glycogen and Weight-Loss

Non-alcoholic fatty liver disease (NAFLD) has emerged as the most prevalent liver disease in industrialized countries. It is regarded as the hepatic manifestation of the metabolic syndrome (MetS) resulting from insulin resistance. Moreover, insulin resistance impairs glycogen synthesis, postprandially diverting a substantial amount of carbohydrates to the liver and storing them there as fat. NAFLD has far-reaching metabolic consequences involving glucose and lipoprotein metabolism disorders and risk of cardiovascular disease, the leading cause of death worldwide. No pharmaceutical options are currently approved for the treatment of NAFLD. Exercise training and dietary interventions remain the cornerstone of NAFLD treatment. Current international guidelines state that the primary goal of nutritional therapy is to reduce energy intake to achieve a 7%-10% reduction in body weight. Meal replacement therapy (formula diets) results in more pronounced weight loss compared to conventional calorie-restricted diets. However, studies have shown that body mass index (BMI) or weight reduction is not obligatory for decreasing hepatic fat content or to restore normal liver function. Recent studies have achieved significant reductions in liver fat with eucaloric diets and without weight loss through macronutrient modifications. Based on this evidence, an integrative nutritional therapeutic concept was formulated that combines the most effective nutrition approaches termed "liver-fasting." It involves the temporary use of a low calorie diet (total meal replacement with a specific high-protein, high-soluble fiber, lower-carbohydrate formula), followed by stepwise food reintroduction that implements a Mediterranean style low-carb diet as basic nutrition.

Topics: Caloric Restriction; Diet, Carbohydrate-Restricted; Diet, Mediterranean; Exercise; Glycogen; Heart Disease Risk Factors; Humans; Insulin Resistance; Lipid Metabolism; Liver; Non-alcoholic Fatty Liver Disease; Nutrition Therapy; Nutritional Physiological Phenomena; Weight Loss

Endurance sports are increasing in popularity and athletes at all levels are looking for ways to optimize their performance by training and nutrition. For endurance exercise lasting 30 min or more, the most likely contributors to fatigue are dehydration and carbohydrate depletion, whereas gastrointestinal problems, hyperthermia, and hyponatraemia can reduce endurance exercise performance and are potentially health threatening, especially in longer events (>4 h). Although high muscle glycogen concentrations at the start may be beneficial for endurance exercise, this does not necessarily have to be achieved by the traditional supercompensation protocol. An individualized nutritional strategy can be developed that aims to deliver carbohydrate to the working muscle at a rate that is dependent on the absolute exercise intensity as well as the duration of the event. Endurance athletes should attempt to minimize dehydration and limit body mass losses through sweating to 2-3% of body mass. Gastrointestinal problems occur frequently, especially in long-distance races. Problems seem to be highly individual and perhaps genetically determined but may also be related to the intake of highly concentrated carbohydrate solutions, hyperosmotic drinks, as well as the intake of fibre, fat, and protein. Hyponatraemia has occasionally been reported, especially among slower competitors with very high intakes of water or other low sodium drinks. Here I provide a comprehensive overview of recent research findings and suggest several new guidelines for the endurance athlete on the basis of this. These guidelines are more detailed and allow a more individualized approach.

Topics: Athletic Performance; Dehydration; Diet; Dietary Carbohydrates; Energy Intake; Fatigue; Gastrointestinal Diseases; Glycogen; Guidelines as Topic; Humans; Muscle Fatigue; Muscle, Skeletal; Nutritional Requirements; Nutritional Status; Physical Endurance; Sports; Sweat; Sweating; Weight Loss

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

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

The present study investigated the effects of three consecutive days of endurance training under conditions of low energy availability (LEA) on the muscle glycogen content, muscle damage markers, endocrine regulation, and endurance capacity in male runners.. Seven male long-distance runners (19.9 ± 1.1 yr, 175.6 ± 4.7 cm, 61.4 ± 5.3 kg, maximal oxygen uptake [V˙O2max]: 67.5 ± 4.3 mL·kg·min) completed two trials consisting of three consecutive days of endurance training under LEA (18.9 ± 1.9 kcal·kg FFM·d) or normal energy availability (NEA) (52.9 ± 5.0 kcal·kg FFM·d). The order of the two trials was randomized, with a 2-wk interval between trials. The endurance training consisted of 75 min of treadmill running at 70% of V˙O2max. Muscle glycogen content, respiratory gas variables, and blood and urine variables were measured in the morning for three consecutive days of training (days 1-3) and on the following morning after training (day 4). As an indication of endurance capacity, time to exhaustion at 19.0 ± 0.8 km·h to elicit 90% of V˙O2max was evaluated on day 4.. During the training period, body weight, fat-free mass, and skeletal muscle volume were significantly reduced in LEA (P = 0.02 for body weight and skeletal muscle volume, P = 0.01 for fat-free mass). Additionally, muscle glycogen content was significantly reduced in LEA (~30%, P < 0.001), with significantly lower values than those in NEA (P < 0.001). Time to exhaustion was not significantly different between the two trials (~20 min, P = 0.39).. Three consecutive days of endurance training under LEA decreased muscle glycogen content with lowered body weight. However, endurance capacity was not significantly impaired.

Topics: Blood Glucose; Body Mass Index; Cross-Over Studies; Energy Intake; Energy Metabolism; Glycogen; Heart Rate; Humans; Insulin-Like Growth Factor I; Lactic Acid; Male; Muscle, Skeletal; Oxygen Consumption; Physical Conditioning, Human; Physical Endurance; Respiratory Mechanics; Running; Testosterone; Weight Loss; Young Adult

The effects of adaptation to a high-fat diet on endurance performance are equivocal, and there is little data regarding the effects on high-intensity exercise performance. This study examined the effects of a high-fat/moderate protein diet on submaximal, maximal, and supramaximal performance. Twenty non-highly trained men were assigned to either a high-fat/moderate protein (HFMP; 61% fat diet) (n = 12) or a control (C; 25% fat) group (n = 8). A maximal oxygen consumption test, two 30-s Wingate anaerobic tests, and a 45-min timed ride were performed before and after 6 weeks of diet and training. Body mass decreased significantly (-2.2 kg; p < or = .05) in HFMP subjects. Maximal oxygen consumption significantly decreased in the HFMP group (3.5 +/- 0.14 to 3.27 +/- 0.09 L x min(-1)) but was unaffected when corrected for body mass. Perceived exertion was significantly higher during this test in the HFMP group. Main time effects indicated that peak and mean power decreased significantly during bout 1 of the Wingate sprints in the HFMP (-10 and -20%, respectively) group but not the C (-8 and -16%, respectively) group. Only peak power was lower during bout 1 in the HFMP group when corrected for body mass. Despite significantly reduced RER values in the HFMP group during the 45-min cycling bout, work output was significantly decreased (-18%). Adaptation to a 6-week HFMP diet in non-highly trained men resulted in increased fat oxidation during exercise and small decrements in peak power output and endurance performance. These deleterious effects on exercise performance may be accounted for in part by a reduction in body mass and/or increased ratings of perceived exertion.

