glycogen and Coma

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

The primary objective of this study was to attempt to induce excessive intraglial acidosis during ischemia by subjecting rats to an initial insult which leads to post insult accumulation of glycogen, presumed to accumulate primarily in astrocytes. The initial insults were 15 min of transient forebrain ischemia, 30 min of hypoglycemic coma, and intraperitonial injection of methionine-sulphoximine (MSO). In the first two of these insults, glycogen content in neocortex increased to 6-7 mM kg(-1) after 6 h of recovery, and in MSO-treated animals even higher values were measured 24 h after administration ( 12 mM kg(-1)). In spite of this glycogen loading, the amount of lactate formed during a subsequent ischemic insult (of 5-30 min duration) did not exceed values usually obtained during complete ischemia in animals with normal glycogen contents (tissue lactate contents of 15 mM kg(-1)) This was because appreciable amounts of glycogen (3-7 mM kg(-1)) remained undegraded even after 30 min of ischemia. The undigested part largely reflected the extra amount of glycogen accumulated after the initial insults. It is discussed whether this part is unavailable to degradation by phosphorylase.

Topics: Acidosis; Animals; Astrocytes; Brain; Brain Ischemia; Coma; Energy Metabolism; Glycogen; Hypoglycemia; Ischemic Attack, Transient; Male; Methionine Sulfoximine; Phosphorylation; Rats; Rats, Wistar; Reperfusion Injury; Seizures

The effect of the anticonvulsant sodium valproate on cerebral brainstem energy metabolism has been investigated. Stupor and coma were produced in mice by the intraperitoneal injection of sodium valproate at a dose of 600 mg/kg. Glucose, glycogen, ATP, and phosphocreatine were measured in small tissue samples from the ascending reticular activating system. Levels of all metabolites were either normal or elevated in precoma and comatose mice as compared to controls. These data are consistent with the concept that sodium valproate does not have a primary action through depletion of high energy phosphates.

Topics: Adenosine Triphosphate; Animals; Brain Stem; Coma; Energy Metabolism; Female; Glucose; Glycogen; Mice; Phosphocreatine; Reticular Formation; Valproic Acid

The medium chain fatty acid octanoic acid was injected i.p. into 20-22 g Swiss-Albino mice at a dose of 15 mumol/g. This dose produced a reproducible response consisting of a 3-4 min period of drowsiness, followed by coma. These mice as well as suitable controls were sacrificed by rapid submersion in liquid N2, or by microwave irradiation in a 7.3 kW microwave oven. Tissue from the reticular formation and the inferior colliculus was prepared for microanalysis of the energy metabolites glucose, glycogen, ATP and phosphocreatine. Results from this study showed a selective effect on energy metabolism in cells of the reticular formation. Both glucose and glycogen were elevated in the coma and precoma state. In addition, ATP and phosphocreatine were decreased in the reticular formation during coma. These results show a selective effect of octanoic acid on energy metabolism in the reticular formation both in the precoma stage, and during overt coma. The selective vulnerability of the reticular formation to metabolic insult may act in a beneficial manner to the animal by inducing coma. This lowers the overall demand for energy, thereby placing the animal in a milieu in which there is an increased chance for correction of the perturbation.

Topics: Adenosine Triphosphate; Animals; Caprylates; Coma; Energy Metabolism; Female; Glucose; Glycogen; Inferior Colliculi; Mice; Phosphocreatine; Reticular Formation

Previous studies have implicated the ascending reticular activating system (RAS) as playing a vital role in ammonia induced coma. It has been shown, for example, that cells of the RAS have selective decreases in the level of energy metabolites such as ATP and phosphocreatine as compared to adjacent tissue during ammonia induced encephalopathy. To determine the utilization rate of metabolites during ammonia induced coma, we have examined the turnover rate of four key energy metabolites in 20-22 gram mice. Results from this study show decreases in the turnover of glucose, glycogen, and phosphocreatine. The derived value for the turnover of energy metabolites was decreased by 49% as compared to that of control mice. These data suggest that energy utilization is decreased at a time when the physiological output of the RAS is also diminished and the animal is comatose.

