Endocrine Abstracts

Cellular Ca2+ signals have been proposed to activate signal for hormone secretion. In pancreatic β cell which produce insulin, Ca2+ signals have been known contributing insulin secretion. Prior to conduct this study, we confirmed calbindin-D9k (CaBP-9k) which responsible for regulation of the distribution offree calcium in the cytoplasm. Hypoxic condition induces endoplasmic reticulum(ER) stress, increase both insulin signaling and insulin resistance. Byexposing hypoxia, CaBP-9k KO mice showed more increased level of ER stressmarker protein than wild type mice. To examine the cumulative effacement of CaBP-9k molecule ablation, we did examined the glucose tolerant test for 6, 12, 18 24 months old mice. After 6 month, CaBP-9k KO mice showed delayedregulation of serum glucose after glucose administration. Serum insulin of CaBP-9k KO mice were decreased compare to wildtype mice. In addition, theinsulin transcription factors of CaBP-9k KO mice (Mafa, Pdx, NeuroD1) have been downregulated. It demonstrated that CaBP-9k is not only the part of the insulin-secreting calcium signaling but also insulin working mechanism which could link to pathology for exacerbating type 1diabetes to type 2 diabetes.