RGD Reference Report - Mitochondrial 3-hydroxy-3-methylglutaryl coenzyme A synthase and carnitine palmitoyltransferase II as potential control sites for ketogenesis during mitochondrion and peroxisome proliferation.

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Mitochondrial 3-hydroxy-3-methylglutaryl coenzyme A synthase and carnitine palmitoyltransferase II as potential control sites for ketogenesis during mitochondrion and peroxisome proliferation.
Authors:	Madsen, L Garras, A Asins, G Serra, D Hegardt, FG Berge, RK
Citation:	Madsen L, etal., Biochem Pharmacol. 1999 May 1;57(9):1011-9.
RGD ID:	2326088
Pubmed:	PMID:10796071 (View Abstract at PubMed)
3-Thia fatty acids are potent hypolipidemic fatty acid derivatives and mitochondrion and peroxisome proliferators. Administration of 3-thia fatty acids to rats was followed by significantly increased levels of plasma ketone bodies, whereas the levels of plasma non-esterified fatty acids decreased. The hepatic mRNA levels of fatty acid binding protein and formation of acid-soluble products, using both palmitoyl-CoA and palmitoyl-L-carnitine as substrates, were increased. Hepatic mitochondrial carnitine palmitoyltransferase (CPT) -II and 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase activities, immunodetectable proteins, and mRNA levels increased in parallel. In contrast, the mitochondrial CPT-I mRNA levels were unchanged and CPT-I enzyme activity was slightly reduced in the liver. The CoA ester of the monocarboxylic 3-thia fatty acid, tetradecylthioacetic acid, which accumulates in the liver after administration, inhibited the CPT-I activity in vitro, but not that of CPT-II. Acetoacetyl-CoA thiolase and HMG-CoA lyase activities involved in ketogenesis were increased, whereas the citrate synthase activity was decreased. The present data suggest that 3-thia fatty acids increase both the transport of fatty acids into the mitochondria and the capacity of the beta-oxidation process. Under these conditions, the regulation of ketogenesis may be shifted to step(s) beyond CPT-I. This opens the possibility that mitochondrial HMG-CoA synthase and CPT-II retain some control of ketone body formation.

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Object Symbol	Species	Term	Qualifier	Evidence	With	Notes	Source	Original Reference(s)
Cpt2	Rat	fatty acid beta-oxidation		IEP			RGD
Cpt2	Rat	response to fatty acid		IEP			RGD
Hmgcs2	Rat	response to fatty acid		IEP		3-thia fatty acids	RGD

Objects Annotated

Genes (Rattus norvegicus)

Cpt2 (carnitine palmitoyltransferase 2)

Hmgcs2 (3-hydroxy-3-methylglutaryl-CoA synthase 2)

Objects referenced in this article

Gene	CPT2	carnitine palmitoyltransferase 2	Homo sapiens
Gene	Cpt2	carnitine palmitoyltransferase 2	Mus musculus

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Mitochondrial 3-hydroxy-3-methylglutaryl coenzyme A synthase and carnitine palmitoyltransferase II as potential control sites for ketogenesis during mitochondrion and peroxisome proliferation.