glycogen and Alcoholism

The pharmacological and toxicological properties of furazolidone have been briefly reviewed. Among the most important pharmacological actions of furazolidone is the inhibition of mono- and diamine oxidase activities, which seem to depend, at least in some species, on the presence of the gut flora. The drug also seems to interfere with the utilization of thiamin, which is probably instrumental in the production of anorexia and loss of body weight of the treated animals. Furazolidone is known to induce a condition of cardiomyopathy in turkeys, which could be used as a model to study alpha 1-antitrypsin deficiency in man. The drug is most toxic to ruminants. The toxic signs observed were of nervous nature. Experiments are in progress in this laboratory to try to explain the mechanism(s) by which this toxicity is brought about. It is uncertain whether the use of furazolidone at the recommended therapeutic dose would result in drug residues in tissues of treated animals. This is a matter of public health importance as the drug has been shown to possess a carcinogenic activity. It is important that a simple and reliable method of identification and estimation of furazolidone residues be devised. More work is needed to elucidate the mode of action and biochemical effects caused by the drug in both the host and the infective organisms.

Topics: Adrenal Glands; Alcoholism; Animals; Anorexia; Brain; Cardiomyopathies; Cattle; Chick Embryo; Chickens; Chromatography, High Pressure Liquid; Ducks; Female; Furazolidone; Glycogen; Guinea Pigs; Humans; In Vitro Techniques; Liver; Mice; Monoamine Oxidase Inhibitors; Poultry Diseases; Pregnancy; Rabbits; Rats; Thiamine Deficiency; Turkeys

Topics: Alcoholic Intoxication; Alcoholism; Animals; Chemical and Drug Induced Liver Injury; Ethanol; Fats; Fatty Liver; Glucose; Glycogen; Hepatomegaly; Humans; Lipid Metabolism; Liver; Liver Cirrhosis; Microsomes, Liver; Social Problems

We report a 55 year old Japanese man with a history of alcohol abuse, who was in a near fasting state for the previous few days.He was admitted to our hospital with abrupt disturbance of consciousness. He presented disturbance of consciousness with extreme hypoglycemia and ketoacidosis with high β-hydroxybutyric acid concentration. Taking into account his living history, we diagnosed with alcoholic ketoacidosis (AKA). Symptoms ameliorated with glucose injection and fluid loading. AKA patients show abdominal pain, nausea or vomiting, but they are usually alert and lucid despite the severe acidosis. This case, however, presented comatose status caused by hypoglycemia. Poor oral intake of this patient was assumed to be the cause of hypoglycemia. Alcoholism may cause hypoglycemia accompanying with AKA, due to a low carbohydrate intake, the inhibition of gluconeogenesis, and reduced hepaticglycogen storage as seen in this case. Here, we report a case of AKA that demonstrated hypoglycemia with the literature review.

Topics: 3-Hydroxybutyric Acid; Alcoholism; Coma; Dietary Carbohydrates; Fluid Therapy; Gluconeogenesis; Glucose; Glycogen; Humans; Hypoglycemia; Ketosis; Liver; Male; Middle Aged; Severity of Illness Index

To prepare an oral nutritional liquid for protecting liver and antialcoholic from defatted oyster powder.. The orthogonal design was used to determine the optimal enzymatic hydrolytic condition and the enzymolysis liquid from oyster was deodorized and seasoned.. The optimum hydrolytic conditions were determined as follows: defatted oyster powder added concentration of 2%, ratio of enzyme to base material 10%, enzymatic hydrolytic time 90 min, temperature 50 degrees C, pH 6.2. The content of glycogen, crude protein and amino acids in the oral nutritional liquid were 461 mg/100 mL, 381 mg/100 mL and 294.5 mg/100 mL, respectively.. The processing conditions are stable and reliable and can be used to provide reference for further pilot scale production.

