Regulation of the expression of the mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase gene : its role in the control of ketogenesis

• Published in: Biochemical journal Vol. 283; no. 1; pp. 261 - 264
• Main Authors: CASALS, N, ROCA, N, GUERRERO, M, GIL-GOMEZ, G, AYTE, J, CIUDAD, C. J, HEGARDT, F. G
• Format: Journal Article
• Language: English
• Published: Colchester Portland Press 01.04.1992
• Subjects: Animals; Biological and medical sciences; Blotting, Northern; Dexamethasone - pharmacology; Diabetes Mellitus, Experimental - enzymology; Diabetes Mellitus, Experimental - genetics; DNA Probes; Fundamental and applied biological sciences. Psychology; Gene expression; Gene Expression Regulation, Enzymologic - drug effects; Gene Expression Regulation, Enzymologic - physiology; Hydroxymethylglutaryl-CoA Synthase - genetics; Ketone Bodies - biosynthesis; Mitochondria, Liver - enzymology; Mitochondria, Liver - physiology; Molecular and cellular biology; Molecular genetics; Rats; Rats, Inbred Strains; Ketogenesis; Rat; Enzyme; Liver; Hydroxymethylglutaryl-CoA synthase; Rodentia; Gene expression; In vivo; Vertebrata; Mitochondria; Regulation(control); Mammalia; Gene
• ISSN: 0264-6021; 1470-8728
• DOI: 10.1042/bj2830261

We have explored the role of mitochondrial 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase in regulating ketogenesis. We had previously cloned the cDNA for mitochondrial HMG-CoA synthase and have now studied the regulation in vivo of the expression of this gene in rat liver. The amount of processed mitochondrial HMG-CoA synthase mRNA is rapidly changed in response to cyclic AMP, insulin, dexamethasone and refeeding, and is greatly increased by starvation, fat feeding and diabetes. We conclude that one point of ketogenic control is exercised at the level of genetic expression of mitochondrial HMG-CoA synthase.