Comparison of adipocyte-specific gene expression from WNIN/Ob mutant obese rats, lean control, and parental control

Adipose tissue development is a highly regulated phenomenon orchestrated by several check points (recruitment of mesenchymal stem cells and their lineage commitment) to form mature adipocytes. Once committed to obesity, expansion of adipose tissue occurs either by hypertrophy or hyperplasia or by both resulting in an altered physiological status. This precipitates as inflammatory responses, leading to endoplasmic reticulum and oxidative stress altering the gene expression of adipose tissue in a depot-specific manner. However, such studies reporting a phased gene expression profile in conditions of rodent obesity are not reported so far. WNIN/Ob mutant obese rat, developed at our institute is an excellent model to study the pathophysiological changes underlying obesity. Here, we report the gene expression profile of this mutant rat (obese and lean), compared with the parental control, with reference to markers of embryonic stem cells, adipogenesis, inflammation, and senescence in both subcutaneous (SCAT) and retroperitoneal (RPAT) adipose depots representing abdominal fat. We demonstrate an upregulation of genes such as Sox-2, Pref-1, PPAR gamma 2, LPL, IRS-1, GLUT-4, IL-6, TNF alpha, and telomerase in SCAT and RPAT depots of the obese rat compared to its lean counterpart indicating no difference in fat depots at different locations. This is suggestive of a similar phenotypic expression of mutant gene. Data form the phased gene expression changes of adipogenesis (embryonic/adipogenic/inflammatory) in the present obese rat model system advocate for inflammatory mediated response(s) associated with obesity-a condition often seen in humans.