Topics: Administration, Oral; Alcoholism; Amino Acids; Animals; Glycogen; Hydrolysis; Materia Medica; Ostreidae; Papain; Powders; Technology, Pharmaceutical; Temperature

Epidemiological studies suggest that alcohol consumption is an independent risk factor for the development of non-insulin-dependent diabetes mellitus (NIDDM). Alcoholism is known to be associated with increased plasma levels of two novel diols, 2,3-butanediol and 1,2-propanediol, metabolites known to impair insulin action in isolated adipocytes. This study examines whether 2,3-butanediol and 1,2-propanediol have the capacity to impair insulin action acutely in vivo in the rat. Using the euglycemic-hyperinsulinemic clamp, it is shown that the two diols reduce whole-body glucose utilization (by approximately 30%), with the onset of insulin resistance in vivo occurring at plasma concentrations of 2,3-butanediol (33 micromol/L) at least one order of magnitude (P < .001) lower than 1,2-propanediol (432 micromol/L). Tracer methodologies using [U-14C]glucose and 2-deoxy[1-(3)H]glucose indicate that the reduction in whole-body glucose utilization is accompanied by a reduction in glucose uptake and glycogen synthesis in the skeletal muscle and heart. The association between elevated plasma diol levels and insulin resistance demonstrated in this report raises the question of whether there is a link between the high plasma diol levels in alcohol abusers and their increased susceptibility to NIDDM.

Topics: Alcoholism; Animals; Blood Glucose; Butylene Glycols; Diabetes Mellitus, Type 2; Glycogen; Insulin; Insulin Resistance; Male; Propylene Glycol; Rats; Rats, Wistar

To determine the effect of alcohol on carbohydrate metabolism, 48 human muscle biopsies from chronic alcoholics were studied. The level of glycogen and the activities of the enzymes catalyzing glycogen and glucose metabolism were analyzed. Chronic alcohol intake produced an increase in glycogen concentration and a decrease in pyruvate kinase activity before the first signs of myopathy appeared. When myopathy was present, glycogen decreased. These changes may contribute to the decline in skeletal muscle performance in these patients.

Topics: Adult; Alcohol Drinking; Alcoholism; Blood Glucose; Glycogen; Glycolysis; Humans; Male; Middle Aged; Muscle, Skeletal; Pyruvate Kinase; Reference Values

Changes in neurobiological parameters were examined from early life (10 days post-natal) until late adulthood (8 months post-natal) in three successive generations of alcoholized rats. The mean daily consumption of alcohol by the 2nd and 3rd generation rats (7.40 +/- 0.22 and 7.70 +/- 0.20 g ethanol/kg body weight, respectively) was significantly greater than that of the 1st generation alcoholized group (4.26 +/- 0.33 g/kg). Brain/body weight ratios of alcoholized rats, 10 days post-natal, were significantly greater than controls, with 1st generation alcoholized rats presenting significantly greater brain/body weight ratios than those of the 2nd or 3rd generation, which tended toward control weights and ratios. This difference between alcoholized rats and controls persisted, although to a lesser extent, at 8 months post-natal. Glycogen content in the brains of rats of all alcoholized generations was significantly lower than in controls at 10 days post-natal, with a reversal of this situation in later life for 2nd and 3rd generation rats, which presented significantly greater cerebral glycogen levels than control or 1st generation alcoholized rats (which had an equivalent cerebral glycogen content). In 10-day-old rat pups, monoamine oxidase (MAO) activity in brain tissues had a tendency (mostly non-significant) to be greater in alcoholized rats than in controls, with a reversal of this situation, ie a statistically significant decrease in MAO activity in the 2nd and 3rd alcoholized generations with respect to controls, in 8-month-old rats. MAO activity in adrenal glands of alcoholized rats was greater than in controls at 10 days post-natal, and this difference persisted at 8 months.