Topics: Adaptation, Physiological; Adult; Carbohydrate Metabolism; Carbohydrates; Dietary Fats; Glycogen; Humans; Male; Middle Aged; Muscle, Skeletal; Oxidation-Reduction; Oxygen Consumption; Physical Endurance; Weight Loss

Well-trained subjects (n = 6) were studied before and after losing a mean 3.0%-4.3% of body mass to determine whether muscle performance could be maintained or even enhanced by dietary creatine supplementation. During a 5-day period of loss of mass the subjects were randomly assigned to a creatine or placebo supplemented diet. All the subjects were measured before and after loss of mass on both supplements for isokinetic peak torque (PT) and work at peak torque (W(PT)) of knee extensors, also for intermittent high intensity working capacity of the same muscle group. The latter test consisted of submaximal isokinetic knee extensions at an angular velocity of 1.57 rad x s(-1) for 45 s at the rate of 30 contractions each min (submaximal work, Ws max) followed by 15-s maximal effort (maximal work, Wmax). Total duration of the test was 3 min. Haematocrit was measured and haemoglobin, ammonia, lactate, glucose and urea concentrations were analysed in blood samples obtained at rest and after cessation of muscle performance tests. The results indicated that creatine supplementation in comparison with placebo treatment during rapid body mass reduction may help to maintain muscle PT and W(PT)1 at high angular velocities, not influencing Wmax and the rate of fatigue development during Wmax, but affecting adversely Ws max. Within the limitations of the present study the reasons for the partially detrimental effect of creatine administration remain obscure, but it is suggested that impaired creatine uptake in muscle during body mass loss as well as creatine induced changes in muscle glucose and glycogen metabolism may be involved.

Topics: Adult; Ammonia; Biomechanical Phenomena; Creatine; Dietary Supplements; Glucose; Glycogen; Humans; Lactic Acid; Male; Muscle Fatigue; Muscle, Skeletal; Physical Exertion; Placebos; Plasma Volume; Weight Loss

To examine the effect of energy restriction and wrestling on muscle glycogen content in highly-trained male wrestlers.. Randomized, unblinded intervention trial.. McMaster University Nutrition and Metabolism Research Laboratory.. Twelve highly trained male wrestlers volunteered as subjects and were randomly assigned to one of two groups (Group A, n = 6; Group B, n = 6) as defined below.. All subjects were free of medical conditions that would preclude participation in the study and all had performed rapid weight loss at least three times/year with no medical complications.. Group A: simulated wrestling tournament, four 5-min wrestling bouts ( > 7 h) following a 5% body weight loss and 17 h repletion period; Group B: 5% weight loss through energy restriction (1,141 kcal/day), exercise, fluid restriction, and dehydration methods (sauna) > 72 h.. Group A: muscle glycogen content before and after wrestling tournament and plasma lactate after each bout; Group B: muscle glycogen before and after weight loss.. Group A: no significant effect on muscle glycogen concentration, yet large increases were observed in blood lactate concentrations (up to 14.7 mmol/L); Group B: weight loss resulted in a 54% (p < 0.018) reduction in muscle glycogen concentration.. The weight loss methods commonly performed by wrestlers resulted in large decreases in muscle glycogen concentration that were largely reversed during the 17-h repletion period between weigh-in and the start of the competition; participation in a wrestling tournament did not have a significant impact upon biceps brachii glycogen concentration when ad libitum feeding is allowed between matches.

Topics: Adult; Analysis of Variance; Biopsy; Glycogen; Humans; Lactates; Male; Muscle, Skeletal; Weight Loss; Wrestling

The aim of this study was to examine the effect of carbohydrate (CHO) ingestion on glycogen degradation in type I and type II muscle fibers during prolonged running by using a quantitative biochemical method. To this end, eight male subjects ran at 70% maximal oxygen uptake to exhaustion on a motorized treadmill on two occasions, 1 wk apart. On each occasion, the subjects ingested 8 ml/kg body wt of either placebo (Pl) or a 5.5% CHO-electrolyte solution (CHO-E) immediately before the start of the run and 2 ml/kg body wt every 20 min thereafter. Needle biopsy samples were obtained from the vastus lateralis muscle before and after each trial and also at the time coinciding with Pl exhaustion in the CHO-E trial. Running time to exhaustion was longer (P < 0.01) in the CHO-E trial compared with the Pl trial (132.4 +/- 12.3 and 104.3 +/- 8.6 min, respectively). A 25% reduction in glycogen utilization in type I fibers only was observed in the CHO-E trial compared with the Pl trial (215.2 +/- 27.5 vs. 285.4 +/- 30.1 mmol/kg dry wt; P < 0.01). Furthermore, in the CHO-E trial, in contrast to the Pl trial, both muscle ATP and phosphocreatine concentrations were well maintained throughout exercise. Therefore, because in both the Pl and CHO-E trials the type I fibers were glycogen depleted at the point of exhaustion (31.6 +/- 10.3 and 28.1 +/- 7.1 mmol/kg dry wt, respectively), it is proposed that CHO ingestion improved endurance capacity by contributing to oxidative ATP production specifically in type I fibers and by doing so delayed the development of glycogen depletion in this fiber type.

Topics: Adult; Anaerobic Threshold; Blood Glucose; Dietary Carbohydrates; Drinking; Exercise; Glycogen; Heart Rate; Humans; Insulin; Lactic Acid; Lipids; Male; Muscle Fatigue; Muscle Fibers, Fast-Twitch; Muscle Fibers, Slow-Twitch; Muscle, Skeletal; Oxygen Consumption; Plasma Volume; Running; Weight Loss

Roux-en-Y gastric bypass (RYGB) surgery has been shown to induce positive metabolic adaptations for individuals with severe obesity (body mass index ≥40 kg/m. To investigate the acute and chronic effects of RYGB surgery on insulin-stimulated glucose metabolism in cultured human primary myotubes derived from nondiabetic severely obese humans.. East Carolina University Bariatric Surgery Center and East Carolina Diabetes and Obesity Institute.. Primary human skeletal muscle cells were isolated from biopsies obtained from 8 women with severe obesity before, 1 month, and 7 months following RYGB surgery. Glucose metabolism, glycogen content, and insulin signal transduction were determined in differentiated myotubes.. Insulin-stimulated glycogen synthesis and glucose oxidation increased in human myotubes derived from patients with severe obesity at both 1 and 7 months post-RYGB. However, there were no alterations indicative of enhanced insulin signal transduction. At 1 month post-RYGB, muscle glycogen levels were lower (-23%) and phosphorylation of acetyl CoA carboxylase 2 (ACC2) was elevated (+16%); both returned to presurgery levels at 7 months after RYGB in myotubes derived from patients. At 7 months post-RYGB, there was an increase in peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α) protein content (+54%).. These data indicate that insulin action intrinsically improves in cultured human primary myotubes derived from nondiabetic severely obese patients following RYGB surgery; however, the cellular alterations involved appear to consist of distinct acute and chronic components.

Topics: Acute Disease; Adult; Biopsy; Cells, Cultured; Chronic Disease; Female; Follow-Up Studies; Gastric Bypass; Glucose; Glycogen; Humans; Hypoglycemic Agents; Insulin; Middle Aged; Muscle Fibers, Skeletal; Obesity, Morbid; Postoperative Period; Signal Transduction; Time Factors; Weight Loss

The impact of diet-induced weight loss and weight loss due to RYGB in patients with (T2DM, N = 16) and without (OB, N = 27) type 2 diabetes was studied.. At inclusion (A), after diet-induced weight loss (B), 4 months post-surgery (C) and 18 months post-surgery (D) body composition, hepatic glucose production (HGP), insulin-mediated glucose uptake (GIR), respiratory exchange ratio, hepatic insulin sensitivity and clearance were determined. GLUT4, intramuscular triglycerides (IMTG) and glycogen content were measured in skeletal muscle.. Weight loss was 35-40 kg, and approximately one-third of the total improvement in GIR in T2DM was observed after the diet-induced weight loss of only ~6 kg (B). Insulin clearance, visceral fat and fasting plasma insulin also improved significantly after the diet (P < 0.05). Throughout the study, HGP, GLUT4 and glycogen content did not change significantly, but IMTG decreased significantly consistent with significant increases in GIR. Metabolic flexibility and hepatic insulin sensitivity improved after RYGB.. Metabolic improvements of RYGB are present already after the diet-induced weight loss prior to surgery. GLUT4 content in skeletal muscle cannot and IMTG content can only partly explain increases in GIR after RYGB.