Topics: Adenosine Triphosphate; Ammonia; Animals; Coma; Energy Metabolism; Glucose; Glycogen; Male; Mice; Reticular Formation

The effects of insulin-induced hypoglycemic stupor and subsequent treatment with glucose on mouse cerebral cortical, cerebellar and brain stem levels of glucose, glycogen, ATP, phosphocreatine, glutamate, aspartate and GABA and on cerebral cortical and cerebellar levels of cyclic AMP and cyclic GMP have been measured. Hypoglycemia decreased glucose, glycogen and glutamate levels and had no effect on ATP levels in all three regions of brain. GABA levels were decreased only in cerebellum. Aspartate levels rose in cerebral cortex and brain stem, and creatine phosphate increased in cerebral cortex and cerebellum. In the hypoglycemic stuporous animals, cyclic GMP levels were elevated in cerebral cortex and depressed in cerebellum whereas cyclic AMP levels were unchanged from control values. Intravenous administration of 2.5-3.5 mmol/kg of glucose to the hypoglycemic stuporous animals produced recovery of near normal neurological function within 45 s. Only brain glucose and aspartate levels returned to normal prior to behavioral recovery. These results suggest that of the several substances examined in this study, only glucose and perhaps aspartate have important roles in the biochemical mechanisms producing neurological abnormalities in hypoglycemic animals.

Topics: Adenosine Monophosphate; Adenosine Triphosphate; Amino Acids; Animals; Aspartic Acid; Behavior, Animal; Central Nervous System; Coma; Cyclic AMP; Cyclic GMP; gamma-Aminobutyric Acid; Glucose; Glutamic Acid; Glycogen; Hypoglycemia; Insulin; Male; Mice; Phosphocreatine; Recovery of Function

Levels of ATP are near normal in the cockroach nerve cord when hypoxia is sufficient to cause coma as determined by behavioral observations and nerve cord electrical activity. During anoxia the major change in ATP occurs after loss of measurable nerve activity. High glycogen levels and reduced energy demands due to coma may contribute to the resistance to anoxic death.

Topics: Adenosine Triphosphate; Animals; Central Nervous System; Cockroaches; Coma; Electrophysiology; Glycogen; Hypoxia; Male; Time Factors

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

Topics: Adrenal Gland Neoplasms; Aged; Androgens; Coma; Glycogen; Humans; Hypoglycemia; Male

Topics: Acridines; Adenosine Triphosphate; Adrenal Medulla; Adrenalectomy; Ammonia; Animals; Blood Glucose; Brain; Brain Chemistry; Carbon Isotopes; Coma; Creatinine; Female; Glucose; Glycogen; Lactates; Liver; Liver Glycogen; Male; Mice; Phosphates; Protein Binding; Rats; Reflex; Tissue Extracts

Interference with cerebral energy metabolism due to excess ammonia has been postulated as a cause of hepatic encephalopathy. Furthermore, consideration of the neurologic basis of such features of hepatic encephalopathy as asterixis, decerebrate rigidity, hyperpnea, and coma suggests a malfunction of structures in the base of the brain and their cortical connections. The three major sources of intracerebral energy, adenosine triphosphate (ATP), phosphocreatine, and glucose, as well as glycogen, were assayed in brain cortex and base of rats given ammonium acetate with resultant drowsiness at 5 minutes and subsequent coma lasting at least 30 minutes. Cortical ATP and phosphocreatine remained unaltered during induction of coma. By contrast, basilar ATP, initially 1.28 +/- 0.15 mumoles per g, was unchanged at 2.5 minutes but fell by 28.1, 27.3, and 26.6% (p < 0.001) at 5, 15, and 30 minutes after NH(4)Ac. At comparable times, basilar phosphocreatine fell more strikingly by 62.2, 96, 77.1, and 71.6% (p < 0.001) from a control level of 1.02 +/- 0.38 mumoles per g. These basilar changes could not be induced by anesthesia, psychomotor stimulation, or moderate hypoxia and were not due to increased accumulation of ammonia in the base. Glucose and glycogen concentrations in both cortex and base fell significantly but comparably during development of stupor, and prevention of the cerebral glucose decline by pretreatment with glucose did not obviate ammonia-induced coma or the basilar ATP fall. These findings represent the first direct evidence that toxic doses of ammonia in vivo acutely affect cerebral energy metabolism and that this effect is preferentially localized to the base of the brain.

Topics: Adenosine Triphosphate; Ammonia; Animals; Brain; Cerebral Cortex; Coma; Glucose; Glycogen; Lactates; Oxygen Consumption; Phosphocreatine; Pyruvates; Rats

Topics: Animals; Brain; Coma; Glycogen; Insulin; Rats