8^th Euro Global Diabetes Summit and Medicare Expo

Biography

Biography: Mercedes Mirecki-Garrido1

Abstract

Currently there has been a rapid increase in the prevalence of diabetes and associated metabolic disorders. Identifying the molecular mechanisms responsible isessential to develop effective strategies. An insufficient number of insulin-producing β cells is a hallmark of both type 1 and type 2 diabetes. SOCS proteins are powerful inhibitors of pathways involved in survival and function of pancreatic β cells [1] also are potent regulators of pro-insulin processing and insulin secretion in β-cells. Moreover, constitutive production of SOCS2 in β-cells leads to hyperglycaemia and glucose intolerance [2]. It is the rationale to investigate, how SOCS2 ablation may influence the development of diabetes in a mice model of autoimmune diabetes and β-cell destruction (multiple low-dose of streptozotocin (MLD-STZ). To analyze SOCS2 glucose homeostatsis and metabolism, all diabetes development parameters were monitored, and both MLD-STZ-treated SOCS2-/- and WT mice developed severe diabetes after day 9 from injecting first dose of STZ. However, SOCS2−/− mice were more resistant to develop diabetes. Also our results suggest higher degree of insulin sensitivity with SOCS2 ablation. Moreover, we further observed higher fasting plasma insulin and the higher HOMA-IR in MLD-STZ- treated SOCS2-/- mice. Taken together, the results suggest that SOCS2 ablation seems to compensate β-cell destruction induced by MLD-STZ. The insulin immunostaining assays showed that SOCS2-/- pancreas have higher β-cell mass and bigger islets size than the control WT pancreas [3].These results seems to explain the augmented serum insulin levels observed in SOCS2-/-, also when treated with the STZ a destruction in the β-cell of the WT was observed, but some conserved structures could be find in the SOCS2-/-. In summary, this study identified SOCS2 as an important regulator of insulin homeostasis in vivo and suggests that inhibition of SOCS2 may be used as therapeutic target to ameliorate diabetes development.