Endocrine Abstracts

Adipose tissue is a highly active metabolic organ which, together with its role as an energy storage depot, produces a wide variety of bioactive molecules (i.e. adipokines) with important roles in the regulation of energy metabolism and homeostasis, immunity and inflammation. Alterations in lipid metabolism and/or in adipokine production associated to the excess of adipose tissue that defines obesity or to adipose tissue deficiency, as occurs in lipodystrophy, are linked to insulin resistance, which represents a major risk factor for the development of type II diabetes, dyslipidemia, hypertension and cardiovascular diseases. In order to identify potential biomarkers of adipose tissue (dys)function, we employed proteomic techniques for the molecular analysis of adipose tissue components (adipocytes and stromal-vascular fraction), adipose tissue depots (subcutaneous (SAT) vs visceral (VAT) adipose tissue), and adipose tissue-related pathologies (insulin resistance associated to obesity). These studies revealed that, in lean individuals, the stromal–vascular faction contributes to major protein differences between VAT and SAT; in particular, we identified several differentially expressed proteins (ezrin, lamin A/C) that could contribute to the distinct association of VAT and SAT to specific adipose tissue-related pathologies (metabolic syndrome and lipodystrophy respectively). Comparative analysis of paired samples of VAT and SAT from lean and obese individuals also unveiled that obesity evokes depot-specific changes in the proteomic profile of adipose tissue. Furthermore, our data support the view that development of insulin resistance linked to obesity involves changes in adipose tissue proteins related to the cytoskeleton, glucose metabolism, cellular iron metabolism and protein folding and stress response. Collectively, our proteomic studies support the relevance of specific biological processes for the maintenance of normal functioning of human adipose tissue and their dysregulation in relation to the development of insulin resistance.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details unavailable.