Topics: Alcoholism; Animals; Body Weight; Brain; Brain Chemistry; Ethanol; Female; Glucose; Glycogen; Male; Monoamine Oxidase; Organ Size; Pregnancy; Prenatal Exposure Delayed Effects; Rats; Rats, Wistar

Topics: Alanine; Alcoholism; Animals; Glycogen; Lactates; Muscles; Organ Specificity; Rats; Reference Values

Topics: Acid Phosphatase; Adult; Alcoholism; Glycogen; Humans; Immunoglobulins; Lymphocytes; Male; Middle Aged; Naphthol AS D Esterase

Acute or chronic intoxication of rats with ethanol (intragastric administration at a dose of 8 g/kg or free-choice drinking of 10% ethanol for 3 months) produced no significant changes in contractile function, glycogen content, glucose uptake and lactate release in isolated hearts. Withdrawal syndrome simulated in rats following a short period of severe intoxication with ethanol at a dose of 4-5 g/kg twice daily has demonstrated a 15 and 28% decrease in peak systolic pressure and tension time index, respectively. In this case glucose uptake and lactate release were 2 times higher. Changes in glycogen level were observed three days after the last ethanol administration. The rats, survived after the abstinence period, revealed areas of perivascular myocardial necrosis. It is concluded that withdrawal syndrome plays an important role in pathogenesis of alcoholic cardiomyopathy.

Topics: Alcoholic Intoxication; Alcoholism; Animals; Ethanol; Glucose; Glycogen; Lactates; Lactic Acid; Myocardial Contraction; Myocardium; Necrosis; Rats; Substance Withdrawal Syndrome

Topics: Adult; Alcoholism; Female; Glycogen; Humans; Lipids; Male; Middle Aged; Mitochondria; Muscles; Necrosis; Sarcoplasmic Reticulum

Muscle biopsies of 20 alcoholic patients (15 males and 5 females), most of whom had liver disease and with no clinical or analytical evidence of neuromyopathy, were studied. 10 abstemious patients with no neuromuscular disease were selected as controls. Conventional histology failed to show significant skeletal muscle changes. A characteristic histochemical picture of tubular aggregates was found in one patient. An enlargement of the intermyofibrillar space with increase in glycogen deposition and fat droplets were detected ultrastructurally while 2 of the patients showed tubular aggregates. The mitochondriae of the alcoholic patients had a smaller perimeter and area than those of the control group (P less than 0.004 and P less than 0.008, respectively). These results suggest that the prolonged ingestion of alcohol can cause a mitochondrial alteration only evidenced by morphometry, with poor clinical, biochemical, electrophysiological and histological expression of myopathy. These findings can represent an early stage of alcoholic skeletal muscle injury.

Topics: Adenosine Triphosphatases; Adult; Alcoholism; Biopsy; Female; Glycogen; Humans; Lipid Metabolism; Liver Cirrhosis, Alcoholic; Male; Middle Aged; Mitochondria, Muscle; Muscles; Myofibrils; Myositis

The capacity for glycolysis in muscle biopsies obtained from long-term heavy alcohol drinking patients has been compared with tissue from control subjects by assay in vitro of the total activities of glycogen phosphorylase, phosphofructokinase and fructose 1,6-bisphosphatase, key regulatory enzymes in the anaerobic glycolytic pathway. Biopsies from 13 of 22 patients had type II fibre atrophy, and the activities of all three enzymes were reduced in these biopsies, when expressed in terms of DNA content, the most striking reduction being in phosphofructokinase activity. The amount of glycogen in the tissue correlated closely with these enzyme activities and was slightly lower in the most atrophic tissue, when expressed in terms of DNA content. The activities of acid and neutral alpha-glucosidases were similar in biopsies from control subjects and patients with various severities of alcohol myopathy. The reduced activities are consistent with a reduced proportion of type II fibre muscle mass in these patients, and suggest that there may be a reduced capacity for glycolysis with resultant reduced lactate production. Whether the changes in enzyme activities are primary to the selective atrophy remains to be established.

