期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 99, 期 17, 页码 11482-11486出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.132384699
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资金
- NHLBI NIH HHS [R01 HL056593, HL-56593] Funding Source: Medline
- NIDDK NIH HHS [R01 DK062388, R01DK-62388, R01DK-58037, R01DK-41096, R01 DK058037, R01 DK041096] Funding Source: Medline
- NIGMS NIH HHS [T32 GM007739, GM07739] Funding Source: Medline
Stearoyl-CoA desaturase (SCD) is a central lipogenic enzyme catalyzing the synthesis of monounsaturated fatty acids, mainly oleate (C18:1) and palmitoleate (C16:11), which are components of membrane phospholipids, triglycerides, wax esters, and cholesterol esters. Several SCID 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.
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