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The role of STIM1 and store operated calcium entry in glucose‐induced insulin secretion
Author(s) -
Zou Luyun,
Chatham John C
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.701.7
Subject(s) - secretion , stim1 , insulin , endocrinology , medicine , chemistry , calcium , glucose homeostasis , homeostasis , biology , insulin resistance
Calcium plays an important role in contributing to glucose homeostasis by regulating insulin secretion in β‐cells, primarily through activation of voltage gated calcium channels. Interestingly, STIM1 and Orail1 proteins, which regulate store operated calcium entry (SOCE) are present in β‐cells; however, the role of SOCE in β‐cells is unknown. Therefore the goal of this study was determine whether STIM1 plays a role in regulating glucose induced insulin secretion and if so whether this was affected by increased O‐GlcNAc levels. We found that STIM1, STIM2, and Orail1 proteins, the molecular machinery for required SOCE, were present in INS‐1 cells. To evaluate the role of STIM1 on insulin secretion INS‐1 cells were either transected with a STIM1 adenovirus over night or pre‐treated with SKF96365 (SKF, 5μM), an inhibitor of SOCE for 2 or 4hrs. Cells were preincubated with 3mM glucose for 2hrs followed by 15mM glucose to induce insulin secretion. STIM1 overexpression had no effect on glucose‐induced insulin secretion; however, SKF treatment (4hrs) decreased insulin secretion almost 2‐fold (p<0.05). These data suggest that SOCE may contribute to glucose‐induced insulin secretion in INS‐1 cells, however further studies are needed to confirm the effects of SKF.