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

Abstract

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.

Lower body adipose tissue removal decreases glucose tolerance and insulin sensitivity in mice with exposure to high fat diet

“…In general, early adipocyte hyperplasia associated HFD feeding is demonstrated to be preceded by an increase in proliferation markers in the stromal vascular cells of adipose tissue. [56][57][58] However, other studies demonstrate HFD-induced proliferation potential is dependent on the magnitude of adiposity, 59 which can vary according to diet composition or experiment length, and/or depot location. 60 In the present experiment 5 week HFD feeding did not alter adipose depot markers of proliferation in Sham mice, but adipose depot compensatory changes at the molecular level were initiated in response to IngX in Chow fed mice only.…”

Serum concentrations of resistin-like molecules β and γ are elevated in high-fat-fed and obese db/db mice, with increased production in the intestinal tract and bone marrow

“…Further analysis, considering the crystal structure data of resistin and RELMβ, is necessary to clarify the mechanism of homo/heterodimer formation of resistin family proteins [20]. This is the first study to investigate the serum concentrations and tissue contents of RELMβ and RELMγ in insulin-resistant animals, while resistin expression has been analysed in several models of obesity and diabetes [8,11,[25][26][27][28][29][30]. In high-fat-fed mice and db/db mice, serum levels of RELMβ and RELMγ were apparently increased.…”

Integrative physiology of human adipose tissue

“…Leptin has angiogenic properties, 42,43 and adipocytes secrete matrix metaloproteinases that may be involved in vascular remodelling. 44 Expression of genes involved in angiogenesis is upregulated during weight gain in animals, 45,46 and inhibition of angiogenesis reduces fat deposition in various obesity models in mice. 47 Situations of negative energy balance involve loss of adipocyte TG stores.…”