Topics: Adult; Aged; Alcoholism; alpha-Glucosidases; Female; Fructose-Bisphosphatase; Glycogen; Glycolysis; Humans; Male; Middle Aged; Muscles; Muscular Diseases; Phosphofructokinase-1; Phosphorylases

The comparative electrophysiologic, histochemical, and biochemical investigation of the anterior tibial muscle of 13 alcoholics indicates that neuropathy could be the cause of the chronic muscle weakness and wasting. Myopathic alterations did not predominate in the findings. It was concluded that the proximal muscle atrophy could also be attributed to neurogenic damage. Histochemical reactions in muscle specimens showed a selective type 2 atrophy and a slight increase of the mean diameter of type 1 fibres. Biochemical investigations revealed that the activities of a number of enzymes representative of energy supplying pathways--the glycogenolysis and glycolysis--as well as acid phosphatase activity in the muscle were lowered. A relationship could be assumed between the lowered glycolytic activity and the decline of the mean diameter of type 2 fibres. Oxidative enzymes were of similar activity in the alcoholics and the control group. The glycolytic enzyme activities were particularly important, being the most sensitive indicators of the onset, intensity, and course of neurogenic damage. These activities probably normalise during reinnervation of a muscle earlier than do the morphologic alterations; however, they were markedly lower in alcoholics with impaired liver function and cachexia, probably because of the catabolic metabolic conditions present in these cases.

Topics: Adenosine Triphosphatases; Adult; Alcoholism; Axons; Dihydrolipoamide Dehydrogenase; Electromyography; Female; Glycogen; Glycolysis; Humans; Male; Middle Aged; Muscles; Muscular Atrophy; Neural Conduction; Reflex, Stretch; Sensation

The effects of chronic ethanol ingestion on a preparation of liver glycogen phsophorylase have been studied. A coupled assay in the direction of glycogenolysis was used. In the absence of AMP, a significant decrease in specific activity was observed in both males (19%) and females (30%). AMP additions stimulated phosphorylase activity and completely obliterated the ethanol-induced decreases in both sexes of animal. Kinetic studies, done in the absence of AMP, showed that only the apparent Vmax had been altered by ethanol. These data suggest that decreases in liver glycogen after chronic ethanol ingestion may not be related to the specific activity of glycogen phosphorylase. Using both glucose and caffeine as negative effectors, addditional studies demonstrated that the inhibitory effects of caffeine had been altered by ethanol in both males and females and that the inhibitory effects of glucose had been altered only in females. Even though the specific activity for phosphorylase did not directly implicate this enzyme in the ethanol-induced decrease in liver glycogen stores, the latter data regarding glucose and caffeine suggest that chronic ethanol ingestion has altererd this enzyme and that differences exist between males and females.

Topics: Adenosine Monophosphate; Alcoholism; Animals; Body Weight; Caffeine; Fasting; Female; Glycogen; Humans; Kinetics; Liver; Male; Phosphorylases; Rats; Sex Factors

Striated muscle from patients taking more than 80 g of alcohol each day shows selective atrophy of the type II fibres which are dependent on glycogenolytic pathways. This atrophy is associated with an excess of glycogen and lipid within the fibres and may represent a selective metabolic insult.

Topics: Adult; Aged; Alcoholism; Cytoplasmic Granules; Female; Glycogen; Humans; Lipids; Male; Microscopy, Electron; Middle Aged; Muscles; Muscular Atrophy

Chronic ethanol ingestion decreased liver glycogen levels in both male and female rats; however plasma glucose was decreased only in males. The decreased levels of liver glycogen were related to increases of 42% and 122% in glycogen phosphorylase in males and females, respectively. Both a and b forms of phosphorylase were increased, but the b form was increased more than the a form. Phosphorylase phosphatase was found to be increased 75% and 267% in males and females, respectively. Studies using positive and negative phosphorylase effector molecules indicated that ethanol ingestion may have altered the structure of phosphorylase a and that the degree of alteration was sex related.

