Gene expression profile of rat adipose tissue at the onset of high-fat-diet obesity.
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 1 wk 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, adipocyte complement-related protein 30 kDa, 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.
Li
Jinping
J
Gifford Laboratories, Touchstone Center for Diabetes Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8854, USA.
Yu
Xinxin
X
Pan
Wentong
W
Unger
Roger H
RH
D017667:Adipocytes / Q000737:chemistry; D052242:Adiponectin; D000273:Adipose Tissue / Q000737:chemistry* / Q000473:pathology; D000818:Animals; D001798:Blood Proteins / Q000235:genetics; D003598:Cytoskeletal Proteins / Q000235:genetics; D004041:Dietary Fats / Q000008:administration & dosage*; D020869:Gene Expression Profiling; D006729:Hormones, Ectopic / Q000235:genetics; D006965:Hyperplasia; D006984:Hypertrophy; D036341:Intercellular Signaling Peptides and Proteins; D020738:Leptin / Q000235:genetics; D008055:Lipids / Q000096:biosynthesis; D008297:Male; D008928:Mitochondria / Q000378:metabolism; D020932:Nerve Growth Factor; D009747:Nutritional Physiological Phenomena; D009765:Obesity / Q000209:etiology / Q000235:genetics* / Q000473:pathology; D010101:Oxygen Consumption / Q000235:genetics; D011506:Proteins / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D052243:Resistin; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction; D014157:Transcription Factors / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
D052242:Adiponectin; D001798:Blood Proteins; D003598:Cytoskeletal Proteins; D004041:Dietary Fats; D006729:Hormones, Ectopic; D036341:Intercellular Signaling Peptides and Proteins; D020738:Leptin; D008055:Lipids; D011506:Proteins; D012333:RNA, Messenger; D052243:Resistin; C499622:Retn protein, rat; C486575:Retnla protein, rat; D014157:Transcription Factors; D014409:Tumor Necrosis Factor-alpha; D020932:Nerve Growth Factor