Topics: Adult; Blood Glucose; Diabetes Mellitus, Type 2; Diet, Reducing; Female; Gastric Bypass; Glycogen; Humans; Insulin; Insulin Resistance; Male; Obesity; Triglycerides; Weight Loss

Obesity is associated with elevated risk of heart disease. A solid understanding of the safety and potential adverse effects of high-fat, low-carbohydrate diet (HFLCD) similar to that used by humans for weight loss on the heart is crucial. High fat intake is known to promote increases in reactive oxygen species and mitochondrial damage. We hypothesized that there would be adverse effects of HFLCD on myocardial ischemia/reperfusion injury through enhancing oxidative stress injury and impairing mitochondrial biogenesis in a nongenetic, diet-induced rat model of obesity. To test the hypothesis, 250-g male Sprague-Dawley rats were fed an obesity-promoting diet for 7 weeks to induce obesity, then switched to HFLCD or a low-fat control diet for 2 weeks. Isolated hearts underwent global low flow ischemia for 60 minutes and reperfusion for 60 minutes. High-fat, low-carbohydrate diet resulted in greater weight gain and lower myocardial glycogen, plasma adiponectin, and insulin. Myocardial antioxidant gene transcript and protein expression of superoxide dismutase and catalase were reduced in HFLCD, along with increased oxidative gene NADPH oxidase-4 transcript and xanthine oxidase activity, and a 37% increase in nitrated protein (nitrotyrosine) in HFLCD hearts. The cardiac expression of key mitochondrial regulatory factors such as nuclear respiratory factor-1 and transcription factor A-mitochondrial were inhibited and myocardial mitochondrial DNA copy number decreased. The cardiac expression of adiponectin and its receptors was down-regulated in HFLCD. High-fat, low-carbohydrate diet impaired recovery of left ventricular rate-pressure product after ischemia/reperfusion and led to 3.5-fold increased injury as measured by lactate dehydrogenase release. In conclusion, HFLCD leads to increased ischemic myocardial injury and impaired recovery of function after reperfusion and was associated with attenuation of mitochondrial biogenesis and enhanced oxidative stress in obese rats. These findings may have important implications for diet selection in obese patients with ischemic heart disease.

Topics: Adiponectin; Animals; Antioxidants; Catalase; Diet, Carbohydrate-Restricted; Diet, High-Fat; DNA Copy Number Variations; DNA, Mitochondrial; Glycogen; Insulin; Male; Mitochondrial Turnover; Myocardial Reperfusion Injury; Myocardium; NADPH Oxidase 4; NADPH Oxidases; Obesity; Oxidative Stress; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Superoxide Dismutase; Tyrosine; Weight Loss; Xanthine Oxidase

Hepatic insulin resistance is the major contributor to fasting hyperglycemia in type 2 diabetes. The protein kinase Akt plays a central role in the suppression of gluconeogenesis involving forkhead box O1 (Foxo1) and peroxisome proliferator-activated receptor gamma co-activator 1 alpha (PGC-1α), and in the control of glycogen synthesis involving the glycogen synthase kinase beta (GSK3β) in the liver. It has been demonstrated that endosomal adaptor protein APPL1 interacts with Akt and blocks the association of Akt with its endogenous inhibitor, tribbles-related protein 3 (TRB3), improving the action of insulin in the liver. Here, we demonstrated that chronic exercise increased the basal levels and insulin-induced Akt serine phosphorylation in the liver of diet-induced obese mice. Endurance training was able to increase APPL1 expression and the interaction between APPL1 and Akt. Conversely, training reduced both TRB3 expression and TRB3 and Akt association. The positive effects of exercise on insulin action are reinforced by our findings that showed that trained mice presented an increase in Foxo1 phosphorylation and Foxo1/PGC-1α association, which was accompanied by a reduction in gluconeogenic gene expressions (PEPCK and G6Pase). Finally, exercised animals demonstrated increased at basal and insulin-induced GSK3β phosphorylation levels and glycogen content at 24 h after the last session of exercise. Our findings demonstrate that exercise increases insulin action, at least in part, through the enhancement of APPL1 and the reduction of TRB3 expression in the liver of obese mice, independently of weight loss.

Topics: Adaptor Proteins, Signal Transducing; Animals; Cell Cycle Proteins; Diabetes Mellitus, Type 2; Diet; Forkhead Box Protein O1; Forkhead Transcription Factors; Gluconeogenesis; Glucose-6-Phosphatase; Glycogen; Glycogen Synthase Kinase 3; Glycogen Synthase Kinase 3 beta; Insulin; Liver; Male; Mice; Mice, Obese; Obesity; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; Phosphorylation; Physical Conditioning, Animal; Physical Endurance; Protein Serine-Threonine Kinases; Proto-Oncogene Proteins c-akt; Signal Transduction; Trans-Activators; Transcription Factors; Weight Loss

This study aimed to investigate the protective and regulatory effects of silymarin (SMN) and melatonin (MEL) on streptozotocin (STZ)-induced diabetic changes in cytochrome P450 3A2 (CYP 3A2) and glutathione peroxidase (GPX) expression and antioxidant status in the liver. Male Wistar rats were divided into five groups, including: control (C), untreated diabetic animals (D), SMN-treated diabetics (S, 50 mg/kg, orally), MEL-treated diabetics (M, 10 mg/kg, i.p.), and SMN plus MEL-treated diabetics (S+M). Diabetes was induced by a single intraperitoneal injection of STZ (50 mg/kg). The blood glucose level, daily urinary volume and body weight changes were measured. After the 28 days treatment period, antioxidant status was analyzed by means of the determination of malondialdehyde (MDA) content, nitric oxide (NO) and total thiol molecules (TTM) levels in the liver. The glycogen depletion in the liver was examined by histochemical staining. The CYP 3A2 and GPX expression at mRNA level was determined using RT-PCT technique. SMN and MEL both individually or in combination prevented from diabetes-induced weight loss and lowered daily urinary volume significantly (p<0.05). None of the test compounds could lower the blood glucose level significantly (p>0.05). Both SMN and MEL could convert the diabetes induced elevated levels of MDA and NO and the diabetes-reduced TTM content to the control level. Moreover, the diabetes-up regulated CYP 3A2 and down regulated GPX, returned to normal values after SMN treatment. Histochemical and histopathological examinations revealed that the diabetes-induced glycogen-depletion and single cell necrosis markedly improved with the SMN and SMN plus MEL treatment. Our data suggest that the STZ-induced diabetes in addition of disturbing the antioxidant status, alters the expression levels of CYP 3A2 and GPX. Moreover, the SMN and SMN plus MEL treatment was able to normalize both the antioxidant status and the expression of CYP 3A2 and GPX in the liver of diabetic rats.

Topics: Animals; Antioxidants; Blood Glucose; Cytochrome P-450 CYP3A; Diabetes Mellitus, Experimental; Drug Therapy, Combination; Glutathione Peroxidase; Glycogen; Liver; Male; Malondialdehyde; Melatonin; Necrosis; Nitric Oxide; Phytotherapy; Plant Extracts; Rats; Rats, Wistar; RNA, Messenger; Silybum marianum; Silymarin; Sulfhydryl Compounds; Urination; Weight Loss

The fruit extracts of Citrus aurantium (bitter orange) are traditionally used as weight-loss products and as appetite supressants. An important fruit component is p-synephrine, which is structurally similar to the adrenergic agents. Weight-loss and adrenergic actions are always related to metabolic changes and this work was designed to investigate a possible action of the C. aurantium extract on liver metabolism. The isolated perfused rat liver was used to measure catabolic and anabolic pathways, including oxygen uptake and perfusion pressure. The C. aurantium extract and p-synephrine increased glycogenolysis, glycolysis, oxygen uptake and perfusion pressure. These changes were partly sensitive to α- and β-adrenergic antagonists. p-Synephrine (200 μM) produced an increase in glucose output that was only 15% smaller than the increment caused by the extract containing 196 μM p-synephrine. At low concentrations the C. aurantium extract tended to increase gluconeogenesis, but at high concentrations it was inhibitory, opposite to what happened with p-synephrine. The action of the C. aurantium extract on liver metabolism is similar to the well known actions of adrenergic agents and can be partly attributed to its content in p-synephrine. Many of these actions are catabolic and compatible with the weight-loss effects usually attributed to C. aurantium.