Topics: Alcoholism; Animals; Blood Glucose; Caffeine; Female; Glycogen; Humans; Liver Glycogen; Male; Phosphorylase Phosphatase; Phosphorylases; Rats; Sex Factors

Topics: Acetate-CoA Ligase; Alcohol Oxidoreductases; Alcoholism; Aldehyde Oxidoreductases; Animals; Cardiomyopathies; Cholesterol; Creatine Kinase; Diet; Disease Models, Animal; Ethanol; Glycogen; Humans; L-Lactate Dehydrogenase; Lipid Metabolism; Male; Mice; Mitochondria, Muscle; Myocardium; Triglycerides

The glucose tolerance curve in alcoholics in delirium tremens was similar to that seen in hepatogenic diabetes. The secretion of immunoreactive insulin and somatotropin after glucose was similar in patients with delirium tremens and alcoholic hallucinosis.

Topics: 17-Hydroxycorticosteroids; Acute Disease; Adult; Alcohol Withdrawal Delirium; Alcoholism; Ammonia; Antigens; Blood Glucose; Chlorpromazine; Chronic Disease; Glucose Tolerance Test; Glycogen; Growth Hormone; Hallucinations; Humans; Insulin; Male; Methotrimeprazine; Promazine; Psychoses, Alcoholic

Biopsies from vastus lateralis muscle of male patients suffering from chronic ethanol abuse were studied with regard to histochemical reactions of ATPase and NADH-diaphorase; enzymatic activities of triosephosphate dehydrogenase (TPD), lactate dehydrogenase (LD), and cytochrome c oxidase (cytox); content of ATP, creatine phosphate, and glycogen; and volume fractions of fat, mitochondria, and fibrillar and extrafibrillar space. The results were compared with those from controls without known abuse of ethanol. The relative numbers of fibers were the same in two groups, but the size of the fast-twitch-glycolytic (white) fibers was diminished in the alcoholic group. The activities of TPD and LD were diminished in skeletal muscle of the alcoholics. This is most probably caused by the reduced amount of fast-twitch-glycolytic tissue, as there was a good correlation between this amount and the activity of the two enzymes. The activity of cytox was slightly lower in muscle of the alcoholics than in that of the controls. The volume fraction of mitochondria was lower in the alcoholic group than in the control group. Volume fractions of fat and fibrillar and extrafibrillar space were equal in the two groups. No significant differences were found in the amount of glycogen and ATP in the muscle of the two groups. However, the content of creatine phosphate is higher in the alcoholic group than in the control group.

Topics: Adenosine Triphosphatases; Adenosine Triphosphate; Adult; Alcoholism; Depression, Chemical; Dihydrolipoamide Dehydrogenase; Electron Transport Complex IV; Ethanol; Glyceraldehyde-3-Phosphate Dehydrogenases; Glycogen; Glycolysis; Humans; L-Lactate Dehydrogenase; Male; Middle Aged; Mitochondria, Muscle; Muscles; Myofibrils; Oxygen Consumption; Phosphocreatine

Topics: Alcoholism; Chlorides; Chronic Disease; Creatine Kinase; Extracellular Space; Fructose-Bisphosphate Aldolase; Glycogen; Humans; Lactates; Male; Membrane Potentials; Muscle Cramp; Muscles; Muscular Diseases; Phosphates; Phosphorus; Potassium; Sodium; Water

A 34-year-old chronic alcoholic with acute alcoholic intoxication was found to have extensive aggregates on muscle biopsy performed 48 hours after admission. Forearm ischemic exercise failed to demonstrate normal generation of lactic acid. Pathologic changes in the muscle biopsy consisted of subsarcolemmal accumulations of bright purple-red material with trichrome reaction. This material stained darkly with NADH-TR but was unstained with myofibrillar ATPase and Pas. Ultrastructural studies revealed that these regions contained tubular aggregates. A second biopsy 7 days later failed to demonstrate any significant abnormalities. Two weeks later, lactate generation was normal. Previous observations by other authors that tubular aggregates may be concerned with correction of metabolic defect or detoxification of endogenous toxins could apply in our case.

