glycogen and Hepatic-Encephalopathy

Topics: Ammonia; Animals; Astrocytes; Brain Edema; Calcium; Cell Size; Cells, Cultured; Cyclic AMP; Cytoskeleton; Glial Fibrillary Acidic Protein; Glycogen; Hepatic Encephalopathy; Humans; Ion Channels; Neurons; Receptors, GABA-A; Signal Transduction

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

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

Most of the brain glycogen, a major energy reserve that can be mobilized in response to increased neuronal activity, resides in the astrocyte, the site of the neuropathological abnormality found in hepatic encephalopathy (HE). Ammonia, a neurotoxin implicated in the pathogenesis of HE, has been reported to cause a depletion of glycogen in primary astrocyte cultures. To further investigate the action of ammonia on glycogen levels, cultured astrocytes were exposed to ammonium chloride (1-5 mM) for various times up to 7 d. Treatment with ammonia for 24 h did not alter deoxyglucose uptake, but significantly lowered peak glycogen values (found at 1.5 h following feeding with medium containing 5.5 mM glucose) in a concentration-dependent manner. This inhibitory effect was not observed after longer exposure times to ammonia. Three day treatment of cells did, however, significantly reduce norepinephrine-stimulated glycogenolysis, an effect not seen after 1 d of ammonia treatment. Part of the neurotoxic action of long term ammonia exposure in humans and experimental animals may be to inhibit the breakdown of glycogen. The effect of ammonia on astrocyte glycogen synthesis and/or breakdown may disrupt glial neuronal signaling and thus play a role in the pathogenesis of HE.

Topics: Ammonia; Animals; Astrocytes; Cells, Cultured; Glycogen; Hepatic Encephalopathy; Norepinephrine; Rats; Rats, Inbred F344

Accumulations of glycogen in leukocytes from patients with hepatic encephalopathy and controls were studied electron-microscopically and biochemically. Extensive glycogen accumulation was observed in polymorphonuclear leukocytes from these patients, the content being 1.5 or 3.4 times higher than in the controls. The absorption spectra of glycogen with an iodine reagent exhibited no difference between patients and controls. Phosphorylasee activity was reduced but acid alpha 1,4-glucosidase activity elevated in the leukocytes from the patients.

Topics: Adult; alpha-Glucosidases; Female; Glycogen; Hepatic Encephalopathy; Humans; Male; Microscopy, Electron; Middle Aged; Neutrophils; Phosphorylases

Brain energy reserve, tricarboxylic cycle intermediate and some putative neurotransmitters were measured in a devascularisation model with portacaval shunt and hepatic artery ligation done in two interventions. Conditions were standardized in that physiologic parameters, i.e. body temperature, systemic arterial pressure, PO2, PCO2 and pH, were kept constant and brain tissue was obtained with the "freeze-blowing" technique designed for deep freezing brain substance in less than one second. 1. Measured values indicative of the brain energy reserve (glucose, glycogen, ATP and phosphocreatin) were not found to differ from those of sham-operated animals. 2. Of the stimulating neurotransmitters, norepinephrine, dopamine, glutamic acid and aspartic acids were reduced with the exception of acetylcholine among the inhibitory neurotransmitters GABA and cAMP were unchanged, while all others including serotonin, octopamine, and phenylethanolamine were increased. 3. The results of these experiments suggest that an inbalance of amino acids with resultant changes in neurotransmitter profiles rather than an energy deficit constitutes the factor underlying hepatic coma.

Topics: Adenosine Diphosphate; Adenosine Monophosphate; Adenosine Triphosphate; Ammonia; Animals; Brain; Energy Metabolism; gamma-Aminobutyric Acid; Glucose; Glutarates; Glycogen; Hepatic Encephalopathy; Malates; Phosphocreatine; Rats

After controlling the physiological parameters during 6 hours of experimental hepatic coma in Sprague-Dawley rats the results show 1. No shortage of brain energy supply of the four main cerebral energy reserves, the brain glycogen is significantly elevated, and the phosphocreatine, ATP and glucose unaltered. 2. No alterations in intermediates of the glycolytic pathway and the tricarboxylic acid cycle in brain tissue. 3. A highly significant decrease in the brain content of the "excitatory" transmitter amino acids glutamate and aspartate. These findings do not support the well-known hypothesis of BESSMAN and BESSMANN and later authors on the role of ammonia in the pathogenesis of hepatic coma.

Topics: Adenosine Triphosphate; Animals; Brain; Brain Chemistry; Female; Glucose; Glycogen; Hepatic Encephalopathy; Ketone Bodies; Lactates; Liver; Male; Neurotransmitter Agents; Phosphocreatine; Rats

Topics: Adenosine Triphosphate; Anesthetics; Brain; Brain Edema; Cerebral Cortex; Cerebrovascular Circulation; Cerebrovascular Disorders; Coma; Consciousness; Diabetic Coma; Glucose; Glycogen; Hepatic Encephalopathy; Humans; Hypoglycemia; Lactates; Oxygen Consumption; Seizures; Sleep