glycogen and Inflammation
glycogen has been researched along with Inflammation* in 120 studies
Reviews
7 review(s) available for glycogen and Inflammation
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Exosomes in Inflammation and Inflammatory Disease.
Exosomes are a subset of extracellular vesicles released by all cell types and involved in local and systemic intercellular communication. In the past decade, research into exosomes has swelled as their important role in the mediation of health and disease has been increasingly established and acknowledged. Exosomes carry a diverse range of cargo including proteins, nucleic acids, and lipids derived from their parental cell that, when delivered to the recipient cell, can confer pathogenic or therapeutic effects through modulation of immunity and inflammation. In this review, the role of exosomes on mediation of immune and inflammatory responses, and their participation in diseases with a significant inflammatory component is discussed. The considerable potential for exosomes in therapy and diagnosis of inflammatory diseases is also highlighted. Topics: Amino Acids; Animals; Cell Proliferation; Exosomes; Fibroblasts; Glycogen; Humans; Inflammation; Lactic Acid | 2019 |
The Intriguing Role of Histamine in Exercise Responses.
In humans, histamine is a molecular transducer of physical activity responses, and antihistamines modify more than 25% of the genes responding to exercise. Although the upstream signal that results in release of histamine within exercising skeletal muscle remains to be identified, it is likely a fundamental exercise response and not an allergic reaction. Topics: Athletic Performance; Exercise; Glucose; Glycogen; Heart Rate; Histamine; Histamine Antagonists; Humans; Inflammation; Muscle, Skeletal; Pain Perception; Receptors, Histamine; Vasodilation | 2017 |
Hypomagnesemia in Type 2 Diabetes: A Vicious Circle?
Over the past decades, hypomagnesemia (serum Mg(2+) <0.7 mmol/L) has been strongly associated with type 2 diabetes mellitus (T2DM). Patients with hypomagnesemia show a more rapid disease progression and have an increased risk for diabetes complications. Clinical studies demonstrate that T2DM patients with hypomagnesemia have reduced pancreatic β-cell activity and are more insulin resistant. Moreover, dietary Mg(2+) supplementation for patients with T2DM improves glucose metabolism and insulin sensitivity. Intracellular Mg(2+) regulates glucokinase, KATP channels, and L-type Ca(2+) channels in pancreatic β-cells, preceding insulin secretion. Moreover, insulin receptor autophosphorylation is dependent on intracellular Mg(2+) concentrations, making Mg(2+) a direct factor in the development of insulin resistance. Conversely, insulin is an important regulator of Mg(2+) homeostasis. In the kidney, insulin activates the renal Mg(2+) channel transient receptor potential melastatin type 6 that determines the final urinary Mg(2+) excretion. Consequently, patients with T2DM and hypomagnesemia enter a vicious circle in which hypomagnesemia causes insulin resistance and insulin resistance reduces serum Mg(2+) concentrations. This Perspective provides a systematic overview of the molecular mechanisms underlying the effects of Mg(2+) on insulin secretion and insulin signaling. In addition to providing a review of current knowledge, we provide novel directions for future research and identify previously neglected contributors to hypomagnesemia in T2DM. Topics: Blood Glucose; Calcium Channels, L-Type; Diabetes Mellitus, Type 2; Dietary Supplements; Disease Progression; Glucokinase; Glycogen; Glycolysis; Humans; Inflammation; Insulin; Insulin Resistance; Insulin Secretion; Insulin-Secreting Cells; KATP Channels; Liver; Magnesium; Magnesium Deficiency; Obesity; Potassium Channels, Inwardly Rectifying; Sodium Chloride Symporters; Sodium-Potassium-Exchanging ATPase; Water-Electrolyte Imbalance | 2016 |
Recovery in soccer : part ii-recovery strategies.
In the formerly published part I of this two-part review, we examined fatigue after soccer matchplay and recovery kinetics of physical performance, and cognitive, subjective and biological markers. To reduce the magnitude of fatigue and to accelerate the time to fully recover after completion, several recovery strategies are now used in professional soccer teams. During congested fixture schedules, recovery strategies are highly required to alleviate post-match fatigue, and then to regain performance faster and reduce the risk of injury. Fatigue following competition is multifactorial and mainly related to dehydration, glycogen depletion, muscle damage and mental fatigue. Recovery strategies should consequently be targeted against the major causes of fatigue. Strategies reviewed in part II of this article were nutritional intake, cold water immersion, sleeping, active recovery, stretching, compression garments, massage and electrical stimulation. Some strategies such as hydration, diet and sleep are effective in their ability to counteract the fatigue mechanisms. Providing milk drinks to players at the end of competition and a meal containing high-glycaemic index carbohydrate and protein within the hour following the match are effective in replenishing substrate stores and optimizing muscle-damage repair. Sleep is an essential part of recovery management. Sleep disturbance after a match is common and can negatively impact on the recovery process. Cold water immersion is effective during acute periods of match congestion in order to regain performance levels faster and repress the acute inflammatory process. Scientific evidence for other strategies reviewed in their ability to accelerate the return to the initial level of performance is still lacking. These include active recovery, stretching, compression garments, massage and electrical stimulation. While this does not mean that these strategies do not aid the recovery process, the protocols implemented up until now do not significantly accelerate the return to initial levels of performance in comparison with a control condition. In conclusion, scientific evidence to support the use of strategies commonly used during recovery is lacking. Additional research is required in this area in order to help practitioners establish an efficient recovery protocol immediately after matchplay, but also for the following days. Future studies could focus on the chronic effects of recovery strategies, on combinations of Topics: Athletic Performance; Beverages; Cold Temperature; Dehydration; Diet Therapy; Dietary Carbohydrates; Dietary Proteins; Electric Stimulation Therapy; Fatigue; Glycogen; Humans; Immersion; Inflammation; Massage; Muscle Proteins; Muscle Stretching Exercises; Recovery of Function; Resistance Training; Sleep Wake Disorders; Soccer; Sodium; Stockings, Compression | 2013 |
Inositol phosphoglycans and preeclampsia: from bench to bedside.
The metabolic syndrome that occurs in preeclampsia reflects the complex interactions between immunological alterations and the systemic inflammation that have been shown to take place during this complication of human pregnancy. Inositol phosphoglycans play a definite role in the insulin resistance in preeclampsia with a higher production and urinary excretion of this molecule before and during preeclampsia. Recent researches suggest that the feto-placental glucose metabolism in the first and early second trimester is mainly linked to the nonoxidative pathway of glycogen catabolism supporting the pivotal role of the inositol phosphoglycan P-type. In this article we present the results of a case-control study carried out in the first trimester to evaluate the potential of urinary P-IPG release as a early marker of the disease. A single mid-stream sample of maternal urine was collected at 11 weeks of gestation for this single centre retrospective study. Twenty-seven patients out of 331 women recruited (8.1%) went on to develop preeclampsia but no sample attained positivity. Further details about the development of the metabolic syndrome during preeclampsia were retrieved also from other studies to implement our knowledge about the pathophysiology of this syndrome and to identify biochemical aspects that could help in clinical practice. Topics: Female; Fetus; Glucose; Glycogen; Humans; Inflammation; Inositol Phosphates; Metabolic Syndrome; Placenta; Polysaccharides; Pre-Eclampsia; Pregnancy; Pregnancy Trimester, First; Pregnancy Trimester, Third | 2011 |
Interleukin 6 as a key regulator of muscle mass during cachexia.
Interleukin 6 (IL-6) has received significant attention for its regulatory role in muscle wasting during cachexia. This review examines the role of circulating IL-6 for decreasing muscle mass during cancer and emphasizes some of the indirect actions of IL-6 that may cause muscle wasting. Topics: Cachexia; Exercise; Glycogen; Humans; Hypertrophy; Inflammation; Interleukin-6; Muscle, Skeletal; Neoplasms; Risk Factors; Signal Transduction | 2010 |
Pathology of viral hepatitis.
Topics: Acute Disease; Biopsy; Cholestasis; Cytoplasm; Feces; Glycogen; Hepatitis A; Hepatitis B; Hepatitis B Antigens; Humans; Inclusion Bodies, Viral; Inflammation; Jaundice; Kupffer Cells; Liver; Lysosomes; Microscopy, Electron; Mitochondria, Liver; Necrosis; Ribosomes | 1972 |
Trials
4 trial(s) available for glycogen and Inflammation
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Alpine Skiing With total knee ArthroPlasty (ASWAP): metabolism, inflammation, and skeletal muscle fiber characteristics.
We investigated the effect of alpine skiing for 12 weeks on skeletal muscle characteristics and biomarkers of glucose homeostasis and cardiovascular risk factors. Twenty-three patients with a total knee arthroplasty (TKA) were studied 2.9 ± 0.9 years (mean ± SD) after the operation. Fourteen patients participated in the intervention group (IG) and nine in the control group (CG). Blood samples and muscle biopsies were obtained before (PRE) and 7.3 ± 0.8 days after (POST) the intervention, and blood samples again after a retention (RET) phase of 8 weeks. With skiing, glucose homeostasis improved in IG (decrease in fasting insulin, increase in muscle glycogen) but not in CG. Fiber type distribution and size, as well as capillary density and number of capillaries around the fibers (CAF), were not different between the operated and the non-operated leg in either group. The relative number of type I fibers increased with skiing in IG with no change in CG. Inflammatory biomarkers, plasma lipids, and mitochondrial proteins and activity did not change. Alpine skiing is metabolically beneficial and can be used as a training modality by elderly people with TKA. Topics: Aged; Arthroplasty, Replacement, Knee; Blood Glucose; C-Reactive Protein; Capillaries; Cholesterol, HDL; Cholesterol, LDL; Cytokines; Female; Glycogen; Humans; Inflammation; Insulin; Male; Middle Aged; Mitochondrial Proteins; Muscle Fibers, Skeletal; Muscle Fibers, Slow-Twitch; Muscle, Skeletal; Osteoarthritis, Knee; Skiing; Triglycerides | 2015 |
Bovine colostrum supplementation's lack of effect on immune variables during short-term intense exercise in well-trained athletes.
The purpose of this study was to investigate the potential of bovine colostrum to attenuate postexercise decline in immune function. The authors evaluated the time course of a number of immune variables after short-term intense exercise in 9 male athletes after 10 d of supplementation with either colostrum or skim-milk powder. To increase the stress on the immune system subjects performed a glycogen-depletion trial the evening before the endurance trial (90 min at 50% Wmax). Blood samples were taken before the glycogen-depletion trial, before and after the endurance trial, and the next morning, ~22 hr after cessation of the exercise. Plasma cortisol levels increased over time, reaching the highest level directly after exercise, and were still elevated ~22 hr after exercise compared with baseline values (p < .001). Neutrophil cell count was increased after exercise and dropped below starting values 22 hr after exercise (time effect p < .001). Circulating immunoglobulins did not change over time. A significant time effect was seen for interleukin (IL)-6, IL-10, IL-1-receptor agonist, and C-reactive protein, with levels being higher directly after exercise (p < .05). Other cytokines (interferon-γ, IL-1a, IL-8, tumor necrosis factor-a) did not show a time effect. No differences were seen between colostrum and skim-milk powder in any of the investigated variables. Our results are consistent with the hypothesis that intense exercise affects several variables of the immune system. Colostrum did not alter any of the postexercise immune variables compared with skim-milk powder, suggesting no role for bovine colostrum supplementation in preventing postexercise immune suppression after short-term intense exercise. Topics: Adult; Animals; Biomarkers; Cattle; Colostrum; Cross-Over Studies; Cytokines; Double-Blind Method; Exercise; Glycogen; Humans; Hydrocortisone; Immune System; Immunoglobulins; Inflammation; Male; Neutrophils; Physical Endurance; Time Factors | 2011 |
Expression profiling of insulin action in human myotubes: induction of inflammatory and pro-angiogenic pathways in relationship with glycogen synthesis and type 2 diabetes.
Myotube cultures from patients with type 2 diabetes mellitus (T2DM) represent an experimental in vitro model of T2DM that offers a possibility to perform gene expression studies under standardized conditions. During a time-course of insulin stimulation (1 microM) at 5.5 mM glucose for 0 (no insulin), 0.5, 1, 2, 4, 8, and 24 h, mRNA contents were analyzed in human myotubes for each time point using Affymetrix DNA chip technology. Insulin treatment induced an inflammatory and pro-angiogenic response in the myotubes, with expression of early response factors followed by inflammatory chemokines, metabolic enzymes, and finally cell cycle regulating genes. One-hundred-forty-four genes were differentially expressed in myotubes from donors with type 2 diabetes compared with control subjects, including HSP70, apolipoprotein D/E, tropomyosin, myosin, and actin previously reported from in vivo studies of diabetic skeletal muscle. We conclude, (i) that insulin induces a time-dependent inflammatory and pro-angiogenic transcriptional response in cultured human myotubes, (ii) that myotubes in vitro retain a gene expression pattern specific for type 2 diabetes and sharing five genes with that of type 2 diabetic skeletal muscle in vivo, and (iii) that insulin, despite similar metabolic effects of glucose uptake and glycogen synthesis, regulates different pools of genes in skeletal muscle during in vivo and in vitro conditions. Topics: Adult; Cells, Cultured; Cytokines; Diabetes Mellitus, Type 2; Dose-Response Relationship, Drug; Gene Expression Profiling; Gene Expression Regulation; Glycogen; Humans; Inflammation; Insulin; Insulin Resistance; Kinetics; Male; Middle Aged; Muscle Fibers, Skeletal; Muscle, Skeletal; Neovascularization, Pathologic; Oligonucleotide Array Sequence Analysis; Signal Transduction | 2004 |
Influence of a prostaglandin-inhibiting drug on muscle soreness after eccentric work.
Since the time sequence of exercise-induced muscle soreness corresponds well with the time sequence of exercise-induced morphological changes in animal skeletal muscle, it has been suggested that muscle soreness is related to an inflammatory response. Prostaglandins are assumed to play a role in the inflammatory process. The influence of a cyclo-oxygenase-inhibiting drug (flurbiprofen) on the subjective symptoms of soreness and eventual structural changes was investigated in six male subjects. The subjects performed one concentric and two eccentric work bouts of 30 min at 80% of the individual maximal work load on the bicycle ergometer. Muscle biopsies taken before, immediately after, and 24 h after work were used to examine structural, ultrastructural changes as well as for assessment of glycogen content. Plasma levels of muscle enzymes and subjective soreness were determined at regular intervals. Eccentric work elicited muscle soreness in all subjects: however, the soreness was consistently less in the second eccentric trial. No significant enzyme release was noticed in any of the subjects, whereas ultrastructural changes were restricted to the mitochondria. No influence of flurbiprofen on subjective soreness was noticed. After both eccentric trials muscle glycogen was lower 24 h after work compared to the content immediately after work. The results suggest that eccentric exercise interferes with glycogen synthesis and that prostaglandins do not play a major role in exercise-induced muscle soreness. Topics: Adult; Exercise Test; Flurbiprofen; Glycogen; Humans; Inflammation; Male; Muscle Contraction; Muscles; Muscular Diseases; Physical Exertion; Propionates | 1985 |
Other Studies
109 other study(ies) available for glycogen and Inflammation
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Effect of source and amount of rumen-protected choline on hepatic metabolism during induction of fatty liver in dairy cows.
Topics: Animals; Cattle; Cattle Diseases; Cholesterol; Choline; Diet; Dietary Supplements; Fatty Acids; Fatty Liver; Female; Glucose; Glycogen; Haptoglobins; Inflammation; Lactation; Liver; Methionine; Milk; Pregnancy; RNA, Messenger; Rumen; Triglycerides | 2023 |
Activated Lymphocyte-Derived DNA Drives Glucose Metabolic Adaptation for Inducing Macrophage Inflammatory Response in Systemic Lupus Erythematosus.
Activated lymphocyte-derived DNA (ALD-DNA) has been reported to drive the polarization of macrophages toward M2b, producing inflammatory cytokines and inducing inflammation, correspondingly playing an essential role in the development of systemic lupus erythematosus (SLE). Recently, accumulating evidence has pinpointed metabolic adaptation as the crucial cell-intrinsic determinant for inflammatory response, in which glucose metabolism is the key event. However, whether and how glucose metabolism was involved in ALD-DNA-induced macrophage inflammatory response and SLE development remains unclear. Herein, we performed glucose metabolomic analyses of ALD-DNA-stimulated macrophages and uncovered increased glycolysis and diminished pentose phosphate pathway (PPP), as well as enhanced glycogenesis. In ALD-DNA-stimulated macrophages, increased glycolysis resulted in higher lactate production, whereas diminished PPP efficiently led to lower levels of nicotinamide adenine dinucleotide phosphate (NADPH) with higher levels of reactive oxygen species (ROS). While blockade of lactate generation exerted no significant effect on macrophage inflammation in response to ALD-DNA, scavenging ROS fundamentally inhibited the inflammatory response of ALD-DNA-stimulated macrophages. Further, cyclic adenosine monophosphate (cAMP), a master for regulating glycogen metabolism, was downregulated by ALD-DNA in macrophages, which subsequently imbalanced glycogen metabolism toward glycogenesis but not glycogenolysis. Administration of cAMP effectively restored glycogenolysis and enhanced PPP, which correspondingly reduced ROS levels and inhibited the inflammatory response of ALD-DNA-stimulated macrophages. Finally, blocking glucose metabolism using 2-deoxy-D-glucose (2-DG) efficiently restricted macrophage inflammatory response and alleviated ALD-DNA-induced lupus disease. Together, our findings demonstrate that ALD-DNA drives the adaptation of glucose metabolism for inducing macrophage inflammatory response in SLE, which might further our understanding of disease pathogenesis and provide clues for interventive explorations. Topics: Cyclic AMP; DNA; Glucose; Glycogen; Humans; Inflammation; Lactic Acid; Lupus Erythematosus, Systemic; Lymphocytes; Macrophages; Reactive Oxygen Species | 2023 |
The effect of coffee consumption on glucose homeostasis and redox-inflammatory responses in high-fat diet-induced obese rats.