Topics: Adrenergic alpha-Antagonists; Adrenergic beta-Antagonists; Animals; Citrus; Dietary Supplements; Fruit; Glycogen; Glycogenolysis; Glycolysis; Liver; Organ Culture Techniques; Oxygen Consumption; Perfusion; Plant Extracts; Rats; Synephrine; Weight Loss

The metabolic syndrome has reached epidemic proportions worldwide, but currently there is a lack of effective therapies for this multifactorial endocrine disease. TCM (traditional Chinese medicine) has been utilized to treat a wide variety of diseases for centuries in the People's Republic of China, subsequently becoming a promising source for the development of new therapeutic agents. Chinese medicinal herbs Gynostemma pentaphyllum, Coptis chinensis and Salvia miltiorrhiza have been shown to have anti-atherosclerotic and antidiabetic properties. In this study, we have investigated the metabolic effects of a mixture of these three herbal extracts (SK0506) in a rodent model of the metabolic syndrome induced by an HFD (high-fat diet). SD (Sprague-Dawley) rats that were fed on an HFD for 4 weeks gained 33% more weight compared with chow-fed rats (P<0.05). Four weeks treatment with SK0506 prevented weight gain with decreased visceral fat (P<0.01 compared with vehicle treatment). SK0506 also significantly reduced plasma triacylglycerols (triglycerides), NEFAs (non-esterified fatty acids) and cholesterol. SK0506 exerted similar effects to RSG (rosiglitazone) on impaired glucose intolerance. SK0506 also significantly enhanced glucose uptake and glycogen synthesis in adipose tissue during hyperinsulinaemic-euglycaemic clamp. Western blotting analysis revealed that SK0506 enhanced GLUT4 (glucose transporter 4) expression in adipose tissue, and RSG markedly up-regulated GLUT4 translocation in skeletal muscle. Overall, the present study has discovered that SK0506 can reverse several components of the metabolic syndrome primarily through acting on hyperlipidaemia and visceral obesity. The results from the present study suggest that it is worthwhile to conduct a randomized clinical trial to confirm the potential that SK0506 may be a new oral agent for treating the metabolic syndrome and preventing Type 2 diabetes.

Topics: Adipose Tissue; Animals; Blood Glucose; Drug Evaluation, Preclinical; Drugs, Chinese Herbal; Glucose Clamp Technique; Glucose Tolerance Test; Glucose Transporter Type 4; Glycogen; Insulin; Lipids; Male; Metabolic Syndrome; Muscle, Skeletal; Phytotherapy; Rats; Rats, Sprague-Dawley; Translocation, Genetic; Weight Loss

The inedible bottom part of asparagus (Asparagus officinalis L.) spears, around one-third to one-half of the total length, is always discarded as by-product. Since it still contains various bioactive substances, this by-product might have potential usage in food supplements for its therapeutic effects. In this study the hypoglycaemic effect of the aqueous extract of asparagus by-product (AEA) was evaluated in a streptozotocin (STZ)-induced diabetic rat model.. Continuous administration of AEA for 21 days significantly decreased fasting serum glucose and triglyceride levels but markedly increased body weight and hepatic glycogen level in diabetic rats. In an oral glucose tolerance test, both the blood glucose level measured at 30, 60 and 120 min after glucose loading and the area under the glucose curve showed a significant decrease after AEA treatment.. The results of this study demonstrate that AEA has hypoglycaemic and hypotriglyceridaemic functions, suggesting that it might be useful in preventing diabetic complications associated with hyperglycaemia and hyperlipidaemia.

Topics: Animals; Asparagus Plant; Diabetes Mellitus, Type 1; Dietary Supplements; Food-Processing Industry; Glucose Intolerance; Glycogen; Hypertriglyceridemia; Hypoglycemia; Hypoglycemic Agents; Industrial Waste; Liver; Male; Plant Extracts; Plant Stems; Random Allocation; Rats; Rats, Sprague-Dawley; Streptozocin; Weight Loss

We examined the physiological mechanisms by which cannabinoid receptor 1 (CB1) antagonism improves glucose metabolism and insulin sensitivity independent of its anorectic and weight-reducing effects, as well as the effects of CB1 antagonism on brown adipose tissue (BAT) function.. Three groups of diet-induced obese mice received for 1 month: vehicle; the selective CB1 antagonist SR141716; or vehicle/pair-feeding. After measurements of body composition and energy expenditure, mice underwent euglycaemic-hyperinsulinaemic clamp studies to assess in vivo insulin action. In separate cohorts, we assessed insulin action in weight-reduced mice with diet-induced obesity (DIO), and the effect of CB1 antagonism on BAT thermogenesis. Surgical denervation of interscapular BAT (iBAT) was carried out in order to study the requirement for the sympathetic nervous system in mediating the effects of CB1 antagonism on BAT function.. Weight loss associated with chronic CB1 antagonism was accompanied by increased energy expenditure, enhanced insulin-stimulated glucose utilisation, and marked activation of BAT thermogenesis. Insulin-dependent glucose uptake was significantly increased in white adipose tissue and BAT, whereas glycogen synthesis was increased in liver, fat and muscle. Despite marked weight loss in the mice, SR141716 treatment did not improve insulin-mediated suppression of hepatic glucose production nor increase skeletal muscle glucose uptake. Denervation of iBAT blunted the effect of SR141716 on iBAT differentiation and insulin-mediated glucose uptake.. Chronic CB1 antagonism markedly enhances insulin-mediated glucose utilisation in DIO mice, independent of its anorectic and weight-reducing effects. The potent effect on insulin-stimulated BAT glucose uptake reveals a novel role for CB1 receptors as regulators of glucose metabolism.

Topics: Adipose Tissue, Brown; Animals; Body Composition; Diet, High-Fat; Energy Metabolism; Gluconeogenesis; Glucose; Glycogen; Insulin; Liver; Male; Mice; Mice, Inbred C57BL; Mice, Obese; Muscle, Skeletal; Piperidines; Pyrazoles; Receptor, Cannabinoid, CB1; Rimonabant; Thermogenesis; Weight Loss

The adaptability/plasticity of the highly oxidative red muscle in Atlantic salmon was demonstrated during spawning migration. Substrate concentrations and the enzymatic pathways of ATP production were examined in red muscle obtained from Atlantic salmon at different sites along their migratory route in the Exploits River, Newfoundland, Canada. Individuals were chronologically sampled from a seawater site, two sites upstream, and at spawning. The 20% decrease in salmon body weight during the later stages of migration was accompanied by large decreases (mg dry weight(-1)) in both glycogen (P < 0.01) and total muscle lipid (P < 0.01). In contrast, water content and protein concentration (mg dry weight(-1)) of the red muscle increased by 25 and 34%, respectively, at spawning. Enzymes of the glycolytic pathways demonstrated a significant (P < 0.001) decrease in maximal activity as migration proceeded whereas enzymes of the oxidative phosphorylation pathways, specifically the citric acid cycle enzymes, exhibited an increase (P < 0.001) in maximal activity at spawning. The antioxidant enzyme superoxide dismutase also demonstrated an increase (P < 0.001) in maximal activity during the latter stages of migration. These adaptations imply that the red epaxial muscle of Atlantic salmon has a more efficient means of oxidizing lipids, while minimizing free radical damage, during the later stages of migration and spawning, thereby potentially increasing post spawning survival.

