose tolerance tests (OGTT) and insulin suppression tests (IST). After training, ET rats were retired for 1, 3, or 7 days (R1, R3, or R7). Initial OGTT and IST studies indicated that sensitivity to insulin-induced glucose uptake was increased in ET rats compared with sedentary control (C) rats and was progressively lost with retirement: ET greater than R1 and R3 greater than R7 and C rats, and this reaction was generally associated with a rapid gain in body weight. Subsequent IST tests were performed on C and R7 rats fed laboratory chow or a hypocaloric diet consisting of equal parts of cellulose and chow for 7 days before the test. The results of these tests showed that steady-state serum glucose (SSSG) levels averaged 165 +/- 12 mg/dl for chow-fed C rats and 172 +/- 11 mg/dl for chow-fed R7 rats that gained body weight at rates twice those of C rats. Chow-fed R7 rats, gaining weight at rates comparable to C rats, had SSSG levels of 104 +/- 6 mg/dl. C and R7 rats fed the hypocaloric diet had SSSG values of 102 +/- 6 and 59 +/- 4 mg/dl, respectively. Muscle glycogen levels were comparable in all groups, and liver glycogen was lower in C and R7 rats fed the hypocaloric diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Blood Glucose; Glucose Tolerance Test; Glycogen; Insulin; Liver Glycogen; Male; Muscles; Physical Conditioning, Animal; Physical Exertion; Rats; Rats, Inbred Strains; Weight Gain

The effects of hyperinsulinaemia imposed on normal rats on the subsequent insulin-responsiveness in vivo of 2-deoxy-D-glucose uptake of white adipose tissue and of various muscle types were investigated. This was done by treating normal rats with insulin via osmotic minipumps, and by comparing them with saline-infused controls. Hyperinsulinaemia produced by prior insulin treatment resulted in a well-tolerated hypoglycaemia. At the end of the treatment, the glucose utilization index of individual tissues was determined by euglycaemic/hyperinsulinaemic clamps associated with the labelled 2-deoxy-D-glucose method. Prior insulin treatment resulted in increased insulin-responsiveness of the glucose utilization index of white adipose tissue, and in increased total lipogenesis in white adipose tissue and fat-pad weight. In contrast, prior insulin treatment resulted in a decreased glucose utilization index of several muscles. These opposite effects of hyperinsulinaemia on glucose utilization in white adipose tissue and muscles persisted when the hypoglycaemia-induced catecholamine output was prevented (adrenomedullectomy, propranolol treatment), as well as when hypoglycaemia was normalized by concomitant insulin treatment and glucose infusion. Insulin suppressed hepatic glucose production during the clamps in insulin-treated rats as in the respective controls, whereas total hepatic lipid synthesis and liver fat content were greater in rats treated with insulin than in controls. It is concluded that hyperinsulinaemia itself could be one of the driving forces responsible for producing increased glucose utilization by white adipose tissue, increased total lipid synthesis with fat accumulation in adipose tissue and the liver, together with an insulin-resistant state at the muscular level.

Topics: Adipose Tissue; Adrenalectomy; Animals; Blood Glucose; Deoxy Sugars; Deoxyglucose; Energy Intake; Female; Glucose; Glycogen; Insulin; Lipids; Liver; Muscles; Propranolol; Rats; Rats, Zucker; Weight Gain

The aim of this work was to find by which mechanisms an increased availability of plasma free fatty acids (FFA) reduced carbohydrate utilization during exercise. Rats were fed high-protein medium-chain triglycerides (MCT), high-protein long-chain triglycerides (LCT), carbohydrate (CHO) or high-protein low-fat (HP) diets for 5 weeks, and liver and muscle glycogen, gluconeogenesis and FFA oxidation were studied in rested and trained runner rats. In the rested state the hepatic glycogen store was decreased by fat and protein feeding, whereas soleus muscle glycogen concentration was only affected by high-protein diets. The percentage decrease in liver and muscle glycogen stores, after running, was similar in fat-fed, high-protein and CHO-fed rats. The fact that plasma glucose did not drastically change during exercise could be explained by a stimulation of hepatic gluconeogenesis: the activity of phosphoenolpyruvate carboxykinase (PEPCK) and liver phosphoenolpyruvate (PEP) concentration increased as well as cyclic adenosine monophosphate (AMPc) while liver fructose 2,6-bisphosphate decreased and plasma FFA rose. In contrast, the stimulation of gluconeogenesis in rested HP-, MCT- and LCT-fed rats appears to be independent of cyclic AMP.

Topics: Animals; Blood Glucose; Carbohydrate Metabolism; Dietary Carbohydrates; Dietary Fats; Dietary Proteins; Eating; Fatty Acids, Nonesterified; Fructosediphosphates; Glycogen; Lactates; Liver Glycogen; Male; Muscles; Phosphoenolpyruvate; Physical Exertion; Pyruvates; Rats; Rats, Inbred Strains; Time Factors; Triglycerides; Weight Gain

Topics: Body Weight; Carbohydrate Metabolism; Carbohydrates; Dietary Carbohydrates; Eating; Glycogen; Humans; Male; Metabolism; Physical Exertion; Weight Gain