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Loss of stearoyl–CoA desaturase-1 function protects mice against adiposity

2002; National Academy of Sciences; Volume: 99; Issue: 17 Linguagem: Inglês

10.1073/pnas.132384699

1091-6490

James M. Ntambi, Makoto Miyazaki, Jonathan P. Stoehr, Lan Hong, Christina Kendziorski, Brian S. Yandell, Yang Song, Paul Cohen, Jeffrey M. Friedman, Alan Attie,

Peroxisome Proliferator-Activated Receptors

Stearoyl–CoA desaturase (SCD) is a central lipogenic enzyme catalyzing the synthesis of monounsaturated fatty acids, mainly oleate (C18:1) and palmitoleate (C16:1), which are components of membrane phospholipids, triglycerides, wax esters, and cholesterol esters. Several SCD isoforms ( SCD1 - 3 ) exist in the mouse. Here we show that mice with a targeted disruption of the SCD1 isoform have reduced body adiposity, increased insulin sensitivity, and are resistant to diet-induced weight gain. The protection from obesity involves increased energy expenditure and increased oxygen consumption. Compared with the wild-type mice the SCD1 −/− mice have increased levels of plasma ketone bodies but reduced levels of plasma insulin and leptin. In the SCD1 −/− mice, the expression of several genes of lipid oxidation are up-regulated, whereas lipid synthesis genes are down-regulated. These observations suggest that a consequence of SCD1 deficiency is an activation of lipid oxidation in addition to reduced triglyceride synthesis and storage.