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Dietary stearate and oleate in the development of hepatic steatosis and obesity
Author(s) -
Sampath Harini,
Miyazaki Makoto,
Ntambi James M
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a85-c
Subject(s) - lipogenesis , steatosis , medicine , endocrinology , triolein , triglyceride , chemistry , fatty liver , insulin resistance , lipid metabolism , biology , biochemistry , obesity , cholesterol , enzyme , lipase , disease
Fatty liver disease or hepatic steatosis, marked by increased accumulation of triglycerides in the liver, is brought on by chronic over‐nutrition and increases the risk for secondary conditions such as insulin resistance. Mice with a targeted mutation in the enzyme stearoyl‐CoA desaturase 1 (SCD1), which catalyzes the conversion of stearic acid into oleic acid, are lean and protected from diet‐induced obesity as well as insulin resistance. This leads us to hypothesize that oleate, the monounsaturated fatty acid product of SCD1, plays a direct role in the development of diet‐induced hepatic steatosis. 8‐week old male wild‐type (WT) and SCD1−/ − mice were fed 20% high‐fat diets containing either tristearin or triolein for 7 days. Triolein feeding resulted in significantly greater body weight and adipose tissue gains, as well as greater hepatic triglyceride and cholesteryl ester accumulation in WT and SCD1−/ − mice. Expression of lipogenic genes and the transcription factors SREBP‐1c and PGC‐1β, as measured by real‐time PCR, were increased by triolein feeding in both WT and SCD1−/ − animals. Conversely, activity of the AMP‐activated protein kinase (AMPK)‐ α1 was significantly higher in livers of SCD1−/ − mice after tristearin feeding but was unchanged in WT animals. Taken together, these results suggest that triolein feeding increases lipogenesis in WT and SCD1−/ − animals and downregulates lipid oxidation in SCD1−/ − animals. These data help clarify the roles of specific fatty acids in the modulation of hepatic lipid metabolism. This work has been supported by NIH Grant NIDDK‐R0162388 (JMN) and American Heart Association Predoctoral fellowship 0415001Z (HS).