: White adipose tissue (WAT) has an important role in the regulation of metabolic homeostasis. It is well known that two distinct WAT depots in mammals, subcutaneous WAT (sWAT) and visceral WAT (vWAT) display different metabolic roles and it could be presumed that exert different response to various hormones. Numerous studies revealed leading role of insulin in both fat accumulation (lipogenesis) and adipocyte differentiation (adipogenesis) although it is not clear is there a difference in response among these two depots. The aim of this study was to reveal effects of insulin treatments on sWAT and vWAT morphology. Male Wistar rats were treated acutely (1 day) or chronically (3 days) with low (0.4 IU/kg bm) or high (4 IU/kg bm) dose of insulin. Saline-treated animals served as controls. The portions of retroperitoneal, epididymal and subcutaneous WAT (rWAT, eWAT, sWAT, respectively) were removed and prepared for microscopic and Western blot analyses. Tissue components (adipocytes, blood vessels and stroma) volume density and cell profile density per unit area were determined. To establish adipogenic origin of multilocular/paucilocular cells PCNA immunoexpression was examined, while protein expression and cell presence of phosphorylated form (phospho-IR) of insulin receptor (IR) was used to analyze insulin signaling. Our results demonstrate slightly higher number of adipocytes and adipogenic cells and increased capillarization in vWAT depots. A stronger response of vWAT to insulin treatment in comparison to sWAT is due to higher phospho-IR expression in endothelial and multilocular/paucilocular cells of analyzed vWAT depots. Namely, in hyperinsulinaemia canonical insulin-signaling pathway favors adipogenesis and capillary remodeling in vWAT to a greater extent than in sWAT depot. Our results suggest that insulin-induced differences in remodeling of sWAT and vWAT depots may contribute to visceral obesity and development and progression of insulin resistance and diabetes type 2 among other visceral obesity-associated metabolic diseases.
20 - 23 May 2017
European Society of Endocrinology