Topics: Adenosine Triphosphate; Analysis of Variance; Animal Migration; Animals; Body Water; Energy Metabolism; Glycogen; Lipid Metabolism; Muscle, Skeletal; Newfoundland and Labrador; Rivers; Salmo salar; Sexual Behavior, Animal; Spectrophotometry, Ultraviolet; Superoxide Dismutase; Weight Loss

Reduced oxidative capacity of skeletal muscle has been proposed to lead to accumulation of intramyocellular triglyceride (IMTG) and insulin resistance. We have measured mitochondrial respiration before and after a 10% low-calorie-induced weight loss in young obese women to examine the relationship between mitochondrial function, IMTG, and insulin resistance. Nine obese women (age, 32.3 years [SD, 3.0]; body mass index, 33.4 kg/m(2) [SD, 2.6]) completed a 53-day (SE, 3.8) very low calorie diet (VLCD) of 500 to 600 kcal/d without altering physical activity. The target of the intervention was a 10% weight loss; and measurements of mitochondrial respiration, IMTG, respiratory exchange ratio, citrate synthase activity, mitochondrial DNA copy number, plasma insulin, 2-hour oral glucose tolerance test, and free fatty acids were performed before and after weight loss. Mitochondrial respiration was measured in permeabilized muscle fibers using high-resolution respirometry. Average weight loss was 11.5% (P < .05), but the levels of IMTG remained unchanged. Fasting plasma glucose, plasma insulin homeostasis model assessment of insulin resistance, and insulin sensitivity index (composite) obtained during 2-hour oral glucose tolerance test improved significantly. Mitochondrial respiration per milligram tissue decreased by approximately 25% (P < .05), but citrate synthase activity and mitochondrial DNA copy number remained unchanged. Respiratory exchange ratio decreased from 0.87 (SE, 0.01) to 0.79 (SE, 0.02) (P < .05) as a sign of increased whole-body fat oxidation. Markers of insulin sensitivity improved after the very low calorie diet; but mitochondrial function decreased, and IMTG remained unchanged. Our results do not support a direct relationship between mitochondrial function and insulin resistance in young obese women and do not support a direct relationship between IMTG and insulin sensitivity in young obese women during weight loss.

Topics: Adult; Biomarkers; Blood Glucose; Caloric Restriction; Cell Respiration; Citrate (si)-Synthase; DNA, Mitochondrial; Fatty Acids, Nonesterified; Female; Glucose Tolerance Test; Glycogen; Humans; Insulin; Insulin Resistance; Ion Channels; Mitochondria, Muscle; Mitochondrial Proteins; Muscle, Skeletal; Obesity; Triglycerides; Uncoupling Protein 3; Weight Loss

The European polecat (Mustela putorius) is a naturally lean carnivore prone to excessive weight gain in captivity. This study assessed its suitability to investigate the natural history of the obese phenotype displayed in overweight humans, domestic animals, and seasonally obese wild mammals. Ten farm-bred polecats were subjected to a 5-day fast with 10 controls. Obesity (40% body fat) was associated with an unfavorable plasma lipid profile and high glucose and insulin concentrations. The polecats were in phase II of fasting with normoglycemia, low liver carbohydrate stores, and decreased plasma concentrations of urea and most amino acids. Although the plasma nonesterified fatty acid (NEFA) levels were elevated, the adipose tissue lipase activities suggested a blunted lipolytic response. Lipid mobilization was more efficient from intraabdominal fat. The animals developed hepatic lipidosis with elevated NEFA influx into the liver and losses of n-3 polyunsaturated fatty acids and arginine as hypothetical etiological factors. The plasma leptin, insulin, and triiodothyronine levels decreased but were not accompanied by reduced sex steroid or increased stress hormone concentrations. The blunted lipolytic response often encountered in obesity suggests that the organism is trying to defend the obese phenotype. Liver lipidosis and decreased insulin and triiodothyronine levels seem to be among the most consistent responses to fasting manifested in diverse mammalian orders and different levels of body fatness. The polecat could be recommended as an easily accessible carnivorean model to study the natural history of the obese phenotype and its comorbidities.

Topics: Animals; Blood Cell Count; Body Temperature; Body Weight; Cholesterol; Europe; Fasting; Female; Ferrets; Food Deprivation; Glycogen; Hormones; Lipase; Liver; Male; Nitrogen Compounds; Obesity; Organ Size; Time Factors; Triglycerides; Weight Loss

Obesity is an important risk factor for the development of type 2 diabetes, but not all obese individuals develop this complication. The clinical signs of type 2 diabetes can often be reversed with weight loss; however, it is unknown whether the skeletal muscle oxidative stress associated with type 2 diabetes remains after weight loss. We hypothesised that chronic exposure to high glucose and insulin would re-elicit impaired metabolism in primary myotubes from patients with a history of type 2 diabetes.. Obese participants with or without type 2 diabetes completed a standardised weight loss protocol, following which all participants were euglycaemic and had similar indices of insulin sensitivity. Satellite cells were isolated from muscle biopsies and differentiated under low or high glucose and insulin conditions (HGI).. Cells from participants with no history of type 2 diabetes showed robust increases in mitochondrial content, citrate synthase and cytochrome c oxidase activities when exposed to HGI. This increase in oxidative capacity was absent in cells from patients with a history of type 2 diabetes. High glucose and insulin caused increased oxidative damage in cells from the latter, despite higher superoxide dismutase expression. Cells from patients with a history of type 2 diabetes were unable to decrease mitochondrial membrane potential in response to HGI, potentially due to lower levels of uncoupling protein-3.. This is the first report to note that primary myotubes from patients with a history of type 2 diabetes are unable to adapt to a hyperglycaemic-hyperinsulinaemic challenge. We have demonstrated that impaired mitochondrial biogenesis and an inability to manage oxidative stress define a muscle phenotype at risk of obesity-associated type 2 diabetes.

Topics: Adult; Body Composition; Body Mass Index; Diabetes Complications; Diabetes Mellitus, Type 2; Female; Glucose Clamp Technique; Glycated Hemoglobin; Glycogen; Humans; Hyperinsulinism; Hypoglycemic Agents; Insulin; Ion Channels; Male; Middle Aged; Mitochondrial Proteins; Muscle Fibers, Skeletal; Muscle, Skeletal; Obesity; Oxidative Stress; Triglycerides; Uncoupling Protein 3; Weight Loss

Here, we investigated the effect of jump exercise on tumor growth, cancer cachexia, lymphocyte proliferation and macrophage function in Walker 256 tumor-bearing rats. Male Wistar rats (60 days) were divided into sedentary (C) and exercised (E) groups. Jump training consisted of six sets of 10 jumps in water with overload of 50% of body mass with 1 min of resting, four times per week for 8 weeks. After 6 weeks of training, half of each group was inoculated with 2 x 10(7) cells of Walker 256 tumor. Sedentary tumor-bearing and exercised tumor-bearing are referred to as T and TE, respectively. Tumor weight in the T group was 25 g. These animals display loss of weight, hypertriacylglycerolemia, hyperlacticidemia, depletion of glycogen stores and increase in PIF expression. Jump exercise (TE) induced a significant lower tumor weight, preserves liver glycogen stores, partly prevented the hypertriacylglycerolemia, hyperlacticidemia and, prevented the fall in body weight and reduced PIF expression. Lymphocyte was increased by tumor burden (T) and was higher by including exercise (TE). The same was observed regarding phagocytosis and lysosomal volume. Anaerobic exercise decreases tumor growth, cancer cachexia and increases innate and adaptative immune function.