Coffee effects on glucose homeostasis in obesity remain controversial. We investigated whether coffee mitigates the negative effects on glucose metabolism induced by a high-fat diet and the interrelationships with redox-inflammatory responses. Rats were treated with: control (CT-); coffee (CT+) 3.9 g of freeze-dried coffee/kg of diet; high-fat (HF-); or high-fat + coffee 3.9 g of freeze-dried coffee/kg of diet (HF+) diet. The high-fat diet increased weight gain, feed efficiency, HOMA β, muscle and hepatic glycogen, intestinal CAT and SOD activity, hepatic protein (CARB) and lipid oxidation (MDA), muscle Prkaa1 mRNA and IL6 levels, and decreased food intake, hepatic GR, GPX and SOD activities, intestinal CARB, intestinal Slc2a2 and Slc5a1 and hepatic Prkaa1 and Prkaa2 mRNA levels, hepatic glucose-6-phosphatase and muscle hexokinase (HK) activities, compared to the control diet. The high-fat diet with coffee increased hepatic GST activity and TNF and decreased IL6 and intestinal glucosidase activity compared with the high-fat diet. The coffee diet increased muscle glycogen, hepatic CARB and PEPCK activity, and decreased hepatic GR and SOD activities and intestinal CARB, compared with the control diet. Coffee increased insulin levels, HOMA IR/β, FRAP, muscle Prkaa1 mRNA levels and hepatic and muscle phosphofructokinase-1, and it decreased intestinal CAT, hepatic Slc2a2 mRNA levels and muscle HK activity, regardless of the diet type. In conclusion, chronic coffee consumption improves antioxidant and anti-inflammatory responses, but does not ameliorate glucose homeostasis in a high-fat diet-induced obesity model. In addition, coffee consumption increases insulin secretion and promotes muscle glycogen synthesis in rats maintained on a control diet. Topics: Animals; Antioxidants; Blood Glucose; Carbohydrate Metabolism; Coffee; Cytokines; Diet, High-Fat; Glycogen; Homeostasis; Inflammation; Insulin; Intestine, Small; Liver; Male; Muscle, Skeletal; Obesity; Oxidation-Reduction; Rats; Rats, Wistar | 2022 |
Oral Subacute Exposure to Cadmium LOAEL Dose Induces Insulin Resistance and Impairment of the Hormonal and Metabolic Liver-Adipose Axis in Wistar Rats.
Cadmium is a nonessential transition metal considered one of the more hazardous environmental contaminants. The population is chronically exposed to this metal at low concentrations, designated as the LOAEL (lowest observable adverse effect level) dose. We aimed to investigate whether oral subacute exposure to cadmium LOAEL disrupts hormonal and metabolic effects of the liver-adipose axis in Wistar rats. Fifty male Wistar rats were separated into two groups: control (standard normocalorie diet + water free of cadmium) and cadmium (standard normocalorie diet + drinking water with 32.5 ppm CdCl Topics: Adipose Tissue; Animals; Cadmium; Glycogen; Inflammation; Insulin; Insulin Resistance; Liver; Male; Rats; Rats, Wistar; Sterol Regulatory Element Binding Protein 1; Triglycerides | 2022 |
Glycogen accumulation in adipocyte precursors from elderly and obese subjects triggers inflammation via SIRT1/6 signaling.
Dysfunctional adipocyte precursors have emerged as key determinants for obesity- and aging-related inflammation, but the mechanistic basis remains poorly understood. Here, we explored the dysfunctional adipose tissue of elderly and obese individuals focusing on the metabolic and inflammatory state of human adipose-derived mesenchymal stromal cells (hASCs), and on sirtuins, which link metabolism and inflammation. Both obesity and aging impaired the differentiation potential of hASCs but had a different impact on their proliferative capacity. hASCs from elderly individuals (≥65 years) showed an upregulation of glycolysis-related genes, which was accompanied by increased lactate secretion and glycogen storage, a phenotype that was exaggerated by obesity. Multiplex protein profiling revealed that the metabolic switch to glycogenesis was associated with a pro-inflammatory secretome concomitant with a decrease in the protein expression of SIRT1 and SIRT6. siRNA-mediated knockdown of SIRT1 and SIRT6 in hASCs from lean adults increased the expression of pro-inflammatory and glycolysis-related markers, and enforced glycogen deposition by overexpression of protein targeting to glycogen (PTG) led to a downregulation of SIRT1/6 protein levels, mimicking the inflammatory state of hASCs from elderly subjects. Overall, our data point to a glycogen-SIRT1/6 signaling axis as a driver of age-related inflammation in adipocyte precursors. Topics: Adipocytes; Adipose Tissue; Adult; Aged; Glycogen; Humans; Inflammation; Obesity; Sirtuin 1; Sirtuins | 2022 |
Glycogen metabolism reprogramming promotes inflammation in coal dust-exposed lung.
Long-term coal dust exposure triggers complex inflammatory processes in the coal workers' pneumoconiosis (CWP) lungs. The progress of the inflammation is reported to be affected by disordered cell metabolism. However, the changes in the metabolic reprogramming associated with the pulmonary inflammation induced by the coal dust particles are unknown. Herein, we show that coal dust exposure causes glycogen accumulation and the reprogramming of glucose metabolism in the CWP lung. The glycogen accumulation caused by coal dust is mainly due to macrophages, which reprogram glycogen metabolism and trigger an inflammatory response. In addition, 2-deoxy-D-glucose (2-DG) reduced glycogen content in macrophages, which was accompanied by mitigated inflammation and restrained NF-κB activation. Accordingly, we have pinpointed a novel and crucial metabolic pathway that is an essential regulator of the inflammatory phenotype of coal dust-exposed macrophages. These results shed light on new ways to regulate CWP inflammation. Topics: Anthracosis; Coal; Coal Mining; Dust; Glycogen; Humans; Inflammation; Lung; Minerals; Pneumoconiosis | 2022 |
High-refined carbohydrate diet alters different metabolic functions in female rats.
A diet containing refined carbohydrate (HCD) caused obesity and white adipose tissue (WAT) abnormalities, but it is unclear if HCD is linked with other metabolic dysfunctions in female models. Thus, we assessed whether HCD results in WAT, pancreas, liver, skeletal muscle (SM) and thyroid (TH) abnormalities in female rats. Female rats were fed with HCD for 15 days and metabolic morphophysiology, inflammation, oxidative stress (OS), and fibrosis markers were assessed. HCD rats presented large adipocytes, hyperleptinemia, and WAT OS. HCD caused irregular glucose metabolism, low insulin levels, and large pancreatic isle. Granulomas, reduced glycogen, and OS were observed in HCD livers. HCD caused hypertrophy and increased in glycogen in SM. HCD caused irregular TH morphophysiology, reduced colloid area and high T3 levels. In all selected tissues, inflammation and fibrosis were observed in HCD rats. Collectively, these data suggest that the HCD impairs metabolic function linked with irregularities in WAT, pancreas, liver, SM and TH in female rats. Topics: Animals; Diet; Diet, High-Fat; Female; Fibrosis; Glucose; Glycogen; Inflammation; Insulins; Rats | 2022 |
β-Hydroxyphosphocarnitine modifies fibrosis, steatosis and improves liver function in non-alcoholic steatohepatitis induced in rats.
Non-alcoholic steatohepatitis (NASH) is a chronic disease characterized by inflammation, steatosis, and liver fibrosis. The liver is particularly affected by alterations in lipid metabolism. Our aim was to evaluate the effect of β-hydroxyphosphocarnitine (β-HPC) on NASH induced in rats.. NASH was characterized by elevated triglycerides, elevated liver damage enzymes, and the presence of necrosis, inflammation, steatosis, and fibrosis. Significant amounts of glycogen were found, along with α-SMA positive cells in fibrosis areas. The over-expression of SREBP-1 in cytoplasm and nuclei was evident. Animals with NASH treated with β-HPC showed a significant reduction in inflammation, necrosis, and glycogen content in the liver. A reduction in α-SMA and SREBP-1 immunopositive cells correlated with a significant reduction in the degree of fibrosis and steatosis found in liver tissue. β-HPC reduced the levels of ALP and GGT, and significantly reduced triglyceride levels. Animals treated with β-HPC did not show any alterations in liver enzyme function.. Our research shows that β-HPC can improve liver function and morphology in the case of NASH induced in rats, suggesting β-HPC could be potentially used in the treatment of NASH. Topics: Animals; Carnitine; Cholesterol; Diet, High-Fat; Disease Models, Animal; Fructose; Glucose; Glycogen; Inflammation; Liver; Liver Cirrhosis; Necrosis; Non-alcoholic Fatty Liver Disease; Organophosphates; Rats; Rats, Wistar; Sterol Regulatory Element Binding Protein 1; Triglycerides | 2022 |
TLR4 deletion increases basal energy expenditure and attenuates heart apoptosis and ER stress but mitigates the training-induced cardiac function and performance improvement.
Strategies capable of attenuating TLR4 can attenuate metabolic processes such as inflammation, endoplasmic reticulum (ER) stress, and apoptosis in the body. Physical exercise has been a cornerstone in suppressing inflammation and dysmetabolic outcomes caused by TRL4 activation. Thus, the present study aimed to evaluate the effects of a chronic physical exercise protocol on the TLR4 expression and its repercussion in the inflammation, ER stress, and apoptosis pathways in mice hearts. Echocardiogram, RT-qPCR, immunoblotting, and histological techniques were used to evaluate the left ventricle of wild-type (WT) and Tlr4 knockout (TLR4 KO) mice submitted to a 4-week physical exercise protocol. Moreover, we performed a bioinformatics analysis to expand the relationship of Tlr4 mRNA in the heart with inflammation, ER stress, and apoptosis-related genes of several isogenic strains of BXD mice. The TLR4 KO mice had higher energy expenditure and heart rate in the control state but lower activation of apoptosis and ER stress pathways. The bioinformatics analysis reinforced these data. In the exercised state, the WT mice improved performance and cardiac function. However, these responses were blunted in the KO group. In conclusion, TLR4 has an essential role in the inhibition of apoptosis and ER stress pathways, as well as in the training-induced beneficial adaptations. Topics: Animals; Apoptosis; Apoptosis Regulatory Proteins; Echocardiography; Endoplasmic Reticulum Stress; Energy Metabolism; Gene Deletion; Glycogen; Heart Rate; Heart Ventricles; Inflammation; Mice; Mice, Knockout; Physical Conditioning, Animal; RNA, Messenger; Toll-Like Receptor 4; Ventricular Function | 2021 |
Non-targeted metabolomics analyses by mass spectrometry to explore metabolic stress after six training weeks in high level swimmers.
Topics: Adolescent; Athletes; Butyric Acid; Carnitine; Cresols; Cross-Over Studies; Fatigue; Female; Glycogen; Humans; Inflammation; Lactic Acid; Male; Mass Spectrometry; Metabolomics; Osmolar Concentration; Pregnanediol; Random Allocation; Stress, Physiological; Sulfuric Acid Esters; Swimming | 2021 |
Restoring metabolism of myeloid cells reverses cognitive decline in ageing.
Ageing is characterized by the development of persistent pro-inflammatory responses that contribute to atherosclerosis, metabolic syndrome, cancer and frailty Topics: Adult; Aged; Aging; Animals; Cell Respiration; Cells, Cultured; Cognitive Dysfunction; Dinoprostone; Energy Metabolism; Glucose; Glycogen; Humans; Inflammation; Macrophages; Memory Disorders; Mice; Microglia; Mitochondria; Myeloid Cells; Receptors, Prostaglandin E, EP2 Subtype; Signal Transduction; Spatial Memory | 2021 |
Role of zonulin and GLP-1/DPP-IV in alleviation of diabetes mellitus by peptide/polypeptide fraction of Aloe vera in streptozotocin- induced diabetic wistar rats.
The genus Aloe has a long history of usage in medicine. Aloe barbadensis Miller, commonly known as Aloe vera, is said to possess anti-diabetic, anti-inflammatory, anti-cancer, anti-microbial, immunomodulation, wound healing properties.. In diabetes mellitus, loss in intestinal permeability is observed with high levels of zonulin and low levels of glucagon-like peptide-1 (GLP-1) leading to hyperglycemia. The aim of the study was to understand the role of peptide/polypeptide fraction (PPF) of Aloe vera in the alleviation of diabetes through maintaining the intestinal permeability by regulating the zonulin and GLP-1 levels.. The PPF of Aloe vera was obtained through trichloroacetic acid precipitation. The anti-diabetic potential of the PPF was tested through DPP-IV inhibition, glucose diffusion assay, and by using Rin-m5F cells. The anti-diabetic potential of the PPF was tested at a dose of 0.450 mg/kg bw in vivo using streptozotocin-induced diabetic Wistar rats. The effect of PPF on fasting plasma glucose, insulin, glucagon, Zonulin, GLP-1, DPP-IV, levels were studied in diabetic rats. The histopathological studies of the pancreas, small intestine, and liver were carried out for organ-specific effects.. PPF has the ability to reduce fasting plasma glucose levels with concomitant increase in insulin levels in streptozotocin-induced diabetic rats. It was also observed that increase in GLP-1 levels with a decrease in DPP-IV and zonulin levels thereby mitigating the loss of intestinal permeability. These findings correlate with the small intestine's histopathological observation where the excessive proliferation of epithelium in the small intestine of diabetic rats was reduced after PPF treatment.. These results suggest that the PPF of Aloe vera alleviates diabetes through islet cell rejuvenation via GLP-1/DPP-IV pathway and thereby suggesting the usage of PPF as an alternate medicine for diabetes mellitus with the possibility to reduce the intestinal permeability and zonulin levels. Topics: Aloe; Animals; Blood Glucose; Cell Survival; Cytokines; Diabetes Mellitus, Experimental; Dipeptidyl Peptidase 4; Glucagon; Glucagon-Like Peptide 1; Glucose-6-Phosphate; Glycogen; Haptoglobins; Hexokinase; Hypoglycemic Agents; Inflammation; Insulin; Intestine, Small; Liver; Nitric Oxide; Pancreas; Plant Extracts; Protein Precursors; Rats, Wistar; Streptozocin | 2021 |
Hypoglycemic and hypolipidemic effects of total glycosides of Cistanche tubulosa in diet/streptozotocin-induced diabetic rats.
Cistanche tubulosa (Schrenk) R. Wight (Orobanchaceae) is a frequently prescribed component in many traditional herbal prescriptions which are used to treat diabetes in China. In recent studies, the antidiabetic activity of Cistanche tubulosa extracts have been confirmed. However, no systematic investigation has been reported on the total glycosides of Cistatnche tubulosa (TGCT).. The present study aimed to investigate the hypoglycemic and hypolipidemic effects of TGCT and the potential mechanisms in diet/streptozotocin (STZ)-induced diabetic rats, and to chemically characterize the main constituents of TGCT.. The major constituents of TGCT were characterized by HPLC/Q-TOF-MS and the analytical quantification was performed with HPLC-DAD. Type 2 diabetic rats were induced by high-fat high-sucrose diet (HFSD) and a single injection of STZ (30 mg/kg). TGCT (50 mg/kg, 100 mg/kg and 200 mg/kg) or metformin (200 mg/kg) were orally administered for 6 weeks. Body weight and calorie intake were monitored throughout the experiment. Fasting plasma glucose (FPG), oral glucose tolerance test (OGTT), area under curve of glucose (AUC-G), glycosylated hemoglobin (HbA1c), fasting insulin, serum C-peptide, glycogen content and insulin sensitivity index were tested. The levels of phosphorylated protein kinase B and phosphorylated glycogen synthase kinase 3β, the activities of hexokinase and pyruvate kinase were assayed. Meanwhile, the changes in serum lipid profiles, superoxide dismutase, glutathione peroxidase, malondialdehyde and inflammatory factors were measured. Histological of pancreas were also evaluated by haematoxylin-eosin stain.. Our investigation revealed the presence of phenylethanoid glycosides (PhGs): echinacoside (500.19 ± 11.52 mg/g), acteoside (19.13 ± 1.44 mg/g) and isoacteoside (141.82 ± 5.78 mg/g) in TGCT. Pharmacological tests indicated that TGCT significantly reversed STZ-induced weight loss (11.1%, 200 mg/kg); decreased FPG (56.4%, 200 mg/kg) and HbA1c (37.4%, 200 mg/kg); ameliorated the OGTT, AUC-G and insulin sensitivity; increased glycogen content (40.8% in liver and 52.6% in muscle, 200 mg/kg) and the activities of carbohydrate metabolizing enzymes; regulated lipid profile changes and the activities of antioxidant enzymes; diminished serum markers of oxidative stress and inflammation in a dose-dependent manner (p < 0.05).. This study confirmed that TGCT was an effective nutritional agent for ameliorating hyperglycemia and hyperlipidemia in diet/STZ-induced diabetic rats, which might be largely attributed to the activities of TGCT on inhibitions of oxidative stress and inflammation. Topics: Animals; Blood Glucose; Body Weight; C-Peptide; Cistanche; Diabetes Mellitus, Experimental; Diet; Eating; Glycated Hemoglobin; Glycogen; Glycosides; Hypoglycemic Agents; Hypolipidemic Agents; Inflammation; Insulin; Male; Oxidative Stress; Pancreas; Phosphotransferases; Plant Extracts; Rats, Sprague-Dawley; Streptozocin | 2021 |
Loss of C2orf69 defines a fatal autoinflammatory syndrome in humans and zebrafish that evokes a glycogen-storage-associated mitochondriopathy.
Human C2orf69 is an evolutionarily conserved gene whose function is unknown. Here, we report eight unrelated families from which 20 children presented with a fatal syndrome consisting of severe autoinflammation and progredient leukoencephalopathy with recurrent seizures; 12 of these subjects, whose DNA was available, segregated homozygous loss-of-function C2orf69 variants. C2ORF69 bears homology to esterase enzymes, and orthologs can be found in most eukaryotic genomes, including that of unicellular phytoplankton. We found that endogenous C2ORF69 (1) is loosely bound to mitochondria, (2) affects mitochondrial membrane potential and oxidative respiration in cultured neurons, and (3) controls the levels of the glycogen branching enzyme 1 (GBE1) consistent with a glycogen-storage-associated mitochondriopathy. We show that CRISPR-Cas9-mediated inactivation of zebrafish C2orf69 results in lethality by 8 months of age due to spontaneous epileptic seizures, which is preceded by persistent brain inflammation. Collectively, our results delineate an autoinflammatory Mendelian disorder of C2orf69 deficiency that disrupts the development/homeostasis of the immune and central nervous systems. Topics: Animals; Biological Evolution; Cell Line; CRISPR-Cas Systems; Encephalitis; Female; Genes, Recessive; Glycogen; Humans; Inflammation; Male; Membrane Proteins; Mitochondrial Diseases; Pedigree; Seizures; Zebrafish | 2021 |
Aloe vera carbohydrates regulate glucose metabolism through improved glycogen synthesis and downregulation of hepatic gluconeogenesis in diabetic rats.
