Journal article

Publication year: 2017

Pages: e005556-

Journal: Journal of the American Heart Association Cardiovascular and Cerebrovascular Disease

Volume number: 6

Issue number: 4

ISSN: 2047-9980

DOI Link: https://doi.org/10.1161/JAHA.117.005556

Publisher: Wiley

Abstract: 
Background-Ketone bodies are known to substitute for glucose as brain fuel when glucose availability is low. Ketogenic diets have been described as neuroprotective. Similar data have been reported for triheptanoin, a fatty oil and anaplerotic compound. In this study, we monitored the changes of energy metabolites in liver, blood, and brain after transient brain ischemia to test for ketone body formation induced by experimental stroke.Methods and Results-Mice were fed a standard carbohydrate-rich diet or 2 fat-rich diets, 1 enriched in triheptanoin and 1 in soybean oil. Stroke was induced in mice by middle cerebral artery occlusion for 90 minutes, followed by reperfusion. Mice were sacrificed, and blood plasma and liver and brain homogenates were obtained. In 1 experiment, microdialysis was performed. Metabolites (eg glucose, P-hydroxybutyrate, citrate, succinate) were determined by gas chromatography-mass spectrometry. After 90 minutes of brain ischemia, beta-hydroxybutyrate levels were dramatically increased in liver, blood, and brain microdialysate and brain homogenate, but only in mice fed fat-rich diets. Glucose levels were changed in the opposite manner in blood and brain. Reperfusion decreased beta-hydroxybutyrate and increased glucose within 60 minutes. Stroke-induced ketogenesis was blocked by propranolol, a beta-receptor antagonist. Citrate and succinate were moderately increased by fat-rich diets and unchanged after stroke.Conclusions-We conclude that brain ischemia induces the formation of beta-hydroxybutyrate (ketogenesis) in the liver and the consumption of beta-hydroxybutyrate in the brain. This effect seems to be mediated by beta-adrenergic receptors.

Harvard Citation style: Koch, K., Berressem, D., Konietzka, J., Thinnes, A., Eckert, G. and Klein, J. (2017) Hepatic Ketogenesis Induced by Middle Cerebral Artery Occlusion in Mice, Journal of the American Heart Association Cardiovascular and Cerebrovascular Disease, 6(4), p. e005556. https://doi.org/10.1161/JAHA.117.005556

APA Citation style: Koch, K., Berressem, D., Konietzka, J., Thinnes, A., Eckert, G., & Klein, J. (2017). Hepatic Ketogenesis Induced by Middle Cerebral Artery Occlusion in Mice. Journal of the American Heart Association Cardiovascular and Cerebrovascular Disease. 6(4), e005556. https://doi.org/10.1161/JAHA.117.005556