Endocrine Abstracts

Obesity is characterized by insulin resistance and pancreatic β-cell dysfunction; moreover, secretion of adipokines from adipocytes may affect metabolic functions in several tissues, including pancreatic β-cells. Extracellular vesicles (EVs), released by cells as exosomes or shedding vesicles, play a key role in cell-to-cell communication, modifying the phenotype and function of recipient cells by delivering proteins, RNAs and microRNAs. The crosstalk between adipocytes and β-cells in the regulation of glucose and lipid metabolism is still unclear. We hypothesized that EVs derived from adipocytes are able to influence the survival and function of β-cells in pathophysiological conditions. In this study, the role of EVs released by murine 3T3-L1 adipocytes was evaluated on cell viability and proliferation, apoptosis and function of rat INS-1E β-cells and human pancreatic islets. INS-1E β-cells and human pancreatic islets were treated for 24 and 72 hours, respectively, with EVs in either presence or absence of CKs or palmitic acid and high glucose (P/G). Our results show that EVs derived from untreated adipocytes promote cell survival and proliferation, inhibit apoptosis in β-cells and pancreatic islets treated with CKs and P/G, and stimulate glucose-induced insulin secretion. Conversely, EVs derived from adipocytes treated with CKs enhanced the detrimental effects of CKs and P/G. These results suggest a functional crosstalk between adipose tissue and β-cells/pancreatic islets. Furthermore, the protective effects of EVs derived from adipocytes on survival and function of β-cells exposed to stress, such as inflammatory CKs or glucolipotoxicity, suggest possible therapeutic implications in pathological conditions like diabetes and obesity.