Aloe vera (L.) Burm.f. is an ancient medicinal plant that belongs to the family Asphodelaceae. It has a rich source of bioactive constituents such as carbohydrates, polyphenols, peptides, sterols and tannins, etc. Aloe vera has multiple biological activities such as anti-inflammatory, antioxidant and antidiabetic activity etc. AIM OF THE STUDY: The present study investigated the antidiabetic mechanism of Aloe vera carbohydrate fraction (AVCF) and aimed to provide insights into the regulation of carbohydrate metabolism enzymes in glucose homeostasis.. The antidiabetic effect of AVCF was evaluated using α-amylase, α-glucosidase inhibition, glucose diffusion and glucose uptake assay. The in vitro AVCF effect on insulin secretion, cell proliferation and inflammatory markers were determined using streptozotocin-induced oxidative stress on RIN-m5F cells. Streptozotocin-induced male Wistar diabetic rats were treated for 21 days with AVCF (54 mg/kg bw). The in vivo AVCF effect was measured on fasting plasma glucose, insulin, glucagon, hexokinase, glycogen synthase and glucose-6-phosphatase, levels in diabetic rats. Histopathological studies for organ-specific effects in the pancreas, liver and small intestine were also conducted.. AVCF-treated RIN-m5F cells significantly increased BrdU levels, with insulin secretion, and decreased TNF-α, IL-6 and nitric oxide levels. AVCF treated streptozotocin-induced diabetic rats showed significantly decreased fasting plasma glucose, glucagon and glucose-6-phosphatase levels with a concomitant increase in insulin, hexokinase, and glycogen synthase levels and, glycogen content. These findings corroborate with the improved hepatic glycogen content in the PAS stained histological section of the liver of AVCF treated diabetic rats.. These results suggest that CF of Aloe vera improved glucose metabolism by activation of glycogenesis and down-regulation of gluconeogenesis thereby, maintaining glucose homeostasis. Hence, AVCF can be used as an alternative medicine in the alleviation of diabetes mellitus symptoms. Topics: Aloe; Animals; Biomarkers; Carbohydrates; Cell Line; Cell Survival; Cytokines; Diabetes Mellitus, Experimental; Down-Regulation; Gene Expression Regulation; Gluconeogenesis; Glucose; Glycogen; Inflammation; Insulin; Islets of Langerhans; Liver; Male; Nitric Oxide; Random Allocation; Rats; Rats, Wistar | 2021 |
Systemic AAV8-mediated delivery of a functional copy of muscle glycogen phosphorylase (Pygm) ameliorates disease in a murine model of McArdle disease.
McArdle disease is a disorder of carbohydrate metabolism that causes painful skeletal muscle cramps and skeletal muscle damage leading to transient myoglobinuria and increased risk of kidney failure. McArdle disease is caused by recessive mutations in the muscle glycogen phosphorylase (PYGM) gene leading to absence of PYGM enzyme in skeletal muscle and preventing access to energy from muscle glycogen stores. There is currently no cure for McArdle disease. Using a preclinical animal model, we aimed to identify a clinically translatable and relevant therapy for McArdle disease. We evaluated the safety and efficacy of recombinant adeno-associated virus serotype 8 (rAAV8) to treat a murine model of McArdle disease via delivery of a functional copy of the disease-causing gene, Pygm. Intraperitoneal injection of rAAV8-Pygm at post-natal day 1-3 resulted in Pygm expression at 8 weeks of age, accompanied by improved skeletal muscle architecture, reduced accumulation of glycogen and restoration of voluntary running wheel activity to wild-type levels. We did not observe any adverse reaction to the treatment at 8 weeks post-injection. Thus, we have investigated a highly promising gene therapy for McArdle disease with a clear path to the ovine large animal model endemic to Western Australia and subsequently to patients. Topics: Animals; Disease Models, Animal; Female; Glycogen; Glycogen Phosphorylase, Muscle Form; Glycogen Storage Disease Type V; Inflammation; Male; Mice; Mice, Inbred C57BL; Muscle, Skeletal | 2020 |
Supplementation of a propionate-producing consortium improves markers of insulin resistance in an in vitro model of gut-liver axis.
Gut-liver cross talk is an important determinant of human health with profound effects on energy homeostasis. While gut microbes produce a huge range of metabolites, specific compounds such as short-chain fatty acids (SCFAs) can enter the portal circulation and reach the liver (Brandl K, Schnabl B. Topics: Biomarkers; Cytokines; Gastrointestinal Microbiome; Gastrointestinal Tract; Glycogen; Hep G2 Cells; Hepatocytes; Humans; Inflammation; Insulin Resistance; Liver; Propionates | 2020 |
Skeletal muscle dysregulation in rheumatoid arthritis: Metabolic and molecular markers in a rodent model and patients.
Rheumatoid arthritis (RA) is accompanied by pain, inflammation and muscle weakness. Skeletal muscle inflammation and inactivity are independently associated with muscle insulin resistance and atrophy. Our objective was to identify early molecular and biochemical markers in muscle from a rodent model of RA relative to control and subsequently identify commonality in muscle gene expression between this model and muscle from RA patients. Pain behaviour and locomotor activity were measured in a collagen-induced arthritis (CIA) model of RA (n = 9) and control (n = 9) rats. Energy substrates and metabolites, total alkaline-soluble protein:DNA ratio and mRNA abundance of 46 targeted genes were also determined in Extensor digitorum longus muscle. Expression of targeted mRNAs was quantified in Vastus Lateralis muscle from RA patients (n = 7) and healthy age-matched control volunteers (n = 6). CIA rats exhibited pain behaviour (p<0.01) and reduced activity (p<0.05) compared to controls. Muscle glycogen content was less (p<0.05) and muscle lactate content greater (p<0.01) in CIA rats. The bioinformatics analysis of muscle mRNA abundance differences from the control, predicted the activation of muscle protein metabolism and inhibition of muscle carbohydrate and fatty acid metabolism in CIA rats. Compared to age-matched control volunteers, RA patients exhibited altered muscle mRNA expression of 8 of the transcripts included as targets in the CIA model of RA. In conclusion, muscle energy metabolism and metabolic gene expression were altered in the CIA model, which was partly corroborated by targeted muscle mRNA measurements in RA patients. This research highlights the negative impact of RA on skeletal muscle metabolic homeostasis. Topics: Aged; Animals; Arthritis, Experimental; Arthritis, Rheumatoid; Biomarkers; Disease Models, Animal; Female; Glycogen; Humans; Inflammation; Locomotion; Middle Aged; Muscle, Skeletal; Muscular Diseases; Myalgia; Rats; Rats, Inbred Lew; RNA, Messenger; Transcriptome | 2020 |
Sea cucumbers-derived sterol sulfate alleviates insulin resistance and inflammation in high-fat-high-fructose diet-induced obese mice.
Sea cucumbers are widely consumed in traditional medicine and food. Sea cucumbers-derived sulfated sterol exhibits a sulfate group at C-3 position, which is different from phytosterol with a hydroxyl group. However, the effect of sterol sulfate on metabolic syndrome remains unknown. The purpose of the present study is to investigate the alleviation of sterol sulfate on high-fat-high-fructose diet (HFFD)-induced insulin resistance and inflammation. After 2 weeks feeding with HFFD, male C57BL/6J mice were continuously fed with HFFD plus 0.4 % (w/w) sterol sulfate or phytosterol for 6 weeks. The OGTT was carried out at 7 weeks. At the end of the experimental period, the changes of glycogen, circulating glucose, insulin, pro-inflammatory cytokine and adiponectin were measured. H&E staining was used to observe the morphological changes in adipose tissue. Furthermore, the underlying molecular mechanisms were investigated. Dietary sterol sulfate was superior to phytosterol in reducing body weight gain, adipocyte hypertrophy, and levels of circulating glucose and insulin, as well as increasing the glycogen content of tissues. Furthermore, sterol sulfate ameliorated insulin resistance mainly due to the inhibition of gluconeogenesis, the promotion of glycogen synthesis and GLUT4 translocation by activating PI3K/Akt signaling pathway. Additionally, sterol sulfate effectively attenuated inflammation by increasing serum adiponectin and reducing pro-inflammatory cytokine release. Sterol sulfate exhibited a more significant effect than phytosterol in alleviating HFFD -induced insulin resistance and inflammation, which might be closely related to the sulfate group. The results might provide insights into the prevention and alleviation of metabolic syndrome. Topics: Adiponectin; Adipose Tissue; Animals; Anti-Inflammatory Agents; Blood Glucose; Cytokines; Diet, High-Fat; Fructose; Glucose Tolerance Test; Glycogen; Inflammation; Insulin Resistance; Male; Mice; Mice, Inbred C57BL; Obesity; Sea Cucumbers; Signal Transduction; Sterols | 2020 |
Absence of HIF1A Leads to Glycogen Accumulation and an Inflammatory Response That Enables Pancreatic Tumor Growth.
Cancer cells respond to hypoxia by upregulating the hypoxia-inducible factor 1α (HIF1A) transcription factor, which drives survival mechanisms that include metabolic adaptation and induction of angiogenesis by VEGF. Pancreatic tumors are poorly vascularized and severely hypoxic. To study the angiogenic role of HIF1A, and specifically probe whether tumors are able to use alternative pathways in its absence, we created a xenograft mouse tumor model of pancreatic cancer lacking HIF1A. After an initial delay of about 30 days, the HIF1A-deficient tumors grew as rapidly as the wild-type tumors and had similar vascularization. These changes were maintained in subsequent passages of tumor xenografts Topics: Animals; Cell Line, Tumor; Cell Proliferation; Glycogen; Hypoxia; Hypoxia-Inducible Factor 1, alpha Subunit; Inflammation; Mice; Mice, Inbred NOD; Mice, SCID; Neovascularization, Pathologic; Pancreas; Pancreatic Neoplasms; Signal Transduction | 2019 |
Hepatic functional and pathological changes of type 1 diabetic mice in growing and maturation time.
To detect the changes in the liver function in both male and female OVE26 mice from young to adults for better understanding of type 1 diabetes-induced hepatic changes, OVE26 mice and wild-type FVB mice were raised in the same environment without any intervention, and then killed at 4, 12, 24 and 36 weeks for examining liver's general properties, including pathogenic and molecular changes. The influence of diabetes on the bodyweight of male and female mice was different. Both male and female OVE26 mice did not obtain serious liver injury or non-alcoholic fatty liver disease, manifested by mild elevation of plasma alanine transaminase, and less liver lipid content along with significantly suppressed lipid synthesis. Uncontrolled diabetes also did not cause hepatic glycogen accumulation in OVE26 mice after 4 weeks. Oxidative stress test showed no change in lipid peroxidation, but increased protein oxidation. Changed endoplasmic reticulum stress and apoptosis along with increased antioxidant capacity was observed in OVE26 mice. In conclusion, uncontrolled type 1 diabetes did not cause hepatic lipid deposition most likely because of reduced lipids synthesis in response to insulin deficiency. Enhanced antioxidant capacity might not only prevent the occurrence of severe acute liver injury but also the self-renewal, leading to liver dysfunction. Topics: Animals; Antioxidants; Autophagy; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; Endoplasmic Reticulum Stress; Glycogen; Inflammation; Insulin; Lipids; Liver; Mice; Oxidative Stress | 2019 |
Akkermansia muciniphila can reduce the damage of gluco/lipotoxicity, oxidative stress and inflammation, and normalize intestine microbiota in streptozotocin-induced diabetic rats.
This study aimed to investigate how Akkermansia muciniphila can implicate type 2 diabetes mellitus and the mechanisms underlying the effects A. muciniphila on type 2 diabetes mellitus. Normal and streptozotocin-induced diabetic Sprague-Dawley rats were orally administered with A. muciniphila and solvent. After 4 weeks of treatment, diabetic rats orally administered with live or pasteurized A. muciniphila exhibited significant increase in the blood concentration of high-density lipoprotein, and decrease in the hepatic glycogen, serum plasminogen activator inhibitor-1, tumor necrosis factor-α, lipopolysaccharide, malondialdehyde and total glucagon-like peptide-1. Moreover, diabetic rats orally administered with A. muciniphila showed significantly increased species alpha diversity and gene function in gut microbes. These results indicated that A. muciniphila can improve liver function, reduce gluco/lipotoxicity, alleviate oxidative stress, suppress inflammation and normalize intestine microbiota of the host animal, thereby ameliorating type 2 diabetes mellitus. Akkermansia muciniphila might be considered as one of the ideal new probiotics used in the management of type 2 diabetes mellitus in future. Topics: Animals; Cholesterol, HDL; Diabetes Mellitus, Experimental; Feces; Gastrointestinal Microbiome; Gene Expression Regulation; Glucagon-Like Peptide 1; Glycogen; Hypoglycemic Agents; Inflammation; Intestinal Mucosa; Intestines; Lipopolysaccharides; Liver; Male; Malondialdehyde; Oxidative Stress; Plasminogen Activator Inhibitor 1; Probiotics; Rats; Rats, Sprague-Dawley; Streptozocin; Tumor Necrosis Factor-alpha; Verrucomicrobia | 2018 |
Pivotal roles of Kupffer cells in the progression and regression of DDC-induced chronic cholangiopathy.
Kupffer cells (KCs) are key players in maintaining tissue homeostasis and are involved in various liver diseases. However, the roles of KCs in the pathogenesis of cholangiopathy are largely unknown. We aimed to investigate the precise roles of KCs in both the progression and regression phases of the 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-induced cholangiopathy model. In the early phase of DDC-induced cholangiopathy, the number of KCs significantly increased over time. Moreover, KCs were associated with abnormal phenotypic changes in other liver cells, such as hepatocytes, biliary epithelial cells, liver sinusoidal endothelial cells, and hepatic stellate cells. In contrast, KC depletion by clodronate administration suppressed the progression of the disease, and maintained the phenotypes of other cells. In the regression phase, the numbers of KCs significantly decreased, and the cells redifferentiated to their quiescent state. In contrast, KC depletion delayed the recovery of cells by maintaining other liver cells in an active state. These findings suggest that KCs play detrimental roles in the progression phase; however, they are beneficial in the regression phase by mediating interactions between other liver cells. Our data provide new insights into the roles of KCs in the pathogenesis of cholangiopathy. Topics: Animals; Bile Duct Diseases; Disease Models, Animal; Disease Progression; Glycogen; Humans; Inflammation; Kupffer Cells; Liver; Mice; Phenotype; Pyridines; Splenomegaly | 2018 |
Adrenal hormones mediate disease tolerance in malaria.
Malaria reduces host fitness and survival by pathogen-mediated damage and inflammation. Disease tolerance mechanisms counter these negative effects without decreasing pathogen load. Here, we demonstrate that in four different mouse models of malaria, adrenal hormones confer disease tolerance and protect against early death, independently of parasitemia. Surprisingly, adrenalectomy differentially affects malaria-induced inflammation by increasing circulating cytokines and inflammation in the brain but not in the liver or lung. Furthermore, without affecting the transcription of hepatic gluconeogenic enzymes, adrenalectomy causes exhaustion of hepatic glycogen and insulin-independent lethal hypoglycemia upon infection. This hypoglycemia is not prevented by glucose administration or TNF-α neutralization. In contrast, treatment with a synthetic glucocorticoid (dexamethasone) prevents the hypoglycemia, lowers cerebral cytokine expression and increases survival rates. Overall, we conclude that in malaria, adrenal hormones do not protect against lung and liver inflammation. Instead, they prevent excessive systemic and brain inflammation and severe hypoglycemia, thereby contributing to tolerance. Topics: Adrenal Glands; Adrenalectomy; Animals; Blood Glucose; Brain; Corticosterone; Cytokines; Dexamethasone; Disease Models, Animal; Epinephrine; Glucocorticoids; Glycogen; Hormones; Hydrocortisone; Hypoglycemia; Inflammation; Liver; Lung; Malaria; Mice; Mineralocorticoids; Norepinephrine; Plasmodium berghei; Plasmodium chabaudi; Survival Rate | 2018 |
2-Arachidonoylglycerol ameliorates inflammatory stress-induced insulin resistance in cardiomyocytes.
Topics: AMP-Activated Protein Kinases; Animals; Anti-Inflammatory Agents; Arachidonic Acids; Calcium-Calmodulin-Dependent Protein Kinase Kinase; Cell Differentiation; Diabetes Mellitus, Experimental; Embryonic Stem Cells; Endocannabinoids; Glucose; Glucose Transporter Type 4; Glycerides; Glycogen; Humans; Inflammation; Insulin Resistance; Male; Mice; Mice, Inbred C57BL; Myocytes, Cardiac; Rats; Rats, Inbred Lew; Receptor, Cannabinoid, CB1; RNA, Messenger; Signal Transduction; Tumor Necrosis Factor-alpha | 2017 |
Prolyl hydroxylase 2 inactivation enhances glycogen storage and promotes excessive neutrophilic responses.
Fully activated innate immune cells are required for effective responses to infection, but their prompt deactivation and removal are essential for limiting tissue damage. Here, we have identified a critical role for the prolyl hydroxylase enzyme Phd2 in maintaining the balance between appropriate, predominantly neutrophil-mediated pathogen clearance and resolution of the innate immune response. We demonstrate that myeloid-specific loss of Phd2 resulted in an exaggerated inflammatory response to Streptococcus pneumonia, with increases in neutrophil motility, functional capacity, and survival. These enhanced neutrophil responses were dependent upon increases in glycolytic flux and glycogen stores. Systemic administration of a HIF-prolyl hydroxylase inhibitor replicated the Phd2-deficient phenotype of delayed inflammation resolution. Together, these data identify Phd2 as the dominant HIF-hydroxylase in neutrophils under normoxic conditions and link intrinsic regulation of glycolysis and glycogen stores to the resolution of neutrophil-mediated inflammatory responses. These results demonstrate the therapeutic potential of targeting metabolic pathways in the treatment of inflammatory disease. Topics: Acute Disease; Animals; Bronchoalveolar Lavage; Colitis; Glycogen; Glycolysis; Humans; Hypoxia-Inducible Factor-Proline Dioxygenases; Immunity, Innate; Inflammation; Leukocytes; Lung Injury; Mice; Mice, Inbred C57BL; Neutrophils; Phenotype; Pneumococcal Infections; Signal Transduction | 2017 |
Interactive effects of chronic stress and a high-sucrose diet on nonalcoholic fatty liver in young adult male rats.
Glucocorticoids have been implicated in nonalcoholic fatty liver diseases (NAFLD). The influence of a palatable diet on the response to stress is controversial. This study explored whether a high-sucrose diet could protect from hepatic steatosis induced by chronic restraint stress in young adult rats. Male Wistar rats aged 21 days were allocated into four groups (n = 6-8 per group): control, chronic restraint stress, 30% sucrose diet, and 30% sucrose diet plus chronic restraint stress. After being exposed to either tap water or sucrose solution during eight weeks, half of the rats belonging to each group were subject or not to repeated restraint stress (1 h per day, 5 days per week) during four weeks. Triacylglycerol (TAG), oxidative stress, activity of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD-1), infiltration of immune cells, and glycogen amount in the liver were quantified. Serum concentrations of corticosterone and testosterone were also measured. The stressed group showed normal serum concentrations of corticosterone and did not have hepatic steatosis. However, this group showed increased glycogen, inflammation, mild fibrosis, oxidative stress, and a high activity of 11β-HSD-1 in the liver. The group exposed to the high-sucrose diet had lower concentrations of corticosterone, hepatic steatosis and moderate fibrosis. The group subject to high-sucrose diet plus chronic restraint stress showed low concentrations of corticosterone, hepatic steatosis, oxidative stress, and high concentrations of testosterone. Thus, restraint stress and a high-sucrose diet each generate different components of nonalcoholic fatty liver in young adult rats. The combination of both the factors could promote a faster development of NAFLD. Topics: 11-beta-Hydroxysteroid Dehydrogenase Type 1; Animals; Chronic Disease; Corticosterone; Diet; Dietary Sucrose; Glycogen; Inflammation; Liver; Liver Cirrhosis; Male; Non-alcoholic Fatty Liver Disease; Oxidative Stress; Rats; Rats, Wistar; Restraint, Physical; Stress, Psychological; Sweetening Agents; Testosterone; Triglycerides | 2017 |
Cartilage rings contribute to the proper embryonic tracheal epithelial differentiation, metabolism, and expression of inflammatory genes.