Topics: Animals; Body Weight; Cachexia; Carcinoma 256, Walker; Cell Proliferation; Disease Models, Animal; Glycogen; Lactates; Lymphocytes; Macrophages; Male; Phagocytosis; Physical Conditioning, Animal; Rats; Rats, Wistar; Triglycerides; Weight Loss

The common hepatic branch of the vagus nerve negatively regulates lard intake in rats with streptozotocin (STZ)-induced, insulin-dependent diabetes. However, this branch consists of two subbranches: the hepatic branch proper, which serves the liver, and the gastroduodenal branch, which serves the distal stomach, pancreas, and duodenum. The aim of this study was to determine whether the gastroduodenal branch specifically regulates voluntary lard intake. We performed a gastroduodenal branch vagotomy (GV) on nondiabetic, STZ-diabetic, and STZ-diabetic insulin-treated groups of rats and compared them with sham-operated counterparts. All rats had high steady-state corticosterone levels to maximize lard intake. Five days after surgery, all rats were provided with the choice of chow or lard to eat for another 5 days. STZ-diabetes resulted in a reduction in lard intake that was partially rescued by either GV or insulin treatment. Patterns of white adipose tissue (WAT) deposition differed after GV- and insulin-induced lard intake, with subcutaneous WAT increasing exclusively after the former and mesenteric WAT increasing exclusively in the latter. GV also prevented the insulin-induced reduction in the STZ-elevated plasma glucagon, triglycerides, free fatty acids, and total ketone bodies but did not alter the effect of insulin-induced reduction of plasma glucose levels. These data suggest that the gastroduodenal branch of the vagus inhibits lard intake and regulates WAT deposition and plasma metabolite levels in STZ-diabetic rats.

Topics: Animals; Blood Glucose; Body Fat Distribution; Corticosterone; Diabetes Mellitus, Experimental; Dietary Fats; Eating; Fatty Acids; Gastric Inhibitory Polypeptide; Glucagon; Glycogen; Hypoglycemic Agents; Insulin; Liver; Male; Rats; Rats, Sprague-Dawley; Vagotomy; Vagus Nerve; Weight Loss

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

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

To describe the degrees of muscle-glycogen depletion and resynthesis in response to a half Ironman triathlon.. One male subject (38 years of age) completed the Grand Columbian half Ironman triathlon (1.9-km swim, 90-km bike, 21.1-km run, Coulee City, Wash). Three muscle biopsies were obtained from his right vastus lateralis (prerace, immediately postrace, and 4 hours postrace). Prerace and postrace body weight were recorded, in addition to macronutrient consumption before, during, and after the race. Energy expenditure and whole-body substrate oxidation were estimated from linear regression established from laboratory trials (watts and run pace relative to VO2 and VCO2).. Body weight decreased 3.8 kg from prerace to postrace. Estimated CHO energy expenditure was 10,003 kJ for the bike segment and 5759 kJ for the run segment of the race. The athlete consumed 308 g of exogenous CHO (liquid and gel; 1.21 g CHO/min) during the race. Muscle glycogen decreased from 227.1 prerace to 38.6 mmol . kg wet weight-1 . h-1 postrace. During the 4 hours postrace, the athlete consumed a mixed diet (471 g CHO, 15 g fat, 64 g protein), which included liquid CHO sources and a meal. The calculated rate of muscle-glycogen resynthesis was 4.1 mmol . kg wet weight-1 . h-1.. Completing a half Ironman triathlon depends on a high rate of muscle glycogenolysis, which demonstrates the importance of exogenous carbohydrate intake during the race. In addition, rates of muscle-glycogen resynthesis might be dampened by the eccentric damage resulting from the run portion of the race.

Topics: Adult; Bicycling; Biopsy; Dietary Carbohydrates; Dietary Fats; Dietary Proteins; Energy Metabolism; Glycogen; Glycogenolysis; Humans; Linear Models; Male; Muscle Contraction; Muscle Fatigue; Nutritional Status; Oxygen Consumption; Physical Endurance; Quadriceps Muscle; Running; Swimming; Time Factors; Weight Loss

Aqueous extract of the fruits of Solanum xanthocarpum Schrad. & Wendl. (Solanaceae) was investigated for hypoglycaemic activity in rats and mice. Screening for the hypoglycaemic activity was assessed on normoglycaemic, alloxan treated hyperglycaemic and glucose loaded rats along with in vitro study on glucose utilization by isolated rat hemidiaphragm. The various haematological and biochemical parameters were also studied. The extract was found to possess significant hypoglycaemic activity when compared with the reference standard glibenclamide. The in vitro study on glucose utilization by isolated rat hemidiaphragm suggests that the aqueous extract may have direct insulin like activity which enhances the peripheral utilization of glucose and have extra pancreatic effect. The toxicity studies report safety usage of the plant extract.

Topics: Alloxan; Animals; Blood Glucose; Cholesterol, VLDL; Diabetes Mellitus, Experimental; Diaphragm; Fatty Liver; Fruit; Glyburide; Glycogen; Hypoglycemic Agents; India; Kidney; Lipoproteins, HDL; Liver; Medicine, Traditional; Mice; Necrosis; Plant Extracts; Rats; Rats, Wistar; Solanaceae; Triglycerides; Water; Weight Loss

The objective of this study was to establish relationships among various physiological parameters in early (through 72 h posthatch) nutrient restricted broiler chicks from young breeder hens. Despite a 19% decrease in mean BW between 0 and 72 h posthatch, there were no chick mortalities. Liver glycogen peaked at 24 h, and peaks in rectal temperature, plasma glucose, and plasma refractive index occurred at 48 h. By 24 h, negative correlations were noted between BW and relative liver weight and between liver glycogen and both refractive index and rectal temperature. By 24 h, positive correlations were noted between relative liver weight and liver glycogen, BW and plasma glucose, rectal temperature and plasma glucose, and rectal temperature and body fat loss score. Mean daily relative egg weight loss between 0 and 19 d of incubation (RIEWL) was positively correlated with rectal temperature at 0 h but was negatively correlated with rectal temperature at 24 h and liver glycogen at 24 and 48 h. Furthermore, mean relative hatching chick weight (RHCW) had significantly positive correlations with plasma glucose at 6 h and rectal temperature at 48 and 72 h. Broilers having a greater RHCW after hatching from eggs with a lower RIEWL may maintain higher metabolic rates between 24 and 72 h posthatch despite nutrient deprivation. However, broiler chicks from eggs exhibiting a higher than optimal RIEWL may have greater dependence on gluconeogenesis, thus requiring stricter management during initial brooding.

Topics: Aging; Animal Nutritional Physiological Phenomena; Animals; Blood Glucose; Body Temperature; Chick Embryo; Chickens; Female; Food Deprivation; Glycogen; Kidney; Liver; Organ Size; Oviposition; Time Factors; Weight Loss

Mice lacking acyl-CoA:diacylglycerol acyltransferase 1 (DGAT1), a key enzyme in triglyceride synthesis, have increased energy expenditure and therefore are resistant to obesity. Because ambient temperature can significantly affect energy expenditure in mice, we undertook these studies to determine the effects of different ambient temperatures on energy expenditure, food intake, and thermoregulation in DGAT1-deficient [Dgat1(-/-)] mice. Dgat1(-/-) mice had increased energy expenditure irrespective of changes in the ambient temperature. Although core temperature was normal, surface temperature was increased in Dgat1(-/-) mice, most likely reflecting an active mechanism to dissipate heat from increased thermogenesis. Dgat1(-/-) mice had increased food intake at baseline, and this hyperphagia became more pronounced upon exposure to cold. When fasted in a cold environment, Dgat1(-/-) mice developed hypothermia, which was associated with hypoglycemia. These results suggest that the hyperphagia in Dgat1(-/-) mice is a secondary mechanism that compensates for the increased utilization of fuel substrates. Our findings offer insights into the mechanisms of hyperphagia and increased energy expenditure in a murine model of obesity resistance.

