Endocrine Abstracts (2018) 56 GP107 | DOI: 10.1530/endoabs.56.GP107

Cumulative effect of glucose regulation in Calbindin-D9k knockout mice

Eui-Bae Jeung, Changhwan Ahn, Bo Hui Jeon, Seon Young Park & Duc Viet Ly

Chungbuk National University, Cheongju, Republic of Korea.

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.

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