The signaling cross talk between the tracheal mesenchyme and epithelium has not been researched extensively, leaving a substantial gap of knowledge in the mechanisms dictating embryonic development of the proximal airways by the adjacent mesenchyme. Recently, we reported that embryos lacking mesenchymal expression of Sox9 did not develop tracheal cartilage rings and showed aberrant differentiation of the tracheal epithelium. Here, we propose that tracheal cartilage provides local inductive signals responsible for the proper differentiation, metabolism, and inflammatory status regulation of the tracheal epithelium. The tracheal epithelium of mesenchyme-specific Sox9 Topics: Animals; Biomarkers; Cartilage; Cell Differentiation; Cell Shape; Chondrocytes; Culture Media, Conditioned; Embryo, Mammalian; Epithelial Cells; Epithelium; Female; Gene Expression Profiling; Gene Expression Regulation, Developmental; Glycogen; Inflammation; Interferon-gamma; Male; Mesoderm; Mice, Knockout; Models, Biological; Mutation; Oxidation-Reduction; Signal Transduction; SOX9 Transcription Factor; Trachea; Transforming Growth Factor beta; Tumor Necrosis Factor-alpha | 2017 |
Associations between the degree of early lactation inflammation and performance, metabolism, and immune function in dairy cows.
The objective of the current study was to determine associations between the severity of systemic inflammation during the early postpartum period and performance, energy metabolism, and immune function in dairy cows. Cows were assigned to categorical quartiles (Q; Q1=0.18-0.59, Q2=0.60-1.14, Q3=1.15-2.05, and Q4=2.06-2.50 g of haptoglobin/L) based on the highest plasma haptoglobin (Hp) concentration measured during wk 1 postpartum. Although cows were assigned to different categories of inflammation during the postpartum period, we detected a quadratic relationship of inflammation on prepartum dry matter intake (DMI) and body weight (BW) such that cows in Q2 had lower prepartum DMI and cows in Q2 and Q3 had lower prepartum BW compared with cows in the other quartiles. We also detected a quadratic association of inflammation with postpartum DMI and BW such that cows in Q2 and Q3 also had generally lower postpartum DMI and BW compared with cows in Q1. There was a tendency for a Q × time interaction for milk yield and Q × time interactions for 3.5% fat-corrected milk and energy-corrected milk yields; quadratic relationships suggested decreased milk yield for Q2 and Q3 cows. We also found Q × parity and Q × time interactions for plasma glucose and insulin concentrations, suggesting alterations with differing degrees of inflammation. There was also a Q × time interaction for plasma nonesterified fatty acids concentration. In addition, alterations in liver triglyceride and glycogen contents for cows with inflammation as well as alterations in [1-(14)C]propionate oxidation in vitro were observed. Although we observed limited effects of inflammation on neutrophil and monocyte phagocytosis at d 7 postpartum, inflammation appeared to alter neutrophil and monocyte oxidative burst. Overall, cows with any degree of elevated haptoglobin in the first week after calving had alterations in both pre- and postpartum intake and postpartum metabolism. Topics: 3-Hydroxybutyric Acid; Animals; Blood Glucose; Body Weight; Cattle; Cattle Diseases; Energy Metabolism; Fatty Acids, Nonesterified; Female; Glycogen; Haptoglobins; Inflammation; Insulin; Lactation; Liver; Monocytes; Neutrophils; Phagocytosis; Postpartum Period; Triglycerides | 2016 |
Altered glycogen metabolism causes hepatomegaly following an Atg7 deletion.
Autophagy is a lysosomal degradation process involved in the turnover of organelles or other cell constituents, in providing sources for energy production under starving conditions and in cell metabolism. A key protein in the macroautophagic machinery is the autophagy-related protein (Atg) 7. Constitutive deletion of Atg7 is lethal at birth. A conditional deletion of Atg7 in hepatocytes leads to hepatomegaly and in aged animals to liver tumors. With this study, we aim at analyzing the hepatomegaly development in more detail. The 3- to 4-fold enlargement of the liver takes place between days 25 and 35 after birth (P25-P35) and persists at least until P90. This is accompanied by a change in the expression of enzymes involved in the glycogen/glucose metabolism. While glycogen synthesis is inhibited, glucose is preferentially kept as glucose-6-phosphate inside the cells, inducing a swelling of the cells caused by hyperosmolarity. An increase of lipogenic enzymes suggests that glucose-6-phosphate is delivered to lipogenic pathways, which is supported by the occurrence of a steatosis around P30. The development of hepatomegaly is accompanied by a polyploidisation of hepatocytes, an enhanced expression of genes related to inflammatory processes and an infiltration of macrophages and granulocytes. Our data provide evidence that the attenuation of macroautophagy in hepatocytes leads to a glucose retention that causes cell swelling. The resulting hepatomegaly, which develops in a time interval of about 10 days, perturbs liver perfusion and induces an inflammatory reaction together with polyploidisation. Topics: Animals; Autophagy-Related Protein 7; Cell Death; Cell Proliferation; Dietary Carbohydrates; Female; Gene Deletion; Gene Expression Regulation; Glucose; Glycogen; Hepatomegaly; Inflammation; Liver; Male; Mice, Inbred C57BL; Mice, Knockout; Organ Specificity; Polyploidy | 2016 |
Transcriptome assessment of the Pompe (Gaa-/-) mouse spinal cord indicates widespread neuropathology.
Pompe disease, caused by deficiency of acid alpha-glucosidase (GAA), leads to widespread glycogen accumulation and profound neuromuscular impairments. There has been controversy, however, regarding the role of central nervous system pathology in Pompe motor dysfunction. We hypothesized that absence of GAA protein causes progressive activation of neuropathological signaling, including pathways associated with cell death. To test this hypothesis, genomic data (Affymetrix Mouse Gene Array 2.0ST) from the midcervical spinal cord in 6 and 16 mo old Pompe (Gaa Topics: alpha-Glucosidases; Animals; Cell Death; Cervical Vertebrae; Gene Expression Profiling; Glycogen; Glycogen Storage Disease Type II; Inflammation; Mice; Nerve Degeneration; Neurons; RNA, Messenger; Signal Transduction; Spinal Cord; Transcriptome | 2016 |
Exercise-induced AMPK and pyruvate dehydrogenase regulation is maintained during short-term low-grade inflammation.
The aim of the present study was to examine the effect of lipopolysaccharide (LPS)-induced inflammation on AMP-activated protein kinase (AMPK) and pyruvate dehydrogenase (PDH) regulation in human skeletal muscle at rest and during exercise. Nine young healthy physically inactive male subjects completed two trials. In an LPS trial, the subjects received a single LPS injection (0.3 ng/kg body weight) and blood samples and vastus lateralis muscle biopsies were obtained before and 2 h after the LPS injection and immediately after a 10-min one-legged knee extensor exercise bout performed approximately 2½ h after the LPS injection. The exercise bout with muscle samples obtained before and immediately after was repeated in a control trial without LPS injection. The plasma tumor necrosis factor α concentration increased 17-fold 2 h after LPS relative to before. Muscle lactate and muscle glycogen were unchanged from before to 2 h after LPS and exercise increased muscle lactate and decreased muscle glycogen in the control (P < 0.05) and the LPS (0.05 ≤ P < 0.1) trial with no differences between the trials. AMPK, acetyl-CoA carboxylase (ACC) and PDH phosphorylation as well as PDHa activity were unaffected 2 h after LPS relative to before. Exercise decreased (P < 0.05) PDH and increased (P < 0.05) AMPK and ACC phosphorylation as well as increased (P < 0.05) PDHa activity similarly in the LPS and control trial. In conclusion, LPS-induced inflammation does not affect resting or exercise-induced AMPK and PDH regulation in human skeletal muscle. This suggests that metabolic flexibility during exercise is maintained during short-term low-grade inflammation in humans. Topics: Acetyl-CoA Carboxylase; Adult; AMP-Activated Protein Kinases; Exercise; Glycogen; Humans; Inflammation; Lactic Acid; Lipopolysaccharides; Male; Muscle, Skeletal; Phosphorylation; Pyruvate Dehydrogenase Complex; Tumor Necrosis Factor-alpha | 2015 |
JNK and IKKβ phosphorylation is reduced by glucocorticoids in adipose tissue from insulin-resistant rats.
Peripheral insulin resistance (IR) is one of the main side effects caused by glucocorticoid (GC)-based therapies, and the molecular mechanisms of GC-induced IR are not yet fully elucidated. Thus, we aimed to investigate the effects of dexamethasone treatment on the main components of insulin and inflammatory signaling in the adipose tissue of rats.. Male Wistar rats received daily injections of dexamethasone (1mg/kg body weight (b.w.), intraperitoneally (i.p.)) for 5 days (DEX), whereas control rats received saline (CTL). The metabolic status was investigated, and the epididymal fat fragments were collected for lipolysis and western blot analyses.. The DEX rats became hyperglycemic, hyperinsulinemic, insulin resistant and glucose intolerant, compared with the CTL rats (P<0.05). The basal glycerol release in the fat fragments was 1.5-fold higher in the DEX rats (P<0.05). The phosphorylation of protein kinase B (PKB) at ser(473) decreased by 44%, whereas, the phosphorylation of insulin receptor substrate (IRS)-1 at ser(307) increased by 93% in the adipose tissue of the DEX rats after an oral bolus of glucose (P<0.05). The basal phosphorylation of c-jun-N-terminal kinase (JNK) and inhibitor of nuclear factor kappa-B (IKKβ) proteins was reduced by 46% and 58%, respectively, in the adipose tissue of the DEX rats (P<0.05). This was paralleled with a significant reduction (47%) in the glucocorticoid receptor (GR) protein content in the adipose tissue of the DEX rats (P<0.05).. The insulin-resistant status of rats induced by dexamethasone administration have PKB and IRS-1 activity attenuated in epididymal fat without increases in the phosphorylation of the proinflammatory signals JNK and IKKβ. Topics: Adipose Tissue; Animals; Body Weight; Cytokines; Dexamethasone; Epididymis; Glucocorticoids; Glycogen; I-kappa B Kinase; Inflammation; Insulin; Insulin Receptor Substrate Proteins; Insulin Resistance; Male; MAP Kinase Kinase 4; Phosphorylation; Proto-Oncogene Proteins c-akt; Pyruvic Acid; Rats; Rats, Wistar; Signal Transduction; Toll-Like Receptor 4 | 2015 |
Transcriptional profiling of human epithelial cells infected with plasmid-bearing and plasmid-deficient Chlamydia trachomatis.
Chlamydia trachomatis is an obligate intracellular epitheliotropic bacterial pathogen of humans. Infection of the eye can result in trachoma, the leading cause of preventable blindness in the world. The pathophysiology of blinding trachoma is driven by multiple episodes of reinfection of conjunctival epithelial cells, producing an intense chronic inflammatory response resulting in submucosal tissue remodeling and scarring. Recent reports have shown that infection with trachoma organisms lacking the cryptic chlamydial plasmid is highly attenuated in macaque eyes, a relevant experimental model of human trachoma infection. To better understand the molecular basis of plasmid-mediated infection attenuation and the potential modulation of host immunity, we conducted transcriptional profiling of human epithelial cells infected with C. trachomatis plasmid-bearing (A2497) and plasmid-deficient (A2497P(-)) organisms. Infection of human epithelial cells with either strain increased the expression of host genes coding for proinflammatory (granulocyte-macrophage colony-stimulating factor [GM-CSF], macrophage colony-stimulating factor [MCSF], interleukin-6 [IL-6], IL-8, IL-1α, CXCL1, CXCL2, CXCL3, intercellular adhesion molecule 1 [ICAM1]), chemoattraction (CCL20, CCL5, CXCL10), immune suppression (PD-L1, NFKB1B, TNFAIP3, CGB), apoptosis (CASP9, FAS, IL-24), and cell growth and fibrosis (EGR1 and IL-20) proteins. Statistically significant increases in the levels of expression of many of these genes were found in A2497-infected cells compared to the levels of expression in A2497P(-)-infected cells. Our findings suggest that the chlamydial plasmid plays a focal role in the host cell inflammatory response to infection and immune avoidance. These results provide new insights into the role of the chlamydial plasmid as a chlamydial virulence factor and its contributions to trachoma pathogenesis. Topics: Bacterial Proteins; CD8-Positive T-Lymphocytes; Cell Line, Tumor; Chlamydia Infections; Chlamydia trachomatis; Cytokines; Epithelial Cells; Gene Expression Profiling; Glycogen; HeLa Cells; Humans; Inflammation; Interleukins; Plasmids; Trachoma; Virulence Factors | 2015 |
Cell lysis-free quantum dot multicolor cellular imaging-based mechanism study for TNF-α-induced insulin resistance.
TNF-α is an inflammatory cytokine that plays an important role in insulin resistance observed in obesity and chronic inflammation. Many cellular components involved in insulin signaling cascade are known to be inhibited by TNF-α. Insulin receptor substrate (IRS)-1 is one of the major targets in TNF-α-induced insulin resistance. The serine phosphorylation of IRS-1 enables the inhibition of insulin signaling. Until now, many studies have been conducted to investigate the mechanism of TNF-α-induced insulin resistance based on Western blot. Intracellular protein kinase crosstalk is commonly encountered in inflammation-associated insulin resistance. The crosstalk among the signaling molecules obscures the precise role of kinases in insulin resistance. We have developed a cell lysis-free quantum dots (QDots) multicolor cellular imaging to identify the biochemical role of multiple kinases (p38, JNK, IKKβ, IRS1ser, IRS1tyr, GSK3β, and FOXO1) in inflammation-associated insulin resistance pathway with a single assay in one run. QDot-antibody conjugates were used as nanoprobes to simultaneously monitor the activation/deactivation of the above seven intracellular kinases in HepG2 cells. The effect of the test compounds on the suppression of TNF-α-induced insulin resistance was validated through kinase monitoring. Aspirin, indomethacin, cinnamic acid, and amygdalin were tested.. Through the measurement of the glycogen level in HepG2 cell treated with TNF-α, it was found that aspirin and indomethacin increased glycogen levels by almost two-fold compared to amygdalin and cinnamic acid. The glucose production assay proved that cinnamic acid was much more efficient in suppressing glucose production, compared with MAP kinase inhibitors and non-steroidal anti-inflammatory drugs. QDot multicolor cellular imaging demonstrated that amygdalin and cinnamic acid selectively acted via the JNK1-dependent pathway to suppress the inflammation-induced insulin resistance and improve insulin sensitivity.. The regulatory function of multiple kinases could be monitored concurrently at the cellular level. The developed cellular imaging assay provides a unique platform for the understanding of inflammation and insulin resistance signaling pathways in type II diabetes mellitus and how they regulate each other. The results showed that amygdalin and cinnamic acid inhibit serine phosphorylation of IRS-1 through targeting JNK serine kinase and enhance insulin sensitivity. Topics: Anti-Inflammatory Agents, Non-Steroidal; Antibodies; Aspirin; Cinnamates; Forkhead Box Protein O1; Forkhead Transcription Factors; Glucose; Glycogen; Hep G2 Cells; Humans; Indomethacin; Inflammation; Insulin Receptor Substrate Proteins; Insulin Resistance; Molecular Imaging; Molecular Targeted Therapy; Protein Kinases; Quantum Dots; Reproducibility of Results; Serine; Tumor Necrosis Factor-alpha | 2015 |
TWIST1 and TWIST2 regulate glycogen storage and inflammatory genes in skeletal muscle.
TWIST proteins are important for development of embryonic skeletal muscle and play a role in the metabolism of tumor and white adipose tissue. The impact of TWIST on metabolism in skeletal muscle is incompletely studied. Our aim was to assess the impact of TWIST1 and TWIST2 overexpression on glucose and lipid metabolism. In intact mouse muscle, overexpression of Twist reduced total glycogen content without altering glucose uptake. Expression of TWIST1 or TWIST2 reduced Pdk4 mRNA, while increasing mRNA levels of Il6, Tnfα, and Il1β. Phosphorylation of AKT was increased and protein abundance of acetyl CoA carboxylase (ACC) was decreased in skeletal muscle overexpressing TWIST1 or TWIST2. Glycogen synthesis and fatty acid oxidation remained stable in C2C12 cells overexpressing TWIST1 or TWIST2. Finally, skeletal muscle mRNA levels remain unaltered in ob/ob mice, type 2 diabetic patients, or in healthy subjects before and after 3 months of exercise training. Collectively, our results indicate that TWIST1 and TWIST2 are expressed in skeletal muscle. Overexpression of these proteins impacts proteins in metabolic pathways and mRNA level of cytokines. However, skeletal muscle levels of TWIST transcripts are unaltered in metabolic diseases. Topics: Animals; Case-Control Studies; Cells, Cultured; Diabetes Mellitus, Type 2; Female; Gene Expression Regulation; Glycogen; Humans; Inflammation; Male; Mice; Mice, Inbred C57BL; Mice, Obese; Mice, Transgenic; Middle Aged; Muscle, Skeletal; Nuclear Proteins; Repressor Proteins; Twist-Related Protein 1 | 2015 |
Liver inflammation and metabolic signaling in ApcMin/+ mice: the role of cachexia progression.