Topics: Adult; Alcoholism; Biopsy; Glycogen; Histological Techniques; Humans; Kinetics; Lactates; Male; Microscopy, Electron; Muscles; Muscular Diseases; Myofibrils

Topics: Adult; Alcohol Oxidoreductases; Alcoholism; Biopsy, Needle; Creatine Kinase; Energy Metabolism; Glycogen; Hexokinase; Humans; L-Lactate Dehydrogenase; Malate Dehydrogenase; Male; Middle Aged; Muscles; Phosphotransferases; Physical Education and Training; Physical Exertion; Succinate Dehydrogenase; Time Factors

Topics: Alcoholism; Blood Platelets; Blood Proteins; Carbon Dioxide; Carbon Radioisotopes; Energy Metabolism; Epinephrine; Ethanol; Glucose; Glycogen; Humans; Lactates; Plasmapheresis; Thrombin; Thrombocytopenia

Topics: Aged; Alcoholism; Autopsy; Biopsy; Diagnosis, Differential; Endoscopy; Epithelium; Esophageal Diseases; Esophagitis; Esophagoscopy; Esophagus; Gastroesophageal Reflux; Glycogen; Humans; Hyperplasia; Intestinal Mucosa; Leukoplakia; Male; Middle Aged; Periodic Acid; Smoking; Staining and Labeling

Topics: Alcoholism; Animals; Bile Ducts, Intrahepatic; Diabetes Mellitus; Glycogen; Golgi Apparatus; Hemochromatosis; Humans; Liver; Lysosomes; Microscopy, Electron; Mitochondria, Liver; Rats

Topics: Alcoholism; Animals; Cholangitis; Dogs; Glucose; Glycogen; Humans; Hypoglycemia; Liver Cirrhosis; Liver Diseases; Liver Neoplasms; Rabbits; Rats

Topics: Alcoholism; Autopsy; Biopsy; Cardiomyopathies; Cytoplasm; Glycogen; Humans; Lipids; Microscopy, Electron; Mitochondria, Muscle; Myocardium; Myofibrils

Topics: Alcoholism; Cholesterol; Chronic Disease; Female; Glycogen; Humans; Liver; Male; Transaminases

Topics: Adult; Alcoholism; Aspartate Aminotransferases; Chronic Disease; Creatine Kinase; Fructose-Bisphosphate Aldolase; Glycogen; Humans; Hypokalemia; Male; Middle Aged; Muscles; Muscular Diseases; Necrosis; Potassium; Sodium

Topics: Alcoholic Intoxication; Alcoholism; Child; Glucagon; Glycogen; Humans; Hypoglycemia

Topics: Adolescent; Adult; Age Factors; Aged; Alcoholism; Animals; Cell Nucleolus; Cell Nucleus; Child; Child, Preschool; Collagen; Cytoplasm; Cytoplasmic Granules; Diabetes Complications; Diabetes Mellitus; Diet, Diabetic; Female; Glycogen; Hepatitis; Hepatomegaly; Humans; Infant; Insulin; Liver Cirrhosis; Liver Function Tests; Lysosomes; Male; Microscopy, Electron; Middle Aged; Mitochondria, Liver; Reticulum; Sex Factors; Splenomegaly; Sulfonamides

Topics: Alcoholism; Animals; Cardiomyopathy, Alcoholic; Electrons; Endoplasmic Reticulum; Glycogen; Heart Diseases; Humans; Lipids; Lysosomes; Microscopy; Microscopy, Electron; Mitochondria; Myocardium; Myofibrils; Nerve Degeneration; Pathology

Topics: Alcoholic Intoxication; Alcoholism; Brain; Brain Chemistry; Glycogen; Histocytochemistry; Metabolism; Rats; Research; Toxicology