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Reduced hepatic fatty acid oxidation in fasting PPARα null mice is due to impaired mitochondrial hydroxymethylglutaryl‐CoA synthase gene expression
Author(s) -
Le May Cédric,
Pineau Thierry,
Bigot Karine,
Kohl Claude,
Girard Jean,
Pégorier Jean-Paul
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)01648-3
Subject(s) - endocrinology , medicine , steatosis , fatty acid synthase , beta oxidation , peroxisome , biology , lipid metabolism , gluconeogenesis , triglyceride , fatty acid , peroxisome proliferator activated receptor , fatty liver , atp synthase , gene expression , metabolism , chemistry , receptor , gene , biochemistry , cholesterol , disease
Glucose and fatty acid metabolism (oxidation versus esterification) has been measured in hepatocytes isolated from 24 h starved peroxisome proliferator‐activated receptor‐α (PPARα) null and wild‐type mice. In PPARα null mice, the development of hypoglycemia during starvation was due to a reduced capacity for hepatic gluconeogenesis secondary to a 70% lower rate of fatty acid oxidation. This was not due to inappropriate expression of the hepatic CPT I gene, which was similar in both genotypes, but to impaired mitochondrial hydroxymethylglutaryl‐CoA synthase gene expression in the PPARα null mouse liver. We also demonstrate that hepatic steatosis of fasting PPARα null mice was not due to enhanced triglyceride synthesis.