The ApcMin/+ mouse exhibits an intestinal tumor associated loss of muscle and fat that is accompanied by chronic inflammation, insulin resistance and hyperlipidemia. Since the liver governs systemic energy demands through regulation of glucose and lipid metabolism, it is likely that the liver is a pathological target of cachexia progression in the ApcMin/+ mouse. The purpose of this study was to determine if cancer and the progression of cachexia affected liver endoplasmic reticulum (ER)-stress, inflammation, metabolism, and protein synthesis signaling. The effect of cancer (without cachexia) was examined in wild-type and weight-stable ApcMin/+ mice. Cachexia progression was examined in weight-stable, pre-cachectic, and severely-cachectic ApcMin/+ mice. Livers were analyzed for morphology, glycogen content, ER-stress, inflammation, and metabolic changes. Cancer induced hepatic expression of ER-stress markers BiP (binding immunoglobulin protein), IRE-1α (endoplasmic reticulum to nucleus signaling 1), and inflammatory intermediate STAT-3 (signal transducer and activator of transcription 3). While gluconeogenic enzyme phosphoenolpyruvate carboxykinase (PEPCK) mRNA expression was suppressed by cancer, glycogen content or protein synthesis signaling remained unaffected. Cachexia progression depleted liver glycogen content and increased mRNA expression of glycolytic enzyme PFK (phosphofrucktokinase) and gluconeogenic enzyme PEPCK. Cachexia progression further increased pSTAT-3 but suppressed p-65 and JNK (c-Jun NH2-terminal kinase) activation. Interestingly, progression of cachexia suppressed upstream ER-stress markers BiP and IRE-1α, while inducing its downstream target CHOP (DNA-damage inducible transcript 3). Cachectic mice exhibited a dysregulation of protein synthesis signaling, with an induction of p-mTOR (mechanistic target of rapamycin), despite a suppression of Akt (thymoma viral proto-oncogene 1) and S6 (ribosomal protein S6) phosphorylation. Thus, cancer induced ER-stress markers in the liver, however cachexia progression further deteriorated liver ER-stress, disrupted protein synthesis regulation and caused a differential inflammatory response related to STAT-3 and NF-κB (Nuclear factor-κB) signaling. Topics: Animals; Cachexia; Endoplasmic Reticulum Stress; Genes, APC; Glycogen; Hyperlipidemias; Inflammation; Insulin Resistance; Lipid Metabolism; Liver; Mice; NF-kappa B; Protein Biosynthesis; Signal Transduction; STAT3 Transcription Factor | 2015 |
Exposure to common food additive carrageenan alone leads to fasting hyperglycemia and in combination with high fat diet exacerbates glucose intolerance and hyperlipidemia without effect on weight.
Major aims were to determine whether exposure to the commonly used food additive carrageenan could induce fasting hyperglycemia and could increase the effects of a high fat diet on glucose intolerance and dyslipidemia.. C57BL/6J mice were exposed to either carrageenan, high fat diet, or the combination of high fat diet and carrageenan, or untreated, for one year. Effects on fasting blood glucose, glucose tolerance, lipid parameters, weight, glycogen stores, and inflammation were compared.. Exposure to carrageenan led to glucose intolerance by six days and produced elevated fasting blood glucose by 23 weeks. Effects of carrageenan on glucose tolerance were more severe than from high fat alone. Carrageenan in combination with high fat produced earlier onset of fasting hyperglycemia and higher glucose levels in glucose tolerance tests and exacerbated dyslipidemia. In contrast to high fat, carrageenan did not lead to weight gain. In hyperinsulinemic, euglycemic clamp studies, the carrageenan-exposed mice had higher early glucose levels and lower glucose infusion rate and longer interval to achieve the steady-state.. Carrageenan in the Western diet may contribute to the development of diabetes and the effects of high fat consumption. Carrageenan may be useful as a nonobese model of diabetes in the mouse. Topics: Animals; Blood Glucose; Body Weight; Carrageenan; Diet; Diet, High-Fat; Disease Models, Animal; Dyslipidemias; Food Additives; Food Deprivation; Glucose; Glucose Tolerance Test; Glycated Hemoglobin; Glycogen; Hyperglycemia; Hyperlipidemias; Inflammation; Lipids; Male; Mice; Mice, Inbred C57BL; Risk Factors | 2015 |
A rare case of multiple clear cell acanthoma with a relatively rapid development of the lower legs.
Clear cell acanthoma, firstly described by Degos as "an epidermal tumor with a particular aspect", although quite a rare lesion, raised an important interest because it may be easily confused with other dermatologic lesions, in the absence of a histopathological examination. Its clinical aspect is of a solitary nodule, with a red-brown varying color, with a size of 3 mm to 2 mm, sometimes covered with a thin scall. We present a case of a multiple rare cell acanthoma (seven nodular formations), having a rapid development (about two months) diagnosed in a 71-year-old patient within the lower 1/3 of the right shin. Topics: Acanthoma; Aged; B-Lymphocytes; Dermis; Female; Glycogen; Humans; Immunohistochemistry; Inflammation; Keratinocytes; Keratins; Leg; Lymphocyte Count; Skin Neoplasms; T-Lymphocytes | 2014 |
Mesenchymal stem cells and Interleukin-6 attenuate liver fibrosis in mice.
Mesenchymal stem cell (MSC) transplantation has emerged as a promising therapy for liver fibrosis. Issues concerning poor MSC survival and engraftment in the fibrotic liver still persist and warrant development of a strategy to increase MSC potency for liver repair. The present study was designed to examine a synergistic role for Interleukin-6 (IL-6) and MSCs therapy in the recovery of carbon tetrachloride (CCl(4)) induced injured hepatocytes in vitro and in vivo.. Injury was induced through 3 mM and 5 mM CCl(4) treatment of cultured hepatocytes while fibrotic mouse model was established by injecting 0.5 ml/kg CCl(4) followed by treatment with IL-6 and MSCs. Effect of MSCs and IL-6 treatment on injured hepatocytes was determined by lactate dehydrogenase release, RT-PCR for (Bax, Bcl-xl, Caspase3, Cytokeratin 8, NFκB, TNF-α) and annexin V apoptotic detection. Analysis of MSC and IL-6 treatment on liver fibrosis was measured by histopathology, PAS, TUNEL and Sirius red staining, RT-PCR, and liver function tests for Bilirubin and Alkaline Phosphatase (ALP).. A significant reduction in LDH release and apoptosis was observed in hepatocytes treated with a combination of MSCs and IL-6 concomitant with upregulation of anti-apoptotic gene Bcl-xl expression and down regulation of bax, caspase3, NFκB and TNF-α. Adoptive transfer of MSCs in fibrotic liver pretreated with IL-6 resulted increased MSCs homing and reduced fibrosis and apoptosis. Hepatic functional assessment demonstrated reduced serum levels of Bilirubin and ALP.. Pretreatment of fibrotic liver with IL-6 improves hepatic microenvironment and primes it for MSC transplantation leading to enhanced reduction of liver injury after fibrosis. Synergistic effect of IL-6 and MSCs seems a favored therapeutic option in attenuation of liver apoptosis and fibrosis accompanied by improved liver function. Topics: Animals; Apoptosis; Carbon Tetrachloride; Coculture Techniques; Female; Gene Expression Regulation; Glycogen; Hepatocytes; Inflammation; Interleukin-6; Liver Cirrhosis; Mesenchymal Stem Cell Transplantation; Mesenchymal Stem Cells; Mice; Mice, Inbred C57BL | 2013 |
Experimental evidence for the use of CCR2 antagonists in the treatment of type 2 diabetes.
CCR2 inhibition has produced promising experimental and clinical anti-hyperglycemic effects. These results support the thesis that insulin resistance and Type 2 diabetes (T2D) are associated with chronic unresolved inflammation. The aim of this study was to provide a broad analysis of the various physiological changes occurring in mouse models of T2D in connection with pharmacological CCR2 inhibition.. A mouse-active chemical analogue of the clinical candidate CCX140-B was tested in diet-induced obese (DIO) mice and db/db mice. Measurements included: adipose tissue inflammatory macrophage counts; peripheral blood glucose levels at steady-state and after glucose and insulin challenges; peripheral blood insulin and adiponectin levels; 24-h urine output and urinary glucose levels; pancreatic islet number and size; hepatic triglyceride and glycogen content; and hepatic glucose-6-phosphatase levels.. In DIO mice, the CCR2 antagonist completely blocked the recruitment of inflammatory macrophages to visceral adipose tissue. The mice exhibited reduced hyperglycemia and insulinemia, improved insulin sensitivity, increased circulating adiponectin levels, decreased pancreatic islet size and increased islet number. It also reduced urine output, glucose excretion, hepatic glycogen and triglyceride content and glucose 6-phosphatase levels. Similar effects were observed in the db/db diabetic mice.. These data indicate that pharmacological inhibition of CCR2 in models of T2D can reduce inflammation in adipose tissue, alter hepatic metabolism and ameliorate multiple diabetic parameters. These mechanisms may contribute to the promising anti-diabetic effects seen in humans with at least one CCR2 antagonist. Topics: Adiponectin; Adipose Tissue; Animals; Biomarkers; Blood Glucose; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 2; Diet, High-Fat; Dose-Response Relationship, Drug; Glucose-6-Phosphatase; Glycogen; Glycosuria; Hypoglycemic Agents; Inflammation; Insulin; Insulin Resistance; Insulin-Secreting Cells; Liver; Macrophages; Male; Mice; Mice, Inbred C57BL; Obesity; Receptors, CCR2; Triglycerides | 2013 |
Transcriptional regulation of cholesterol and bile acid metabolism after dietary soyabean meal treatment in Atlantic salmon (Salmo salar L.).
Inclusion of plant protein sources such as soyabean meal (SBM) in aquafeeds is associated with decreased lipid digestibility, reduced bile acid levels and hypocholesterolaemia. The mechanism for these metabolic abnormalities is unknown. The present study aimed at gaining further insight into how cholesterol and bile acid metabolism is modulated by SBM feeding by quantifying a number of mRNA species corresponding to key proteins involved in cholesterol and bile acid metabolism using quantitative real-time PCR. A 21 d feeding trial with sequential sampling at ten time points following initiation of 20% SBM exposure was conducted on Atlantic salmon. A histological evaluation confirmed distal intestinal enteritis after 5 d of dietary exposure to the SBM, whereas diminished glycogen/lipid deposition was the only relevant finding observed in the liver. SBM inclusion resulted in reduced body pools of cholesterol and bile acids. Hepatic gene expression profiles revealed up-regulation of genes encoding rate-limiting enzymes in cholesterol (3-hydroxy-3-methyl-glutaryl-CoA reductase; HMGCR) and bile acid (cytochrome P4507A1 (CYP7A1)) biosynthesis, as well as up-regulation of their associated transcription factors (sterol regulatory element binding proteins 1 and 2, liver X receptor, farnesoid X receptor and PPAR isoforms). Hepatic gene expressions of cholesterol (ATP binding cassette G5 (ABCG5)) and bile acid (ATP binding cassette B11 (ABCB11)) transporters were, by and large, not influenced by the SBM, but distal intestinal expression patterns of ABCG5 and apical Na-dependent bile acid transporter indicated impaired cholesterol and bile acid reabsorption. In conclusion, hepatic gene expression profiles indicated that the capacity for cholesterol and bile acid synthesis was up-regulated, whereas the indicated impaired cholesterol and bile acid reabsorption probably occurred as a direct result of distal intestinal inflammation. Topics: Animal Feed; Animals; Bile Acids and Salts; Cholesterol; Gene Expression Regulation; Glycine max; Glycogen; Hydroxymethylglutaryl CoA Reductases; Inflammation; Intestinal Mucosa; Lipid Metabolism; Protein Isoforms; Real-Time Polymerase Chain Reaction; RNA, Messenger; Salmo salar; Time Factors; Transcription, Genetic; Transcriptome; Up-Regulation | 2013 |
Citrus unshiu peel extract ameliorates hyperglycemia and hepatic steatosis by altering inflammation and hepatic glucose- and lipid-regulating enzymes in db/db mice.
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 | 2013 |
Chronic DPP-IV inhibition with PKF-275-055 attenuates inflammation and improves gene expressions responsible for insulin secretion in streptozotocin induced diabetic rats.
Inhibitors of dipeptidyl peptidase-4 (DPP-IV), a key regulator of the actions of incretin hormones, exert antihyperglycemic effects in type 2 diabetic patients. A major question concerns the potential ability of long term DPP-IV inhibition to have beneficial disease-modifying effects, specifically to attenuate loss of pancreatic β-cell mass due to oxidative stress induced inflammation. Here, we investigated the effects of a potent and selective DPP-4 inhibitor, an analog of vildagliptin (PKF-275-055), on glycemic control, pancreatic β-cell mass, genes and proteins expressions, tumor necrosis factor-alpha, and nitric oxide in an n2-STZ diabetic model of rat with defects in insulin sensitivity and secretion. To induce NIDDM, streptozotocin (STZ) 90 mg/kg was administered i.p. to a group of 2 days old pups. Diabetic rats were administered orally with vildagliptin analog PKF-275-055. Saline treated animals served as diabetic control. Significant and dose-dependent correction of postprandial hyperglycemia was observed in diabetic rats following 8 weeks of chronic therapy. Treatment with PKF-275-055 showed increased the number of insulin-positive β-cells in islets and improved the expressions of genes and proteins are responsible for insulin secretions. In addition, treatment of rats with PKF-275-055 significantly increased insulin content, glycogen content and total proteins content; and decreased the inflammatory markers i.e. nitric oxide and TNF-alpha. The present studies indicate that PKF-275-055 is a novel selective DPP-IV inhibitor having potential to reduce inflammation that might be a potential agent for type 2 diabetes. Topics: Adamantane; Animals; Blood Glucose; Blood Proteins; Diabetes Mellitus, Experimental; Dipeptidyl-Peptidase IV Inhibitors; Gene Expression Regulation; Glucagon-Like Peptide 1; Glucose Transporter Type 2; Glucose Transporter Type 4; Glycogen; Hypoglycemic Agents; Inflammation; Insulin; Insulin Secretion; Liver; Muscle, Skeletal; Nitrates; Nitriles; Nitrites; Pancreas; Pyrrolidines; Rats; Rats, Wistar; RNA, Messenger; Tumor Necrosis Factor-alpha | 2012 |
Ultrastructure of gingival epithelium in chronic gingivitis.
We studied ultrastructural reorganization of the gingival mucosa in chronic gingivitis. It was found that chronic inflammation leads to significant intracellular reorganization of epitheliocytes in the basal and prickle cell layers of gingival epithelium and their pronounced structural and functional heterogeneity. The main ultrastructural alterations of epitheliocytes in the basal and prickle cell layers include pronounced vacuolization of the perinuclear zone (partial necrosis), formation of thick tonofilament bundles, focal lysis and sequestration of glycogen, and destruction and reduction of intracellular junctions in some cases accompanied by acantholytic alterations. Chronic inflammation in the gingival mucosa induced extensive remodeling of the lamina propria manifested in multiplication of the basement membrane and obturation of blood vessels with collagen fibrils. Topics: Adult; Basement Membrane; Biopsy; Blood Vessels; Chronic Disease; Cytoplasm; Epithelial Cells; Gingiva; Gingivitis; Glycogen; Humans; Inflammation; Intercellular Junctions; Microscopy, Electron; Mucous Membrane; Necrosis | 2012 |
Modified Si-Miao-San extract inhibits inflammatory response and modulates insulin sensitivity in hepatocytes through an IKKβ/IRS-1/Akt-dependent pathway.
Modified Si-Miao-San (mSMS) has showed anti-inflammatory potency and has been used in the clinic to treat metabolic disorders such as obesity and diabetes, but whether its anti-inflammatory activity contributes to improving insulin resistance remains to be determined. This study aims to investigate the mechanistic relationship between its anti-inflammatory activity and modulation of insulin sensitivity in free fatty acid-stimulated HepG2 cells.. HepG2 cells were stimulated with palmitate (PA) and the effect of mSMS on insulin mediated-glycogen synthesis and triglyceride secretion was observed. The inhibition of mSMS on gene expression of proinflammatory cytokine tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and inhibitor of NF-κB kinase-β (IKKβ) activation was investigated. In addition, the effects of mSMS on insulin signaling transduction along insulin receptor substrates-1 (IRS-1)/Akt pathway were also evaluated. Furthermore, the effect of mSMS on glucose intolerance induced by conditioned-medium derived from activated macrophages was also assessed in normoglycemic mice.. Treatment of hepatocytes with PA reduced insulin sensitivity and mSMS effectively increased insulin-mediated glycogen synthesis and restored insulin inhibition of triglyceride secretion. mSMS suppressed IKKβ activation and down-regulated TNF-α and IL-6 gene over-expression, demonstrating its anti-inflammatory activity in hepatocytes. PA-evoked inflammation impaired insulin signaling cascades and mSMS improved insulin signaling transduction by modification of Ser/Thr phosphorylation of IRS-1 and downstream Akt (T308), thereby improved insulin sensitivity in hepatocytes. mSMS also improved glucose intolerance induced by inflammatory cytokines in normoglycemic mice, which further demonstrated its modulation toward insulin sensitivity in vivo.. The results suggest that mSMS inhibited inflammatory response and improved insulin sensitivity in hepatocytes via an IKKβ/IRS-1/Akt-dependent pathway. Topics: Animals; Anti-Inflammatory Agents; Atractylodes; Coix; Coptis; Down-Regulation; Drugs, Chinese Herbal; Glycogen; Hep G2 Cells; Hepatocytes; Humans; I-kappa B Kinase; Inflammation; Inflammation Mediators; Insulin; Insulin Receptor Substrate Proteins; Insulin Resistance; Interleukin-6; Male; Mice; Mice, Inbred ICR; Phytotherapy; Plants, Medicinal; Proto-Oncogene Proteins c-akt; Signal Transduction; Triglycerides; Tumor Necrosis Factor-alpha | 2011 |
Interleukin-6 signaling in liver-parenchymal cells suppresses hepatic inflammation and improves systemic insulin action.
The contribution of interleukin (IL)-6 signaling in obesity-induced inflammation remains controversial. To specifically define the role of hepatic IL-6 signaling in insulin action and resistance, we have generated mice with hepatocyte-specific IL-6 receptor (IL-6R) alpha deficiency (IL-6Ralpha(L-KO) mice). These animals showed no alterations in body weight and fat content but exhibited a reduction in insulin sensitivity and glucose tolerance. Impaired glucose metabolism originated from attenuated insulin-stimulated glucose transport in skeletal muscle and fat. Surprisingly, hepatic IL-6Ralpha-disruption caused an exaggerated inflammatory response during euglycemic hyperinsulinemic clamp analysis, as revealed by increased expression of IL-6, TNF-alpha, and IL-10, as well as enhanced activation of inflammatory signaling such as phosphorylation of IkappaBalpha. Neutralization of TNF-alpha or ablation of Kupffer cells restored glucose tolerance in IL-6Ralpha(L-KO) mice. Thus, our results reveal an unexpected role for hepatic IL-6 signaling to limit hepatic inflammation and to protect from local and systemic insulin resistance. Topics: Adiposity; Animals; Energy Metabolism; Glucose; Glycogen; Homeostasis; Humans; Inflammation; Insulin; Insulin Resistance; Interleukin-10; Interleukin-6; Kupffer Cells; Liver; Mice; Mice, Knockout; Receptors, Interleukin-6; Signal Transduction; Tumor Necrosis Factor-alpha | 2010 |
Homocysteine induces oxidative stress, inflammatory infiltration, fibrosis and reduces glycogen/glycoprotein content in liver of rats.