Topics: Acyltransferases; Animals; Blood Glucose; Body Temperature; Body Temperature Regulation; Carrier Proteins; Cold Temperature; Diacylglycerol O-Acyltransferase; Eating; Energy Metabolism; Fasting; Female; Gene Expression; Glycogen; Hyperphagia; Hypoglycemia; Hypothermia; Ion Channels; Liver; Membrane Proteins; Mice; Mice, Inbred C57BL; Mice, Knockout; Mitochondrial Proteins; Muscle, Skeletal; Obesity; Temperature; Uncoupling Protein 1; Weight Loss

To determine the effects of weight loss on intramyocellular energy substrates, vastus lateralis muscle biopsies were taken from six obese subjects (body mass index 34 +/- 5 kg/m(2)) before, after 15 wk of energy restriction (ER; -700 kcal/day), and after a further average 20.7 +/- 1.6 wk of endurance training plus low-fat diet (ET-LFD). Body weight fell from 100 +/- 6 to 89 +/- 6 kg during ER and to 84 +/- 4 kg after ET-LFD. Lipids and glycogen were histochemically measured in type I, IIA, and IIB fibers. Total muscle glycogen content (MGC; per 100 fibers) decreased after ER [from 72 +/- 13 to 55 +/- 8 arbitrary units (AU)]. A similar but not significant decrease was seen in total muscle lipid content (MLC; 14 +/- 5 to 9 +/- 1 AU). After ET-LFD, MGC returned to initial values (74 +/- 8 AU), and MLC approached near-initial values (12 +/- 3 AU). Individual fiber lipid concentration did not change throughout the protocol in all fiber types, whereas glycogen concentration increased after ET-LFD. The training effects of ET-LFD were measured as increasing activities of key mitochondrial enzymes. Although total muscle energy reserves can be reduced after weight loss, their concentration within individual myofibers remains elevated. Weight loss does not appear sufficient to correct the potential detrimental effects of high intracellular lipid concentrations.

Topics: Adult; Anthropometry; Diet, Fat-Restricted; Exercise; Female; Glycogen; Humans; Lipid Metabolism; Male; Muscle, Skeletal; Obesity; Osmolar Concentration; Physical Education and Training; Physical Endurance; Tissue Distribution; Weight Loss

The aim of the study was to elucidate whether combustion of skeletal muscle glycogen during a very low calorie diet (VLCD) was associated with decreased muscle potassium content. A comparison between different methods was also performed to evaluate body composition during a VLCD and a low calorie diet (LCD).. Dietary treatment of obese women by VLCD and LCD. Measurements after 1 and 2 weeks of VLCD and 6 months of LCD.. Fifteen perimenopausal obese women aged 46.5+/-1.3 y and 15 of 48.0+/-0.7 y of age.. Skeletal muscle biopsies under local anaesthesia. Body composition measurements by means of deal-energy X-ray absorptiometry (DEXA), and measurements of total body potassium (40K) and total body nitrogen (TBN). Measurements of electrolytes and glycogen concentration in muscle samples.. In the first study (1 week of VLCD) skeletal muscle glycogen decreased (P<0.01), but muscle potassium increased (P<0.01). Muscle sodium decreased (P<0.01), while muscle magnesium was unaltered. Body weight decreased by 2.9+/-0.5 kg and 40K decreased. Fat-free mass (FFM) calculated from 40K and DEXA decreased by 2.7 vs 1.9 kg (P<0.001). Body fat measured with DEXA decreased by 1.1 kg (P<0.01), but not body fat calculated from 40K. TBN decreased by 0.03+/-0.01 kg (P<0.05) and FFM calculated from TBN by 2.9+/-0.5 kg (P<0.002). In the second study, 6 months on the LCD resulted in 17.0+/-2.0 kg weight reduction and this was mainly due to reduced body fat, 14. 0+/-2.0 kg measured with DEXA and from 40K (P<0.001). The decrease in FFM was slight.. One week of VLCD resulted in muscle glycogen depletion but increased muscle potassium content in spite of decreased total body potassium. FFM contributed to the main part of body weight loss during short periods of severe energy restriction, but remained unchanged during long-term dietary treatment. Body fat became mostly responsible for the body weight loss during long-term LCD. Calculations of changes of FFM from 40K and TBN seem to overestimate the FFM decrease associated with short-term VLCD. International Journal of Obesity (2000)24, 101-107

Topics: Absorptiometry, Photon; Anthropometry; Body Composition; Diet, Reducing; Female; Glycogen; Humans; Middle Aged; Muscle, Skeletal; Obesity; Potassium; Premenopause; Time Factors; Weight Loss

Food restriction is known to ameliorate many of the adverse physiologic effects of age. In this study, we have examined the effect of food restriction on the induction of the gluconeogenic enzyme, phosphoenolpyruvate carboxykinase (PEPCK) in liver and kidney following a 12-h fasting period in young (6 month) and old (24 month) ad libitum-fed and food-restricted male Fischer 344 rats. In the liver, following the 12-h fast, the activity of PEPCK increased approximately 2-fold in the young ad libitum fed rats and 3-fold in the young restricted animals. However, PEPCK activity remained unchanged in response to the 12-h fast in the 24 month old ad libitum fed rats. In the old restricted rats, the induction of PEPCK mimicked that of the young rats (PEPCK activity increased 2-fold within the 12-h fasting period). Therefore, dietary restriction not only enhanced the induction response in the liver in young rats, but also restored the induction of hepatic PEPCK in the old animals. In the kidney, there was no effect of age or dietary restriction on the induction of PEPCK as the activity of renal PEPCK did not change in response to the 12-h fast in any of the four groups of rats.

Topics: Aging; Animals; Eating; Enzyme Induction; Glycogen; Kidney; Liver; Male; Phosphoenolpyruvate Carboxykinase (ATP); Rats; Rats, Inbred F344; Weight Loss

The objective of this study was to determine the effects of an alcoholic beverage (Toddy) and the equivalent quantity of ethanol on carbohydrate metabolism in utero. Female rats were exposed to Toddy from coconut palm (24.5 ml/kg body weight/day) and ethanol (0.52 ml/kg body weight/day) for 15 days before conception and throughout gestation. On the 19th day of gestation, hypoglycemia was seen in both the treated groups, but it was more in the Toddy-treated group. Synthesis of glycogen was elevated on exposure to ethanol/Toddy but its degradation was enhanced only in alcohol-exposed rats. Key enzymes of citric acid cycle and gluconeogenesis were inhibited on administration of both alcohol and Toddy. Activity of glycolytic enzymes were increased. Toddy seemed to potentiate the toxicity induced by alcohol, indicating the additive effects of congeners.

Topics: Animals; Blood Glucose; Carbohydrate Metabolism; Citric Acid Cycle; Drug Synergism; Enzyme Inhibitors; Ethanol; Female; Fetus; Gluconeogenesis; Glycogen; Liver; Pregnancy; Rats; Weight Loss; Wine

Owing to a substantial increase in glucose uptake by working muscle, glucose homeostasis during sustained aerobic exercise requires a severalfold increase in hepatic glucose output. As exercise continues and liver glycogen declines, an increasing proportion of this elevated glucose output must be provided by gluconeogenesis. Increased gluconeogenic efficiency in trained individuals is a key adaptation promoting increased endurance, since failure of hepatic glucose output to keep pace with muscle uptake rapidly leads to hypoglycaemia and exhaustion. Pre-administration of (-)-hydroxycitrate, a potent inhibitor of citrate lyase found in fruits of the genus Garcinia, may aid endurance during post-absorptive aerobic exercise by promoting gluconeogenesis. Carnitine and bioactive chromium may potentiate this benefit. The utility of this technique may be greatest in exercise regimens designed to promote weight loss.

