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Am J Physiol Endocrinol Metab (February 11, 2002). doi:10.1152/ajpendo.00516.2001
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Articles in PresS, published online ahead of print February 11, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00516.2001
Submitted on November 16, 2001
Accepted on February 4, 2002

Gene expression profile of rat adipose tissue at the onset of high fat diet obesity

Jinping Li1, Xinxin Yu1, Wentong Pan1, and Roger H Unger2*

1 Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA
2 Research, Veterans Affairs Medical Center, Dallas, Texas, USA; Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA

* To whom correspondence should be addressed. E-mail: Roger.Unger{at}UTSouthwestern.edu.

Morbid obesity is the result of massive expansion of white adipose tissue (WAT) and requires recruitment of adipocyte precursor cells and their supporting infrastructure. To characterize the change in the expression profile of the preexisting WAT at the start of obesity, when adipocyte hypertrophy is present but hyperplasia is still minimal, we employed a cDNA subtraction screen for genes differentially expressed in epididymal fat pads harvested one week after the start of a 60% fat diet. Ninety-six genes were upregulated by at least 50% above the WAT of control rats receiving a 4% fat diet. Of these genes, 30 had not previously been identified. Sixteen of the 96 genes, including leptin, Acrp30 and resistin, were predicted to encode a signal peptide. Ten of the 16 had been previously identified in other tissues and implicated in cell growth, proliferation, differentiation, cell cycle control and angiogenesis. One was a novel gene. Twenty-nine novel fragments were identified. Thus, at the onset of high fat diet-induced obesity in rats, adipose tissue increases its expression of factors previously implicated in the expansion of nonadipocyte tissues, and of several uncharacterized novel factors. The only one of these thus far characterized functionally was found to promote lipogenesis.




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