Hyperhomocysteinemia has been related to various diseases, including homocystinuria, neurodegenerative and hepatic diseases. In the present study we initially investigated the effect of chronic homocysteine administration on some parameters of oxidative stress, named total radical-trapping antioxidant potential, total antioxidant reactivity, catalase activity, chemiluminescence, thiobarbituric acid-reactive substances, and total thiol content in liver of rats. We also performed histological analysis, evaluating steatosis, inflammatory infiltration, fibrosis, and glycogen/glycoprotein content in liver tissue sections from hyperhomocysteinemic rats. Finally, we evaluated the activities of aminotransferases in liver and plasma of hyperhomocysteinemic rats. Wistar rats received daily subcutaneous injection of Hcy from their 6th to their 28th day of life. Twelve hours after the last injection the rats were sacrificed, liver and plasma were collected. Hyperhomocysteinemia decreased antioxidant defenses and total thiol content, and increased lipid peroxidation in liver of rats, characterizing a reliable oxidative stress. Histological analysis indicated the presence of inflammatory infiltrate, fibrosis and reduced content of glycogen/glycoprotein in liver tissue sections from hyperhomocysteinemic rats. Aminotransferases activities were not altered by homocysteine. Our data showed a consistent profile of liver injury elicited by homocysteine, which could contribute to explain, at least in part, the mechanisms involved in human liver diseases associated to hyperhomocysteinemia. Topics: Animals; Antioxidants; Female; Fibrosis; Glycogen; Glycoproteins; Homocysteine; Humans; Inflammation; Lipid Peroxidation; Liver; Male; Oxidative Stress; Rats; Sulfhydryl Compounds; Thiobarbituric Acid Reactive Substances | 2009 |
Gene expression profiling in equine polysaccharide storage myopathy revealed inflammation, glycogenesis inhibition, hypoxia and mitochondrial dysfunctions.
Several cases of myopathies have been observed in the horse Norman Cob breed. Muscle histology examinations revealed that some families suffer from a polysaccharide storage myopathy (PSSM). It is assumed that a gene expression signature related to PSSM should be observed at the transcriptional level because the glycogen storage disease could also be linked to other dysfunctions in gene regulation. Thus, the functional genomic approach could be conducted in order to provide new knowledge about the metabolic disorders related to PSSM. We propose exploring the PSSM muscle fiber metabolic disorders by measuring gene expression in relationship with the histological phenotype.. Genotypying analysis of GYS1 mutation revealed 2 homozygous (AA) and 5 heterozygous (GA) PSSM horses. In the PSSM muscles, histological data revealed PAS positive amylase resistant abnormal polysaccharides, inflammation, necrosis, and lipomatosis and active regeneration of fibers. Ultrastructural evaluation revealed a decrease of mitochondrial number and structural disorders. Extensive accumulation of an abnormal polysaccharide displaced and partially replaced mitochondria and myofibrils. The severity of the disease was higher in the two homozygous PSSM horses.Gene expression analysis revealed 129 genes significantly modulated (p < 0.05). The following genes were up-regulated over 2 fold: IL18, CTSS, LUM, CD44, FN1, GST01. The most down-regulated genes were the following: mitochondrial tRNA, SLC2A2, PRKCalpha, VEGFalpha. Data mining analysis showed that protein synthesis, apoptosis, cellular movement, growth and proliferation were the main cellular functions significantly associated with the modulated genes (p < 0.05). Several up-regulated genes, especially IL18, revealed a severe muscular inflammation in PSSM muscles. The up-regulation of glycogen synthase kinase-3 (GSK3beta) under its active form could be responsible for glycogen synthase (GYS1) inhibition and hypoxia-inducible factor (HIF1alpha) destabilization.. The main disorders observed in PSSM muscles could be related to mitochondrial dysfunctions, glycogenesis inhibition and the chronic hypoxia of the PSSM muscles. Topics: Animals; Female; Gene Expression Profiling; Gene Expression Regulation; Genotype; Glycogen; Horse Diseases; Horses; Hypoxia; Inflammation; Male; Mitochondria; Muscle, Skeletal; Muscular Diseases; Phenotype; Polysaccharides | 2009 |
Increased inflammation, impaired bacterial clearance, and metabolic disruption after gram-negative sepsis in Mkp-1-deficient mice.
MAPKs are crucial for TNF-alpha and IL-6 production by innate immune cells in response to TLR ligands. MAPK phosphatase 1 (Mkp-1) deactivates p38 and JNK, abrogating the inflammatory response. We have previously demonstrated that Mkp-1(-/-) mice exhibit exacerbated inflammatory cytokine production and increased mortality in response to challenge with LPS and heat-killed Staphylococcus aureus. However, the function of Mkp-1 in host defense during live Gram-negative bacterial infection remains unclear. We challenged Mkp-1(+/+) and Mkp-1(-/-) mice with live Escherichia coli i.v. to examine the effects of Mkp-1 deficiency on animal survival, bacterial clearance, metabolic activity, and cytokine production. We found that Mkp-1 deficiency predisposed animals to accelerated mortality and was associated with more robust production of TNF-alpha, IL-6 and IL-10, greater bacterial burden, altered cyclooxygenase-2 and iNOS expression, and substantial changes in the mobilization of energy stores. Likewise, knockout of Mkp-1 also sensitized mice to sepsis caused by cecal ligation and puncture. IL-10 inhibition by neutralizing Ab or genetic deletion alleviated increased bacterial burden. Treatment with the bactericidal antibiotic gentamicin, given 3 h after Escherichia coli infection, protected Mkp-1(+/+) mice from septic shock but had no effect on Mkp-1(-/-) mice. Thus, during Gram-negative bacterial sepsis Mkp-1 not only plays a critical role in the regulation of cytokine production but also orchestrates the bactericidal activities of the innate immune system and controls the metabolic response to stress. Topics: Animals; Cyclooxygenase 2; Dual Specificity Phosphatase 1; Enzyme-Linked Immunosorbent Assay; Escherichia coli; Escherichia coli Infections; Glucose; Glycogen; Gram-Negative Bacterial Infections; Hyperlipidemias; Inflammation; Interleukin-10; Interleukin-6; Lipid Metabolism; Mice; Mice, Knockout; Nitric Oxide Synthase Type II; Sepsis; Tumor Necrosis Factor-alpha | 2009 |
The metabolic changes caused by dexamethasone in the adjuvant-induced arthritic rat.
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 | 2007 |
Effect of in vivo phenol or hydroquinone exposure on events related to neutrophil delivery during an inflammatory response.
Phenol (PHE) and hydroquinone (HQ) are metabolites of benzene that affect leukocytes after solvent intoxication. Hence, we investigated the effects of PHE or HQ exposure on neutrophil mobilization during an inflammatory response. Male Wistar rats received intraperitoneal injections of PHE, HQ or vehicle only and assays were performed 24 h after the last dose. Quantifications of bone marrow or circulating leukocytes showed that only HQ exposure induced neutrophilia, probably due to the accelerated mobilization from the bone marrow compartment, since reduced numbers of segmented cells in the last phase of maturation were detected there. Intravital microscopy showed that circulating leukocytes of HQ-exposed rats increased their rolling behavior and adherence to the mesenteric postcapillary venule wall in vivo. The enhanced leukocyte-endothelium interaction was not dependent on microvascular reactivity or perivascular mast cell degranulation. Instead, it was the result of neutrophil activation, demonstrated by a decrease in L-selectin and an increase in beta2 integrin expression on neutrophil membranes. This pattern of neutrophil activation may have contributed to the higher number of neutrophils in the subcutaneous inflammatory response of HQ-exposed rats after oyster glycogen injection. Taken together, our results indicate that HQ exposure alters neutrophil mobilization, which results in an exacerbated response after an injury. Although PHE is endogenously metabolized to HQ, PHE exposure only induced an increment in rolling behavior, which was not sufficient to alter the inflammatory response. Topics: Animals; Glycogen; Hydroquinones; Inflammation; Leukocyte Count; Leukocyte Rolling; Leukocytes; Male; Mesentery; Neutrophil Activation; Neutrophil Infiltration; Neutrophils; Phenol; Rats; Rats, Wistar | 2006 |
Insight into the involvement of Kupffer cell-derived mediators in the hepatoprotective effect of glycine upon inflammation: study on rat precision-cut liver slices.
To investigate the role of inflammatory mediators in the hepatoprotective effect of glycine against lipopolysaccharide (LPS)-induced liver injury in rats.. Male Wistar rats were used (N = 4 or 5 per group). Precision-cut liver slices (PCLS) were prepared for in vitro studies.. Glycine (10 mM) and LPS (10 mug/ml) were added to the incubation medium of PCLS obtained 3 h after LPS intraperitoneal (i. p.) administration (10 mg/kg) or saline injection to rats. Glycine effects were also investigated in vivo by treating rats with a diet containing glycine (5%) during 3 days.. Tissue injury was assessed by measuring adenosine triphosphate (ATP) and glycogen contents of liver tissue as well as by measuring aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) activity in the medium (in vitro) or in the serum (in vivo). Tumor necrosis factor-alpha (TNF-alpha), prostaglandin E(2)(PGE(2)) and NOx (reflecting nitric oxide production) were measured in the incubation medium or in the serum. Histological detection of both ED-2 and peroxidase activity were used as Kupffer cell markers. Student t test or two-way ANOVA were used for statistic analysis.. Glycine added to the culture medium increased both ATP and glycogen contents of PCLS from LPS-treated rats, reduced the production of TNF-alpha and NOx whereas PGE(2) secretion by PCLS increased. In contrast to the in vitro effect of glycine, we observed that a glycine-enriched diet decreased PGE(2) secretion in the serum after LPS challenge.. The effect of glycine on LPS-induced mediator secretion is different considering in vitro or in vivo situations. Interestingly, glycine in vitro is able to prevent energy status depletion of PCLS occurring upon inflammation, a phenomenon probably linked to change in inflammatory mediator secretion pattern by hepatic immune cells, namely Kupffer cells. Topics: Adenosine Triphosphate; Alanine Transaminase; Analysis of Variance; Animals; Aspartate Aminotransferases; Culture Media; Dinoprostone; Free Radicals; Glycine; Glycogen; Inflammation; Kupffer Cells; L-Lactate Dehydrogenase; Lipopolysaccharides; Liver; Male; Nitric Oxide; Oxygen; Rats; Rats, Wistar; Tumor Necrosis Factor-alpha | 2005 |
Timp3 deficiency in insulin receptor-haploinsufficient mice promotes diabetes and vascular inflammation via increased TNF-alpha.
Activation of inflammatory pathways may contribute to the beginning and the progression of both atherosclerosis and type 2 diabetes. Here we report a novel interaction between insulin action and control of inflammation, resulting in glucose intolerance and vascular inflammation and amenable to therapeutic modulation. In insulin receptor heterozygous (Insr+/-) mice, we identified the deficiency of tissue inhibitor of metalloproteinase 3 (Timp3, an inhibitor of both TNF-alpha-converting enzyme [TACE] and MMPs) as a common bond between glucose intolerance and vascular inflammation. Among Insr+/- mice, those that develop diabetes have reduced Timp3 and increased TACE activity. Unchecked TACE activity causes an increase in levels of soluble TNF-alpha, which subsequently promotes diabetes and vascular inflammation. Double heterozygous Insr+/-Timp3+/- mice develop mild hyperglycemia and hyperinsulinemia at 3 months and overt glucose intolerance and hyperinsulinemia at 6 months. A therapeutic role for Timp3/TACE modulation is supported by the observation that pharmacological inhibition of TACE led to marked reduction of hyperglycemia and vascular inflammation in Insr+/- diabetic mice, as well as by the observation of increased insulin sensitivity in Tace+/- mice compared with WT mice. Our results suggest that an interplay between reduced insulin action and unchecked TACE activity promotes diabetes and vascular inflammation. Topics: Analysis of Variance; Animals; Deoxyglucose; Diabetes Mellitus; Electrophoresis, Polyacrylamide Gel; Gene Expression Profiling; Genetic Vectors; Glucose; Glucose Tolerance Test; Glycogen; Heterozygote; Homeostasis; Hyperglycemia; Hyperinsulinism; Inflammation; Insulin; Liver; Mice; Mice, Inbred C57BL; Mice, Transgenic; Muscle, Skeletal; Muscles; Phosphorylation; Promoter Regions, Genetic; Protein Binding; Receptor, Insulin; Reverse Transcriptase Polymerase Chain Reaction; RNA; RNA, Messenger; RNA, Small Interfering; Signal Transduction; Time Factors; Tissue Inhibitor of Metalloproteinase-3; Tumor Necrosis Factor-alpha | 2005 |
Effects of different dietary oils on inflammatory mediator generation and fatty acid composition in rat neutrophils.
Virgin olive oil (VOO) compared with fish oil (FO) and evening primrose oil (PO) on the ability of stimulated leukocytes to produce inflammatory mediators was investigated in rats. Weaned Wistar rats were fed a basal diet (BD) (2% by weight of corn oil) or diets containing 15% by weight of VOO, PO, or FO. After 8 weeks, glycogen-elicited peritoneal polymorphonuclear leukocytes, mainly neutrophils, were isolated. The calcium-ionophore stimulated neutrophils (2.5 x 10(6) cells/mL) obtained from rats fed the different oils produced a higher release of lysosomal enzymes (beta-glucuronidase, lysozyme, and myeloperoxidase [MPO]) compared with those fed BD. The production of reactive oxygen species (ROS) in response to the stimulant, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), by neutrophils from the VOO group (15.44 nmol of O(2)(-) and 6.56 nmol of H(2)O(2)) was similar to the BD group (12.01 nmol O(2)(-) and 8.49 nmol H(2)O(2)) and significantly lower than the PO (20.90 nmol O(2)(-) and 10.84 nmol H(2)O(2)) and FO (20.93 nmol O(2)(-) and 12.79 nmol H(2)O(2)) groups. The cyclooxygenase-derived eicosanoid production was reduced by the lipid enrichment of the diets. Whereas the generation of prostaglandin E(2) (PGE(2)) was significantly decreased in VOO (5.40 ng/mL), PO (4.95 ng/mL), and FO (1.44 ng/mL) groups compared with BD (8.19 ng/mL), thromboxane B(2) (TXB(2)) reduction was especially significant in neutrophils from the FO diet group (14.67 ng/mL compared with 26.69 ng/mL from BD). These experimental data suggest that FO and PO, as well as VOO, could be considered a valuable strategy in preventing the generation of some inflammatory mediators. Topics: Animals; Arachidonic Acid; Calcimycin; Dietary Fats, Unsaturated; Dinoprostone; Eicosanoids; Fatty Acids; Fatty Acids, Essential; Fish Oils; gamma-Linolenic Acid; Glucuronidase; Glycogen; Hydrogen Peroxide; Inflammation; Linoleic Acid; Linoleic Acids; Lysosomes; Male; Muramidase; Neutrophils; Oenothera biennis; Oleic Acid; Olive Oil; Peritoneum; Peroxidase; Plant Oils; Rats; Rats, Wistar; Reactive Oxygen Species; Superoxides; Tetradecanoylphorbol Acetate; Thromboxane B2 | 2004 |
Dual role of polymorphonuclear neutrophils on the growth of Ehrlich ascites tumor (EAT) in mice.
We show that granulocytes (PMN) have a dual role in the development of Ehrlich Ascites Tumor (EAT) in mice. EAT intraperitoneal inoculation causes a local inflammatory reaction, ascites development and mortality that distinguish resistant and susceptible strains. In resistant mice (CAF1), there is a less pronounced PMN influx after EAT inoculation than in susceptible Swiss mice. Accordingly, the increase in peritoneal PMN numbers enhanced tumor growth in CAF1 mice, but had no effect in the susceptible Swiss animals. Contrastingly, PMN depletion had no effect in resistant mice but facilitated tumor growth in susceptible animals. Though no differences were noted between the strains in peritoneal cell spreading and hydrogen peroxide release after tumor inoculation, in vitro PMN cytotoxic activity against EAT was significantly higher in susceptible Swiss mice. These data indicate a paradoxical dual role for PMN against EAT: while they help control tumor development in susceptible animals, they seem to enhance tumor growth in resistant mice. Topics: Analysis of Variance; Animals; Antibodies, Monoclonal; Body Weight; Carcinoma, Ehrlich Tumor; Cytotoxicity, Immunologic; Glycogen; Hydrogen Peroxide; Inflammation; Injections, Intraperitoneal; Male; Mice; Mice, Inbred BALB C; Neoplasm Transplantation; Neutrophils; Tetrazolium Salts; Thiazoles; Time Factors | 2004 |
Glutamine improves impaired cellular exudation and polymorphonuclear neutrophil phagocytosis induced by total parenteral nutrition after glycogen-induced murine peritonitis.
Clinical and laboratory evidence shows that enteral feeding significantly reduces pneumonia and intra-abdominal abscess formation after celiotomy for severe trauma. Supplementation of total parenteral nutrition (TPN) with glutamine (GLN) supports impaired immunity induced by TPN in several animal and human studies. This work investigates the peritoneal cellular response and polymorphonuclear neutrophil (PMN) bactericidal function after mouse chemical peritonitis after TPN with and without GLN. Thirty-three mice received chow, TPN, or 2% GLN-supplemented TPN (GLN-TPN) for 5 days. All mice then received 2 mL of a 1% glycogen solution intraperitoneally to induce cell exudation, and peritoneal exudative cells (PECs) were recovered 4 h later. Total and differential PEC numbers, as well as PMN phagocytosis, reactive oxygen intermediate production (ROI), CD11b (integrin aM chain) expression, and CD16/32 (Fcgamma II/III receptor) expression were measured. PMN, macrophage, and lymphocyte cell numbers were significantly lower with TPN than with chow or GLN-TPN groups, with no differences between chow and GLN-TPN. TPN significantly lowered peritoneal PMN phagocytosis compared with chow (P < 0.05) and approached significance with GLN-TPN (P = 0.06). There were no significant differences in ROI production or CD11b and CD16/32 expression on peritoneal PMN. GLN supplementation improved the reduction in cell exudation and PMN phagocytosis induced by TPN after chemical peritonitis. Topics: Animals; Body Weight; CD11b Antigen; Cell Adhesion; Flow Cytometry; Glutathione; Glycogen; Inflammation; Macrophages; Mice; Neutrophils; Phagocytosis; Reactive Oxygen Species; Receptors, IgG | 2003 |
CXC chemokine redundancy ensures local neutrophil recruitment during acute inflammation.
