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 of free calcium in the cytoplasm. We confirmed Insulin-secreting β cell express CaBP-9k and assumed that CaBP-9k play a certain role in β cell insulin synthesis or secretion. Using CaBP-9k knock out (CaBP-9k KO) mice, we demonstrate ablation of CaBP-9k induces reduction of insulin secretion and hyperglycemia. Furthermore, to find the role of CaBP-9k in pathophysiologic condition, we evaluate the pathophysiology of aged wild-type and CaBP-9k KO mice. Compare to the aged wild-type mice accumulates abdominal fat, CaBP-9k KO mice does not. CaBP-9k mice showed decreased expression of PPARγ in liver, results in decreased lipid synthesis. Furthermore, CaBP-9k KO ablation induces endoplasmic reticulum (ER) stress, which increase insulin resistance. CaBP-9k KO mice showed more increased level of ER stress marker protein than wild type mice. Taken together, we assumed that CaBP-9k play a certain role in glucose homeostasis accompanying decreased lipid metabolism.