Topics: Aerobiosis; Animals; Carnitine; Chromium Compounds; Citrates; Gluconeogenesis; Glucose; Glycogen; Glycolysis; Hormones; Humans; Lipid Metabolism; Liver; Multienzyme Complexes; Muscle, Skeletal; Oxo-Acid-Lyases; Physical Endurance; Physical Exertion; Rats; Weight Loss

Topics: Adipose Tissue; Adult; Body Composition; Body Water; Body Weight; Diet, Reducing; Glycogen; Humans; Middle Aged; Minerals; Models, Biological; Neutron Activation Analysis; Nitrogen; Obesity; Proteins; Weight Loss

Effects of carbohydrate (CHO) supplementation on muscle glycogen utilization and endurance were evaluated in seven well-trained male cyclists during continuous cycling exercise that varied between low [45% maximal O2 uptake (VO2 max)] and moderate intensity (75% VO2 max). During each exercise bout the subjects received either artificially flavored placebo (P), 10% liquid CHO supplement (L; 3 x 18 g CHO/h), or solid CHO supplement (S; 2 x 25 g CHO/h). Muscle biopsies were taken from vastus lateralis during P and L trials immediately before exercise and after first (124 min) and second set (190 min) of intervals. Subjects then rode to fatigue at 80% VO2 max. Plasma glucose and insulin responses during L treatment reached levels of 6.7 +/- 0.7 mM and 70.6 +/- 17.2 microU/ml, respectively, and were significantly greater than those of P treatment (4.4 +/- 0.1 mM and 17.7 +/- 1.6 microU/ml) throughout the exercise bout. Plasma glucose and insulin responses of S treatment were intermediate to those of L and P treatments. Times to fatigue for S (223.9 +/- 3.5 min) and L (233.4 +/- 7.5 min) treatments did not differ but were significantly greater than that of P treatment (202.4 +/- 9.8 min). After the first 190 min of exercise, muscle glycogen was significantly greater during L (79 +/- 3.5 mumol/g wet wt) than during P treatment (58.5 +/- 7.2 mumol/g wet wt). Furthermore, differences in muscle glycogen concentrations between L and P treatments after 190 min of exercise and in time to fatigue for these treatments were positively related (r = 0.76, P < 0.05). These results suggest that CHO supplementation can enhance prolonged continuous variable-intensity exercise by reducing dependency on muscle glycogen as a fuel source.

Topics: Adult; Bicycling; Blood Glucose; Carbon Dioxide; Dietary Carbohydrates; Drinking; Ergometry; Exercise; Fatty Acids, Nonesterified; Glycogen; Heart Rate; Humans; Insulin; Lactates; Lactic Acid; Male; Muscles; Oxidation-Reduction; Oxygen Consumption; Weight Loss

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

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

This study was conducted to develop a testing protocol which would determine the extent of upper-body power output decrements in subjects following weight loss. Five athletes who had trained via upper-body exercise performed a 6-minute variable intensity arm crank test on an isokinetic ergometer before and after a 3-day, 4.5% body weight loss. Blood samples were drawn from a forearm vein pre- and 1, 3, and 5 min post-arm cranking for assessment of lactate, pH, hemoglobin, and hematocrit. The work performed pre-weight loss was significantly (paired t-test, p less than 0.05) greater than that performed post-weight loss. Repeated measures ANOVA yielded no significant differences in blood variables; however, pre-weight loss lactate values were higher and hemoglobin, hematocrit, and pH values were lower than post-weight loss values. It was concluded that a 4.5% body weight reduction resulted in performance decrements during this arm crank test. Survey information obtained from collegiate wrestlers (n = 14) subsequently tested under this protocol indicates the physical demands of this test approximate the physical demands of actual wrestling competition. It would therefore be appropriate to use this protocol during future testing of wrestlers in weight loss studies.

Topics: Adult; Dehydration; Exercise Test; Glycogen; Humans; Lactates; Male; Physical Education and Training; Physical Endurance; Weight Loss; Wrestling

To assess muscle function after a period of negative energy balance, 32 obese women were placed on a 544-kcal/d, high-protein diet for 4 wk. Weight loss was associated with a decrease in the waist-to-hip-circumference ratio (WHR) and significantly higher emptying of abdominal than gluteal fat cells. The low-calorie regimen was associated with a significant increase in isokinetic muscle endurance, a decrease in glycogen concentration, and an increase in glycogen synthase (GS) activity and its fractional velocity (FV). The GS activity and its FV were negatively correlated with the WHR before treatment whereas their subsequent increase was correlated with the decrease in WHR. Dietary treatment produced a decrease in the isokinetic muscle strength, which was correlated with the reduction in lean body mass. The improvement in dynamic endurance observed after energy restriction parallels not only the increase in GS activity in muscle but also the decrease in glycogen stores and glucose oxidation, and most probably depends on the increased utilization of fatty acids.

Topics: Adipose Tissue; Adult; Diet, Reducing; Energy Intake; Energy Metabolism; Exercise Test; Fatty Acids; Female; Glucose; Glycogen; Glycogen Synthase; Humans; Muscles; Obesity; Oxidation-Reduction; Physical Endurance; Weight Loss

The effects of weight loss (dehydration) techniques (which mimicked techniques used prior to actual competition) used by intercollegiate wrestlers on selected physiological parameters (strength, anaerobic power, anaerobic capacity, the lactate threshold (LT), and peak aerobic power) were examined in seven intercollegiate wrestlers. During the 36 h weight loss period, subjects lost 3.3 kg (4.9% body weight), all of which occurred during the 12 h prior to weigh-in, using exercise in a rubberized sweat suit. Weight loss resulted in a reduction in upper body but not lower body strength measures (peak torque and average work per repetition). Anaerobic power and anaerobic capacity were significantly reduced in a dehydrated state (81.4 kgm.s-1, normal weight; 63.9 kgm.s-1, weight loss; 1984.3 kgm.40 s-1, normal weight; 1791.4 kgm.40 s-1, weight loss). Analyses of treadmill data revealed the following: 1) velocity was decreased at LT (4.4%) and peak (6.5%) during weight loss (P less than 0.05); 2) VO2 peak was significantly reduced with weight loss (6.7%, P less than 0.05); 3) treadmill time to exhaustion was significantly reduced in the weight loss state (12.4%) (35.7 min, normal weight; 31.3 min, weight loss). It was concluded that typical wrestling weight loss techniques result in deleterious effects on strength, anaerobic power, anaerobic capacity, the lactate threshold, and aerobic power.

Topics: Adolescent; Adult; Dehydration; Exercise Test; Glycogen; Humans; Lactates; Male; Muscles; Oxygen; Weight Loss; Wrestling

A group of 13 apparently healthy, premenopausal obese women (134-196% ideal weight) volunteered in a weight reduction study for 8 wk on a 4200 kJ (1000 kcal) diet. Before and after the weight reduction period body composition was measured by densitometry and by the bioelectrical impedance method. Changes in fat mass and fat-free mass were calculated. Mean weight loss was 10.0 +/- 2.8 kg and loss of fat-free mass was measured to be 2.3 +/- 1.7 kg (23%) by densitometry and 0.6 +/- 1.9 kg (6%) by impedance measurements. The underestimation of the change in fat-free mass measured by the impedance method could be due to losses of water bound to glycogen after the weight-reduction period. For this reason the impedance method may be not applicable in studies in which changes in glycogen stores can be expected.

Topics: Adult; Body Composition; Body Height; Densitometry; Diet, Reducing; Electric Conductivity; Female; Glycogen; Humans; Middle Aged; Weight Loss

Twelve healthy volunteers consumed a very-low-calorie diet for 2 d to achieve a body-weight loss mainly from a loss of fat-free mass, ie, of glycogen plus water. Body weight, body density, and bioelectrical impedance were measured before and after weight loss. Body-weight loss was 1.3 +/- 0.5 kg. Loss of fat-free mass as measured by densitometry was 1.2 +/- 0.8 kg. Changes in body weight and fat-free mass measured by densitometry did not differ significantly and were significantly different from zero. Reduction of fat-free mass as determined by bioelectrical impedance was 0.5 +/- 0.8 kg, which was significantly different from body-weight loss and loss of fat-free mass as measured by densitometry but not significantly different from zero. The results show that after weight loss the bioelectrical impedance method overestimates the fat-free mass by approximately 1 kg.

Topics: Adult; Body Composition; Diet, Reducing; Electric Conductivity; Female; Glycogen; Humans; Intracellular Fluid; Male; Weight Loss