Previous publications demonstrated that elevated systemic levels of interleukin (IL)-8 decrease local neutrophil recruitment. We tested whether sustained, high plasma levels of IL-8 would prevent local inflammation after inflammatory insults. Mice carrying the transgene for human IL-8 were separated on the basis of their plasma levels of IL-8 into IL-8-positive (plasma levels >90 ng/ml) and IL-8-negative (IL-8 below detection). Presence of the IL-8 transgene did not improve survival or morbidity nor did it alter peritoneal neutrophil recruitment induced by the cecal ligation and puncture model of sepsis. In an acute lung injury model created by intratracheal injection of acid, IL-8-positive mice showed no reduction in alveolar neutrophil recruitment. There was no difference in the local recruitment of neutrophils when either thioglycollate or glycogen was injected intraperitoneally. We examined the chemotactic response to murine chemokines to test how neutrophil recruitment occurs in the setting of elevated plasma IL-8 and found that neutrophils from both IL-8-positive and -negative mice respond equally well to recombinant KC or macrophage inflammatory protein (MIP)-2. We measured KC and MIP-2 in the peritoneum after thioglycollate injection and demonstrated that IL-8-positive mice have significantly higher levels of the chemokines compared to the IL-8-negative mice. Antibody inhibition of KC and MIP-2 in the IL-8-positive mice significantly decreased peritoneal neutrophil recruitment in response to thioglycollate, clarifying their important role in the local neutrophil recruitment. Our data demonstrate that despite the presence of high plasma levels of IL-8, neutrophils may still be recruited to sites of local inflammation because of chemokine redundancy. Topics: Acute Disease; Animals; Cecum; Chemokines, CXC; Glycogen; Humans; Hydrochloric Acid; Inflammation; Interleukin-8; Ligation; Lung Diseases; Mice; Mice, Transgenic; Morbidity; Neutrophil Infiltration; Peritoneum; Punctures; Reference Values; Thioglycolates; Transgenes | 2001 |
Glycogen granules in resting and inflammatory rainbow trout phagocytes--an ultrastructural study.
The ultrastructural image of glycogen granules in the cytoplasm of rainbow trout phagocytes in sections stained by the conventional lead or uranyl-lead stains is highly dependent on fixation conditions, the granules being visible only when adequate fixation protocols are used. Morphometry of samples processed for the detection of peroxidase or esterase activities (to specifically label neutrophils and macrophages, respectively), and simultaneously stained for the specific detection of glycogen, showed that inflammatory peritoneal neutrophils were richer in glycogen granules than resting neutrophils. This increase in glycogen content occurs after the migration from the haematopoietic tissues and peripheral blood to the inflamed foci. Glycogen granules could not be found in resting peritoneal macrophages but were found in inflammatory macrophages. The macrophage granules occurred in smaller amounts than in neutrophils, and consisted of granules identical to those of neutrophils together with significantly smaller granules. No evidence for the utilization of glycogen by neutrophils phagocytosing bacteria within the peritoneal cavity was found. Topics: Animals; Aquaculture; Blood Glucose; Cytoplasmic Granules; Fish Diseases; Glycogen; Inflammation; Macrophages, Peritoneal; Neutrophils; Oncorhynchus mykiss; Phagocytes; Yersinia; Yersinia Infections | 2000 |
Role of inducible nitric oxide synthase in leukocyte extravasation in vivo.
Several recent studies have suggested that nitric oxide (NO) derived from the inducible isoform of NO synthase (NOS) may act as an endogenous modulator of the inflammatory response by inhibiting adhesion of leukocytes to endothelial cells in vitro. Few studies have addressed specifically the role of iNOS in regulating leukocyte recruitment in vivo in a model of acute inflammation. Thus, the objective of this study was to assess the role of iNOS in modulating neutrophil (PMN) extravasation in an oyster glycogen-induced model of acute peritonitis in rats. Data obtained in the present study demonstrates that injection (IP) of oyster glycogen induces massive and selective PMN recruitment into the peritoneal cavity of rats at 6 hrs following OG administration. These extravasated cells were found to contain significant amounts of iNOS protein as assessed by Western blot analysis. Treatment of rats with the selective iNOS inhibitor L-iminoethyl-lysine (L-NIL) dramatically reduced NO levels in lavage fluid as measured by decreases in nitrate and nitrite concentrations without significantly affecting iNOS protein levels. Although L-NIL inhibited NO production by >70%, it did not alter oyster glycogen-induced PMN recruitment when compared to vehicle-treated rats. We conclude that PMN-associated, iNOS-derived NO does not play an important role in modulating extravasation of these leukocytes in this model of acute inflammation. Topics: Acute Disease; Animals; Ascitic Fluid; Blotting, Western; Cell Movement; Disease Models, Animal; Enzyme Induction; Female; Glycogen; Inflammation; Lysine; Neutrophils; Nitrates; Nitric Oxide; Nitric Oxide Synthase; Nitric Oxide Synthase Type II; Nitrites; Ostreidae; Peritonitis; Rats; Rats, Inbred Lew | 1999 |
Atypical stromal cells in inflammatory nasal polyps: immunohistochemical and ultrastructural analysis in defining histogenesis.
The authors investigated 29 cases of sinonasal polyps with atypical stromal cells (ASC). The clinicopathologic features of these lesions were of benign inflammatory polyps except for the presence of ASC. Misinterpretation of these cells resulted in contributor diagnosis of sarcoma (rhabdomyosarcoma). Immunohistochemical study of the ASC demonstrated the presence of actin (smooth muscle and muscle specific), KP-1, and vimentin; no reactivity was seen with desmin, myoglobin, S-100 protein, or glial fibrillary acidic protein (GFAP). Unexpectedly, cytokeratin reactivity was identified in more than 75% of the cases analyzed. Ultrastructural analysis revealed that the ASC shared morphologic features in common with fibroblasts and smooth muscle cells. Based on the light microscopic, immunohistochemical, and ultrastructural findings, it was concluded that the ASC represent reactive myofibroblasts and not a neoplastic proliferation. Follow-up data supported this contention indicating the absence of an aggressive biological course. Misinterpretation as a malignant neoplasm might result in unwarranted and unnecessary therapeutic intervention. Topics: Actins; Adolescent; Adult; Antigens, CD; Biomarkers, Tumor; Child; Diagnosis, Differential; Female; Follow-Up Studies; Glycogen; Humans; Inflammation; Lysosomal Membrane Proteins; Male; Membrane Glycoproteins; Microscopy, Electron; Middle Aged; Morphogenesis; Nasal Polyps; Stromal Cells; Vimentin | 1995 |
The effect of psychological stress on neutrophil superoxide release.
Stress has long been suggested to exacerbate symptom expression in people with chronic inflammatory disorders. The release of oxidative metabolites from activated PMN plays a significant role in the pathophysiology of inflammation. Thus, we examined the effects of psychological stress on release of superoxide anions from PMN of rats with or without an inflammation induced by injection of shellfish glycogen (SFG). Psychological stress was found to significantly increase PMN superoxide release in both healthy and SFG-injected animals. Total amounts of superoxide release were similar between the two groups, suggesting that PMN from animals with a mild inflammatory condition were not more susceptible to the effects of stress than PMN from healthy animals. However, this study should be repeated using an animal model of chronic inflammation, such as airway hyperactivity or rheumatoid arthritis. Topics: Analysis of Variance; Animals; Glycogen; Inflammation; Male; Neutrophils; Random Allocation; Rats; Rats, Sprague-Dawley; Shellfish; Stress, Psychological; Superoxides | 1994 |
Smoke inhalation with a concurrent systemic stress results in lung alveolar injury.
Smoke inhalation causes injuries to lung airways, and, at times, alveolar inflammation also develops over approximately 24 h. The pathophysiology of parenchymal lung injuries is unknown, and it is often fatal. We hypothesized that an inflammatory stress remote from the smoke-related lung insult was required for development of alveolar injuries. Spontaneously breathing rats were exposed, head only, to smoke generated by nonflaming pyrolysis (smoldering) of Douglas fir wood (DF), polyvinylchloride (PVC), or the combination of DF+PVC. Intraperitoneal injection of sterile oyster shell glycogen 4 h before smoke inhalation was used as an extra inflammatory stimulus. Histologic examinations revealed extensive airway inflammation in all smoke-exposed groups. Glycogen peritonitis alone caused no lung injuries, and in the absence of glycogen, smoke inhalation caused neither parenchymal lung injuries, assessed by [125I]bovine serum albumin (BSA) leakage, nor neutrophil infiltration, quantified by myeloperoxidase (MPO) activity. However, in rats pretreated with glycogen and studied 24 h after exposure to smoke from burning DF+PVC, [125I]BSA permeability was increased by 232 +/- 41% (SE; n = 13), MPO activity was increased 5-fold, from 2.6 +/- 0.4 (n = 7) to 13.9 +/- 1.4 (n = 19) A460/min/g lung, and histopathologic findings included extensive pulmonary inflammation. We conclude that inhalation of certain types of smoke will trigger pulmonary injury when an inflammatory process remote from the lungs is present. Topics: Analysis of Variance; Animals; Blood Gas Analysis; Bronchoalveolar Lavage Fluid; Capillary Permeability; Fires; Glycogen; Inflammation; Male; Neutrophils; Peritonitis; Peroxidase; Polyvinyl Chloride; Pulmonary Alveoli; Rats; Rats, Inbred F344; Serum Albumin, Bovine; Smoke Inhalation Injury; Stress, Physiological; Wood | 1994 |
[Histochemical investigation on glycogen in the epithelium of mucosa under denture base].
Accumulation of glycogen in the epithelium of the oral mucosa was evaluated in relation to the existence of wound and inflammation of the oral mucosa histochemically and histopathologically. Antemolar rhombus (the anterior part of the intermolar palate) of adult Wistar rat was employed as experimental area. Experimental wound of palatal mucosa was made by excision of crestal one third of the palatine ruga. Inflammation of the connective tissue was artificially induced by the insertion of silk thread or silk thread immersed in 5% formalin in the connective tissue parallel to the crest line of palatine ruga. The experimental area was examined histochemically and histopathologically up to 72 hours after experimental operation. In excision wound the accumulation of glycogen was observed in prickle cell layer of the epithelium after 24 hours. Although the inflammatory reaction was observed more prominently in the thread inserted connective tissue, the accumulation of glycogen in the epithelium could not be detected. The findings of this study suggested that inflammation itself does not induce the accumulation of glycogen in the epithelium of the oral mucosa and the accumulation could be an indication of wound and/or its healing process of oral epithelium. Topics: Animals; Denture Bases; Epithelium; Glycogen; Inflammation; Mouth Mucosa; Rats; Rats, Inbred Strains; Wound Healing | 1989 |
Measurement of inflammatory reactions by a dye dilution method.
Topics: Animals; Carrageenan; Dye Dilution Technique; Exudates and Transudates; Glycogen; Inflammation; Male; Rats; Rats, Inbred Strains | 1982 |
Studies of glycogen-induced inflammation of mice. Dynamics of inflammatory responses and influence of antiinflammatory drugs and protease inhibitors.
The intraperitoneal injection of glycogen in the mouse resulted, shortly thereafter, in the accumulation of 14-23 million neutrophils in the peritoneal cavity and a four-fold increase in the numbers of circulating neutrophils. Preceding the influx of leukocytes, the exudation of plasma proteins and the chemotactic activity for mouse neutrophil in vitro increased in the peritoneal fluid. Among various protease inhibitors examined, chymostatin alone suppressed the plasma protein exudation. Indomethacin and dexamethasone reduced the accumulation of white cells and protein exudation. These nonsteroidal and steroidal antiinflammatory drugs were equally effective whether given simultaneously with or 60 min before glycogen or whether administered intraperitoneally or orally. Colchicine showed a suppressive effect on the leukocyte accumulation but enhanced the protein exudation. Topics: Animals; Anti-Inflammatory Agents; Glycogen; Inflammation; Kinetics; Mice; Protease Inhibitors; Time Factors | 1982 |
Glycogen accumulation in polymorphonuclear leukocytes, and other intracellular alterations that occur during inflammation.
Neutrophils isolated from the blood were compared to those from inflammatory exudates in the peritoneal cavity of guinea pigs. Inflammatory neutrophils were shown to have 10-fold more glycogen than blood neutrophils. This was also reflected in the morphology of these cells. The large accumulations of glycogen in inflammatory neutrophils exists in ordered arrays of beta-granules. Other morphological changes including accumulations of lipid droplets and a decrease in the number of lysosomal granules also accompany the change from blood neutrophils to inflammatory neutrophils. These results show that there are major metabolic differences in the two types of neutrophils. Topics: Animals; Ascitic Fluid; Bone Marrow Cells; Caseins; Cytoplasmic Granules; Endoplasmic Reticulum; Glycogen; Guinea Pigs; Inflammation; Lipids; Lipopolysaccharides; Lysosomes; Male; Neutrophils | 1982 |
[Inflammation and regeneration in the tissues of purulent wounds closed with primary sutures].
Topics: Adolescent; Adult; Aged; DNA; Female; Glycogen; Humans; Inflammation; Male; Middle Aged; Neutrophils; Staphylococcal Infections; Surgical Wound Infection; Suture Techniques; Wound Healing | 1981 |
The effect of stress on the migration of leucocytes into the peritoneal cavity of rats following injection of an inflammatory agent.
Although previous studies have shown that the injection of exogenous corticosteroids suppresses the inflammatory response, no study has been made on the effect on inflammation of endogenous corticosteroids released in response to stress. In the present study a reduction was observed in the total number of leucocytes migrating into the peritoneal cavity of stressed rats in response to the injection of an inflammatory agent. The reduction of total counts was due to a stress-induced reduction of both polymorph and mononuclear cells. Permeability studies and blood leucocyte counts were conducted to determine the mode of action of the stress-induced reduction of leucocyte migration. In the case of the polymorphs, evidence is presented to implicate both a reduced release of these cells into the blood stream from storage sites and a blockade of the increased vascular permeability. The situation is not as clear for the mononuclear cells where no change in the circulating levels of these cells was observed in either stressed or control rats following induction of an inflammatory response. Topics: Animals; Capillary Permeability; Cell Movement; Glycogen; Hematocrit; Humans; Inflammation; Leukocyte Count; Leukocytes; Male; Peritoneal Cavity; Rats; Stress, Psychological | 1981 |
Nonantibiotic effects of macrolide antibiotics of the oleandomycin-erythromycin group with special reference to their "steroid-sparing" effects.
Certain macrolide antibiotics, such as troleandomycin (TAO), oleandomycin, and erythromycin estolate (Ilosone), can lower the maintenance dose of glucocorticoids required by severely asthmatic patients. These effects were postulated to be caused by an as yet undefined steroid-sparing effect. In this study, TAO in combination with methylprednisolone, when compared with methylprednisolone alone, was demonstrated to significantly increase liver glycogen deposition in adrenalectomized mice, intact mice, and adrenalectomized rats; protect histamine-sensitized mice following beta adrenergic blockade or adrenalectomy; further decrease the steroid-lowered glucose tolerance of mice and significantly increase the plasma corticosteroid levels in rats. TAO alone did not have these effects. TAO plus betamethasone, and erythromycin estolate plus methylprednisolone also increased liver glycogen deposition. However, TAO did not appear to potentiate the effects of hydrocortisone. Erythromycin stearate and to a lesser degree erythromycin ethylsuccinate when combined with methylprednisolone also decreased histamine lethality in mice. Leucomycin and tetracycline did not enhance the effects of methylprednisolone. TAO, alone or with methylprednisolone, did not alter serum glutamic oxaloacetic transaminase (SGOT) levels in rats. Thus, TAO and some other macrolides did not exert their effects on corticosteroids as antimicrobial agents, adrenocorticotropic hormone (ACTH)--like compounds, or quasisteroids, but as steroid-sparing agents by some undefined mechanism. Topics: Anaphylaxis; Animals; Aspartate Aminotransferases; Carrageenan; Epinephrine; Erythromycin; Erythromycin Estolate; Female; Glucose Tolerance Test; Glycogen; Guinea Pigs; Histamine; Hydrocortisone; Inflammation; Liver; Methylprednisolone; Mice; Rats; Steroids; Troleandomycin | 1980 |
Secretion of a hyperemia-inducing moiety by mitogen or glycogen stimulated mononuclear inflammatory cells of sheep and rabbit.
A nonlymphokine mediator of hyperemia has been shown to be secreted by both rabbit peritoneal exudate cells stimulated with 5% glycogen and by concanavalin A treated cells from afferent lymph of sheep. This mediator is not stored in an active form in cells, but is either activated or synthesized de novo in response to antigenic or mitogenic stimuli. Secretion of the mediator is inhibited by culturing cells in the presence of dexamethasone but not indomethacin. However, expression of the activity is inhibited by pretreatment of the assay animals with indomethacin, suggesting a two-step induction of hyperemia. A similar mediator was found to be secreted by sheep and rabbit alveolar lavage cells, and rat peritoneal exudate cells. The presence of this hyperemia-inducing activity from diverse species suggests a fundamental role in controlling blood flow. Alteration of blood flow may modulate delivery of blood-borne cells and factors to sites of chronic inflammation. Topics: Animals; Cells, Cultured; Concanavalin A; Culture Media; Dexamethasone; Female; Glycogen; Guinea Pigs; Hyperemia; Indomethacin; Inflammation; Injections, Intradermal; Kinetics; Lung; Mice; Mitogens; Phagocytes; Rabbits; Rats; Sheep; Sonication; Therapeutic Irrigation; Time Factors | 1980 |
Investigation of an inflammatory humoral factor as a stimulator of fibrinogen synthesis.
Topics: Animals; Blood Transfusion; Cell Extracts; Fibrinogen; Glycogen; Inflammation; Leukocytes; Lysine; Male; Plasma; Rabbits; Serum Albumin | 1979 |
Reduction in inflammatory response by prior injection of a different agent at the same site: an experimental study in the rat.
Glycogen, producing a weak PMN response, and BHI/PP, which induces a strong response, have been injected both separately and sequentially into the peritoneal cavity of the rat. It was found that the first stimulus, glycogen, had a modifying effect on the response to the second stimulus, which was reduced. Changes in the number of PMNs in the peritoneal cavity were found to correspond to PMN count changes in the blood, which were monitored simultaneously. This suggests the possibility that the number of PMNs in an exudate is dependent on blood PMN numbers. The point at which the modifying mechanism has its effect remains to be demonstrated, and an assessment of the importance of the changes in blood counts is crucial in locating the point at which the two stimuli interact. Topics: Animals; Antigens; Ascitic Fluid; Glycogen; Inflammation; Leukocyte Count; Male; Neutrophils; Rats; Time Factors | 1978 |
Pulmonary carcinoma (Jaagsiekte) of sheep. Ultrastructural study of early and advanced tumor lesions.
Lung carcinoma of sheep (Jaagsiekte) is a bronchiolar-alveolar cell carcinoma. Differences in the ultrastructural patterns of early and advanced lesions of the disease are described. A-type and C-type viruses were observed in advanced tumors and were absent in early lesions. Numerous microtubules were characteristic in the epithelial tumor cells of the early lesions and were absent in the advanced tumor. In comparison to the early lesions, extensive cytosome production, surfactant secretion, and glycogen accumulation were observed in the advanced tumor. The immune response to the early tumor lesion was restricted to the peribronchiolar lymph aggregates, while in the advanced stages of the disease the systemic immune response was markedly increased. Topics: Adenocarcinoma, Bronchiolo-Alveolar; Animals; Cytoplasmic Granules; Glycogen; Inflammation; Lung Neoplasms; Neoplasm Metastasis; Oncogenic Viruses; Retroviridae; Sheep; Sheep Diseases | 1977 |
Effect of cyclophosphamide on delayed hypersensitivity to Staphylococcus aureus in mice.
