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Beta-hydroxybutyrate reverses insulin-induced hypoglycemic coma in suckling-weanling mice despite low blood and brain glucose levels.
Metab Brain Dis. 1986 Mar; 1(1):63-82.MB

Abstract

In normal suckling-weanling mice, DL-beta-hydroxybutyrate (30 mmol/kg ip) stimulated insulin secretion and reduced plasma glucose levels. In the brains of these animals, glucose levels were tripled due to a reduced rate of glucose utilization (determined by deoxyglucose phosphorylation). Other metabolite changes were compatible with inhibition of hexokinase, phosphofructokinase, glyceraldehyde-P-dehydrogenase, and pyruvate dehydrogenase activities. In contrast to the decrease in cerebral glycolysis, metabolite changes were compatible with an increase in the Krebs citric acid metabolic flux. The brain energy charge was also elevated. While it is generally believed that ketone bodies cannot sustain normal brain metabolism and function in the absence of glucose, DL-beta-hydroxybutyrate (20 or 30 mmol/kg ip) reversed insulin (100 U/kg sc)-induced hypoglycemia despite the persistence of a critically reduced plasma glucose concentration and near-zero brain glucose levels. Metabolic correlates of possible significance in the behavioral recovery from coma were reductions of the elevated levels of brain aspartate to below normal and ammonia levels to normal. Levels of acetyl CoA were unchanged both before and after treatment with beta-hydroxybutyrate.

Authors+Show Affiliations

Washington University School of Medicine, Department of Pediatrics, Children's Hospital, St. Louis, Missouri 63110.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

3334063

Citation

Thurston, J H., et al. "Beta-hydroxybutyrate Reverses Insulin-induced Hypoglycemic Coma in Suckling-weanling Mice Despite Low Blood and Brain Glucose Levels." Metabolic Brain Disease, vol. 1, no. 1, 1986, pp. 63-82.
Thurston JH, Hauhart RE, Schiro JA. Beta-hydroxybutyrate reverses insulin-induced hypoglycemic coma in suckling-weanling mice despite low blood and brain glucose levels. Metab Brain Dis. 1986;1(1):63-82.
Thurston, J. H., Hauhart, R. E., & Schiro, J. A. (1986). Beta-hydroxybutyrate reverses insulin-induced hypoglycemic coma in suckling-weanling mice despite low blood and brain glucose levels. Metabolic Brain Disease, 1(1), 63-82.
Thurston JH, Hauhart RE, Schiro JA. Beta-hydroxybutyrate Reverses Insulin-induced Hypoglycemic Coma in Suckling-weanling Mice Despite Low Blood and Brain Glucose Levels. Metab Brain Dis. 1986;1(1):63-82. PubMed PMID: 3334063.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Beta-hydroxybutyrate reverses insulin-induced hypoglycemic coma in suckling-weanling mice despite low blood and brain glucose levels. AU - Thurston,J H, AU - Hauhart,R E, AU - Schiro,J A, PY - 1986/3/1/pubmed PY - 1986/3/1/medline PY - 1986/3/1/entrez SP - 63 EP - 82 JF - Metabolic brain disease JO - Metab Brain Dis VL - 1 IS - 1 N2 - In normal suckling-weanling mice, DL-beta-hydroxybutyrate (30 mmol/kg ip) stimulated insulin secretion and reduced plasma glucose levels. In the brains of these animals, glucose levels were tripled due to a reduced rate of glucose utilization (determined by deoxyglucose phosphorylation). Other metabolite changes were compatible with inhibition of hexokinase, phosphofructokinase, glyceraldehyde-P-dehydrogenase, and pyruvate dehydrogenase activities. In contrast to the decrease in cerebral glycolysis, metabolite changes were compatible with an increase in the Krebs citric acid metabolic flux. The brain energy charge was also elevated. While it is generally believed that ketone bodies cannot sustain normal brain metabolism and function in the absence of glucose, DL-beta-hydroxybutyrate (20 or 30 mmol/kg ip) reversed insulin (100 U/kg sc)-induced hypoglycemia despite the persistence of a critically reduced plasma glucose concentration and near-zero brain glucose levels. Metabolic correlates of possible significance in the behavioral recovery from coma were reductions of the elevated levels of brain aspartate to below normal and ammonia levels to normal. Levels of acetyl CoA were unchanged both before and after treatment with beta-hydroxybutyrate. SN - 0885-7490 UR - https://www.unboundmedicine.com/medline/citation/3334063/Beta_hydroxybutyrate_reverses_insulin_induced_hypoglycemic_coma_in_suckling_weanling_mice_despite_low_blood_and_brain_glucose_levels_ DB - PRIME DP - Unbound Medicine ER -