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J. Lipid Res.
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Originally published In Press as doi:10.1194/jlr.M300013-JLR200 on March 16, 2003

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Journal of Lipid Research, Vol. 44, 1199-1208, June 2003
Copyright © 2003 by Lipid Research, Inc.

Fatty acid flux suppresses fatty acid synthesis in hamster intestine independently of SREBP-1 expression

F. Jeffrey Field1, Ella Born and Satya N. Mathur

Department of Veterans Affairs and Department of Internal Medicine, University of Iowa, Iowa City, IA 52242

1 To whom correspondence should be addressed. e-mail: f-jeffrey-field{at}uiowa.edu

Hamsters were fed a control diet or diets containing palm, olive, safflower, or fish oil for 2 weeks. In villus cell populations from duodenum, jejunum, and ileum, rates of intestinal fatty acid and cholesterol synthesis were estimated, as were sterol regulatory element-binding protein (SREBP)-1a, SREBP-1c, SREBP-2, HMG-CoA synthase, fatty acid synthase, ATP citrate lyase, acetyl-CoA carboxylase mRNA levels, and SREBP-1 and SREBP-2 mass. Plasma cholesterol and triacylglcerol levels were increased in animals ingesting palm oil and decreased in animals ingesting fish oil. Fatty acid synthesis and fatty acid synthase activity were decreased in the proximal intestine of animals ingesting all the fat-containing diets. Intestinal cholesterol synthesis was unaltered. In animals fed fat, SREBP-1c gene expression was modestly increased in the duodenum of hamsters fed palm oil or olive oil, and decreased in animals ingesting safflower oil or fish oil. Fatty acid synthase, acetyl-CoA carboxylase, ATP citrate lyase, SREBP-2, and HMG-CoA synthase mRNA levels were not altered, nor were SREBP-1 or SREBP-2 mass. In the intestine, dietary polyunsaturated fatty acids suppress SREBP-1c mRNA without altering expression of its target genes, fatty acid synthase, acetyl-CoA carboxylase, or ATP citrate lyase.

Fatty acid influx decreases intestinal fatty acid synthesis by a posttranscriptional mechanism independent of the SREBP pathway.

Abbreviations: SREBP, sterol regulatory element-binding protein

Supplementary key words fat diet • cholesterol • triacylglycerol • gene expression


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