Mice given cyclophosphamide 2-3 days before a single subcutaneous infection with Staphylococcus aures on cotton dust develop much more delayed type hypersensitivity (DTH) than normal. The enhancement is due to removal of rapidly dividing cells from the spleen. Passive transfer experiments before infection or before challenge show that immune serum suppresses the induction but not the expression but do not prevent induction. There may therefore be 2 suppressor or regulating systems involved. Cell commitment to suppressor function may be self-limiting. The results explain why DTH to staphylococci is only fully established after repeated infections and support the view that the suppressor system may function as a check on the excessive and potentially harmful development of DTH. Topics: Animals; Cyclophosphamide; Elapid Venoms; Female; Glycogen; Hypersensitivity, Delayed; Immunity; Immunization, Passive; Inflammation; Mice; Mice, Inbred BALB C; Spleen; Splenectomy; Staphylococcus aureus; Time Factors | 1977 |
Changes in the concentration of leucocytes and platelets in the peripheral blood during sterile inflammation in rabbits.
Glycogen in isotonic saline was infused into the peritoneal cavities of rabbits to produce sterile inflammation. This caused a small increase in the haematocrit value and larger decreases in the concentrations of circulation leucocytes and platelets. Circulating granulocytes decreased by about 40% in 2 h and increased in the next 2 h to about 4 times their initial concentration. Acetyl salicyclic acid (ASA) (10 mg/kg) infused with the glycogen did not affect the decrease significantly but accelerated the subsequent increase. Circulating mononuclear leucocytes, mostly lymphocytes, decreased progressively by about 75% after 4-5 h. This decrease was not affected by ASA. Circulating platelets decreased by about 30% in the first hour; this decrease was accelerated and augmented by ASA. Subsequently the platelet concentrations remained constant for at least 4-5 h. Glycogen so infused is known to activate complement, and ASA to inhibit prostaglandin synthetase. Therefore the results suggest that (i) the initial decrease in circulating granulocytes is mediated by activated complement; (ii) the emigration of granulocytes from blood into the inflammatory exudate is increased by prostaglandins; (iii) the initial decrease in circulating platelets is mediated by activated complement and antagonized by prostaglandins; and (iv) the decrease in circulating lymphocytes is mediated by activated complement and uninfluenced by prostaglandins. Topics: Animals; Aspirin; Blood Cell Count; Blood Platelets; Glycogen; Inflammation; Leukocyte Count; Leukocytes; Male; Peritoneal Cavity; Prostaglandins; Rabbits | 1977 |
Glycogen metabolism in inflammatory macrophages.
Topics: Animals; Glucosidases; Glycogen; Glycogen Synthase; Hydrogen-Ion Concentration; Inflammation; Lysosomes; Macrophages; Male; Neutrophils; Phosphorylases; Rats | 1976 |
[Bioptic changes in juvenile diabetes mellitus].
Topics: Adolescent; Biopsy; Child; Child, Preschool; Diabetes Mellitus, Type 1; Female; Glycogen; Hepatomegaly; Humans; Inflammation; Liver; Male | 1976 |
Ultrastructural studies on the endometrium of women wearing TCu-200 intrauterine devices by means of transmission and scanning electron microscopy and x-ray dispersive analysis.
Endometrial biopsies obtained from 12 young women wearing TCu-200 intrauterine contraceptive devices from six to 12 months were studied by means of transmission and scanning electron microscopes as well as with the use of rubeanic acid stains and x-ray dispersive analysis. Six biopsies were taken at Day 10 and six were taken at Day 20 of the menstrual cycle. The aim was to investigate epithelial and stromal changes possibly related to copper deposition. The main changes were located in the cell organelles at Day 10 of the cycle. The mitochondria disclosed vacuolization of the matrix and myelin figure formation in 70 to 80% of the epithelial cells. There were also increased numbers of lysosomes. There were similar alterations of secretory endometrium in only a few cases. Instead, there was an increased number of mitochondria, and most of them were dividing. Rubeanic acid stains as well as energy-dispersive x-ray analysis failed to reveal significant amounts of copper in the various cell organelles studied. The above observations seem to indicate that there is a definite alteration of the mitochondria of epithelial cells which may result in impairment of respiratory mechanisms and energy production, rendering the endometrial environment inhospitable to the fertilized egg. These changes are thought to be reversible. The absence of copper is explained on the basis of a rapid turnover of the endometrium or to a problem in sampling common to this methodology. Topics: Cilia; Copper; Endometrium; Epithelium; Female; Glycogen; Golgi Apparatus; Histocytochemistry; Humans; Inflammation; Intrauterine Devices; Microscopy, Electron, Scanning; Mitochondria; Mitochondrial Swelling; Vacuoles; X-Rays | 1976 |
Observations on phagocytosis of urate crystals by polymorphonuclear leucocytes.
The sequence of events that may initiate the inflammatory reaction in acute gout has been investigated with specific reference to phagocytosis of urate crystals by polymorphonuclear leucocytes and the results have shown (1) that neutrophil leucocytes avidly ingest microcrystals of sodium monourate, (2) that this causes the rapid degranulation and disintegration of the leucocytes, (3) that fresh leucocytes ingest the debris and crystals liberated by the dead cells, and in their turn degranulate and die, thus possibly establishing a vicious circle in the system. Topics: Animals; Cell Nucleus; Cells, Cultured; Glycogen; Humans; Inflammation; Leukocytes; Microscopy, Electron; Microscopy, Fluorescence; Microscopy, Phase-Contrast; Motion Pictures; Neutrophils; Phagocytosis; Pseudopodia; Rabbits; Staining and Labeling; Uric Acid | 1975 |
Cytochemical study of exfoliated cells of oral mucosa. I. The glycogen deposition and keratinization.
Cytochemical studies of glycogen of oral mucosa cells have been made on the smears by freeze-drying and PAS staining. The specimens were obtained from different areas of oral cavity of 77 human subjects and an attempt was made to find some interrelation amoung glycogen deposition, keratinization and inflammation. The largest glycogen deposition was found in the mucosa cells from mouth floor and cheek, a little in those from gingiva and quite a small or no glycogen in those from mucosa of hard palate and tongue. In gingiva the cells showing much more keratinization were less in glycogen contents, and vice versa. In inflammation some increase in glycogen contents were found in the gingivitis and the highest glycogen content in the cases of denture irritation of the palate as far as the present observation is concerned. Topics: Adolescent; Adult; Aged; Cheek; Denture, Complete; Female; Gingiva; Gingivitis; Glycogen; Humans; Inflammation; Keratins; Male; Middle Aged; Mouth Diseases; Mouth Floor; Mouth Mucosa; Palate; Stomatitis, Aphthous; Tongue | 1975 |
Studies in myoclonus epilepsy. (Lafora body form). IV. Skeletal muscle abnormalities.
Topics: Adult; Amylases; Biopsy; Cytoplasmic Granules; Diagnosis, Differential; Epilepsy; Glycogen; Humans; Inflammation; Male; Microscopy, Electron; Muscles; Myoclonus; NADH, NADPH Oxidoreductases; Staining and Labeling; Tetrazolium Salts | 1974 |
Leucocyte glycogen response in inflammatory exudates.
Topics: Animals; Carbon Radioisotopes; Caseins; Exudates and Transudates; Gluconeogenesis; Glucose; Glycogen; Glycogen Synthase; Guinea Pigs; Inflammation; Injections, Intraperitoneal; Kinetics; Leukocytes; Phosphorylases | 1974 |
Glycogen metabolism in macrophages: effect of exogenous glycogen on glucogenesis in inflammatory exudate leukocytes and macrophages.
Topics: Animals; Bucladesine; Cell Nucleus; Cyclic AMP; Dextrans; Exudates and Transudates; Fluorides; Glucose; Glycogen; Glycosides; Hydrogen-Ion Concentration; Inflammation; Leukocytes; Macrophages; Male; Molecular Weight; Peritoneal Cavity; Phagocytosis; Rats; Sodium | 1974 |
Sequestration of macrophages in growing tumours and its effect on the immunological capacity of the host.
The effects of rat tumours of various macrophage contents on the syngeneic host's ability to produce either: (1) an inflammatory exudate in response to intraperitoneal oyster glycogen or (2) a cutaneous delayed hypersensitivity (DHS) response to PPD or SRBC after appropriate sensitization, were studied as a function of tumour growth.Both these reactions were found to be markedly decreased as the tumours grew. The suppression was greatest in animals bearing tumours of high macrophage content. The suppression of the DHS response could be reversed by a local injection of normal peritoneal macrophages with the eliciting antigen, and lymphocytes from tumour bearing animals exhibiting poor DHS responses were able to adoptively transfer DHS reactivity to normal unsensitized recipients. The monocyte infiltration in response to oyster glycogen was also decreased, and these data indicate a monocyte, rather than a lymphocyte defect in the tumour induced "anergy" in this system. Topics: Animals; Antigen-Antibody Reactions; BCG Vaccine; Erythrocytes; Glycogen; Hypersensitivity, Delayed; Immune Tolerance; Inflammation; Macrophages; Neoplasm Transplantation; Ostreidae; Peritoneal Cavity; Rats; Sarcoma, Experimental; Sheep; Skin Tests; Transplantation, Homologous; Tuberculin | 1974 |
[Accumulation of glycogen in the neutrophilic granulocytes in experimental inflammatory reaction of the cornea].
Topics: Animals; Cattle; Cornea; Corneal Injuries; Eye Burns; Eye Diseases; Eye Injuries; Glycogen; Graft vs Host Reaction; Histocytochemistry; Inflammation; Microscopy, Electron; Neutrophils; Phagocytosis; Rabbits; Rats | 1973 |
An ultrastructural study of ovine polio-encephalomalacia.
Topics: Animals; Blood Proteins; Cerebral Cortex; Cytoplasmic Granules; Edema; Encephalomalacia; Endothelium; Extracellular Space; Glycogen; Golgi Apparatus; Histocytochemistry; Inflammation; Microscopy, Electron; Mitochondria; Nerve Degeneration; Neuroglia; Neurons; Nissl Bodies; Ribosomes; Sheep; Sheep Diseases; Thiamine | 1973 |
Ultrastructural and associated observations on clinical cases of mastitis in cattle.
Topics: Animals; Basement Membrane; Cattle; Cell Membrane; Cell Nucleus; Collagen; Connective Tissue; Cytoplasm; Cytoplasmic Granules; Endoplasmic Reticulum; Epithelium; Extracellular Space; Female; Fibrin; Glycogen; Inflammation; Leukocytes; Lipids; Mammary Glands, Animal; Mastitis, Bovine; Microscopy, Electron; Milk Proteins; Organoids; Staphylococcal Infections; Streptococcal Infections | 1973 |
[Histological studies on normal and pathological Vater's ampulla].
Topics: Age Factors; Aged; Ampulla of Vater; Cholecystitis; Cholelithiasis; Diverticulum; Endometriosis; Epispadias; Epithelial Cells; Female; Glycogen; Humans; Inflammation; Intestinal Mucosa; Male; Microscopy, Electron; Middle Aged; Sclerosis; Staining and Labeling | 1972 |
Acute changes in the central nervous system of monkeys exposed to protons.
Topics: Acute Disease; Animals; Brain; Cerebellum; Cerebral Cortex; Choroid Plexus; Glycogen; Hypertrophy; Inflammation; Macaca; Necrosis; Neuroglia; Protons; Radiation Dosage; Radiation Injuries, Experimental; Spinal Cord | 1972 |
Biological activity of complement in vivo. Role of C5 in the accumulation of polymorphonuclear leukocytes in inflammatory exudates.
The importance of C5 in the generation of complement (C)-dependent chemotactic activity in vitro is well recognized. However, the actual role C5 may play in the accumulation of polymorphonuclear leukocytes (PMN) at inflammatory sites in vivo has not been established. Injection of glycogen or endotoxin into the peritoneal cavities of guinea pigs resulted, shortly thereafter, in the local accumulation of PMN. Preceding the influx of leukocytes, the peritoneal fluid became chemotactic for rabbit PMN in vitro. The majority of this activity could be attributed to a cleavage product of C5 (C5a). Similarly, injection of endotoxin into the peritoneal cavity of C5-normal mice resulted in the generation of a chemotactic factor for mouse PMN which was followed by the accumulation of PMN in the peritoneal fluid. In contrast, injection of endotoxin into the peritoneal cavity of C5-deficient mice resulted in the generation of virtually no detectable chemotactic activity and a markedly depressed accumulation of PMN during the first 24 hr after injection. The data suggest that C5 plays an important role in the early phases of PMN accumulation in response to inflammatory stimuli. The rapid accumulation of PMN in response to an inflammatory stimulus such as bacterial endotoxin would be expected to be a major factor in host defense against proliferation and dissemination of infectious agents. Topics: Animals; Ascitic Fluid; Chemotaxis; Chromatography, Gel; Complement System Proteins; Endotoxins; Exudates and Transudates; Glycogen; Guinea Pigs; Immunologic Deficiency Syndromes; Inflammation; Kinetics; Leukocytes; Male; Mice; Rabbits | 1971 |
Glycogen in inflammatory mononuclear cells of premature and mature newborn infants.
Topics: Glycogen; Humans; Infant, Newborn; Infant, Premature; Inflammation; Monocytes | 1970 |
Glycogen in clinical leukoplakia. Distribution and fine structure in human buccal mucosa.
Topics: Cell Membrane; Cell Nucleus; Cheek; Cytoplasmic Granules; Epithelium; Glycogen; Histocytochemistry; Humans; Inflammation; Keratins; Keratosis; Leukoplakia; Leukoplakia, Oral; Lichen Planus; Microscopy, Electron; Mouth Mucosa; Mouth Neoplasms; Smoking | 1970 |
[Inflammation cells in the cornea after injection of heterogenous protein].
Topics: Albumins; Animals; Cornea; Fibroblasts; Glycogen; Inflammation; Keratitis; Leukocytes; Photomicrography; Rabbits | 1970 |
Effects of an intra-uterine foreign body (IUFB) on glycogen accumulation and lysosomal enzyme activity in rat uterus.
Topics: Acid Phosphatase; Animals; Estrus; Female; Glucuronidase; Glycogen; Inflammation; Intrauterine Devices; Leukocytes; Lysosomes; Pregnancy; Rats; Serum Albumin, Bovine; Uterus | 1969 |
Energization of lymphocytes transforming to macrophages in human inflammation.
Topics: Antigens; Diabetes Mellitus; Diphtheria Toxoid; Energy Transfer; Escherichia coli; Exudates and Transudates; Glycogen; Histiocytes; Histocytochemistry; Humans; Inflammation; Insulin; Lymphocytes; Macrophages; Monocytes; Skin; Skin Window Technique | 1968 |
[Morphological and cytochemical studies of inflammatory exudate cells and peripheral blood cells in healthy persons and leukaemic patients].
Topics: Adult; Aged; Esterases; Exudates and Transudates; Female; Glycogen; Histocytochemistry; Humans; Inflammation; Leukemia; Leukemia, Lymphoid; Leukemia, Myeloid; Leukemia, Myeloid, Acute; Leukocytes; Lipids; Male; Middle Aged; NADP; Phagocytosis; Phosphoric Monoester Hydrolases; Skin Window Technique; Succinate Dehydrogenase | 1967 |
[Changes in internal organs under combined effect (experimental study)].
Topics: Animals; Blast Injuries; Blood Vessels; Burns; Coal; Dogs; Dust; Explosions; Gastric Mucosa; Glycogen; Hemorrhage; Hemostasis; Histocytochemistry; Inflammation; Intestinal Mucosa; Kidney; Liver; Liver Circulation; Liver Glycogen; Lung; Methane; Methods; Myocardium; Pulmonary Circulation; Regeneration | 1967 |
Studies in oral leukoplakias. 10. Periodic-acid-Schiff staining of normal and leukoplakic epithelium before and after vitamin A application.
Topics: Adult; Aged; Female; Glycogen; Histocytochemistry; Humans; Inflammation; Keratins; Leukoplakia; Male; Middle Aged; Mouth Mucosa; Staining and Labeling; Vitamin A | 1966 |
[Biochemistry of inflammation. II. Concluded].
Topics: Collagen; Dentistry; Glycogen; Glycosaminoglycans; Inflammation | 1966 |
The mononuclear response to intrapleural injection in the rat.
Topics: Animals; Dextrans; Glycogen; Histamine; Inflammation; Injections; Klebsiella; Pleural Effusion; Rats | 1966 |
Human epidermal glycogen after inflammatory stimuli.
Topics: Acetylcholine; Adult; Bradykinin; Glycogen; Histamine; Histocytochemistry; Humans; Hypersensitivity, Delayed; Inflammation; Injections, Intradermal; Male; Skin; Skin Tests | 1965 |
POLYSACCHARIDE EFFECTS SIMULATING HYPERSENSITIVITY RESPONSES IN THE RABBIT.
Topics: Antigen-Antibody Reactions; Blood Coagulation; Blood Group Antigens; Chlorpheniramine; Eosinophils; Glycogen; Inflammation; Leukocyte Count; Liver; Myocardium; Pharmacology; Phenylbutazone; Physiology; Polysaccharides; Precipitins; Rabbits; Research; Spleen; Starch; Sucrose | 1964 |
Histochemical studies of leukocytes from an inflammatory exudate. Glycogen and phosphorylase.
Topics: Exudates and Transudates; Glycogen; Inflammation; Leukocytes; Phosphorylases | 1962 |
[On glycogen storage in neutrophil leukocytes in the peripheral blood in aseptic inflammations].
Topics: Glycogen; Glycogenolysis; Humans; Inflammation; Leukocytes; Neutrophils | 1961 |
The effects of some 21-methyl-substituted corticoids on inflammation, liver glycogen and electrolyte-regulating activity in the rat.
Topics: Adrenal Cortex Hormones; Animals; Electrolytes; Glycogen; Glycogenolysis; Inflammation; Liver Glycogen; Rats | 1961 |
[The influence of the glycogen level in tissue inflammations].
Topics: Glycogen; Inflammation; Muscles; Skin | 1961 |
Effects of 2-methylation on glucocorticoid activity of various C-21 steroids.
Topics: Glucocorticoids; Glycogen; Glycogenolysis; Humans; Inflammation; Methylation; Steroids | 1957 |
Effect of alterations in side chain upon anti-inflammatory and liver glycogen activities of hydrocortisone esters.
Topics: Anti-Inflammatory Agents; Esters; Glycogen; Glycogenolysis; Hydrocortisone; Inflammation; Liver; Liver Glycogen | 1957 |