The role of primary cilia on cell to cell communication in pancreatic islets

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K08488
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General physiology
• Research Institution: Ritsumeikan University
• Principal Investigator: Mukai Eri 立命館大学, 生命科学部, 准教授 (60362539)
• Project Period (FY): 2016-04-01 – 2019-03-31
• Keywords: 細胞間情報伝達 / インスリン分泌 / 糖代謝

Outline of Final Research Achievements

Pancreatic b cells within islets synchronize functionally by cell to cell communication, therefore, necessary and enough insulin secretory response is observed. However, the regulatory mechanism has not been unclear. We investigated the involvement of primary cilia on synchronized secretory function of b cells within islets. Glucose-stimulated insulin secretion (GSIS) from pseudoislets of b cells was increased more than that from b cells in monolayer. Inhibitory effect of somatostatin on GSIS was augmented in pseudoislets compared with b cells in monolayer. Defect of primary cilia resulted in a decrease in inhibitory effect of somatostatin on GSIS in pseudoislets. These results indicate that primary cilia is involved in synchronized secretory function of b cells within islets.

Free Research Field

基礎医学、代謝学、生理学

Academic Significance and Societal Importance of the Research Achievements

我が国の2型糖尿病では膵β細胞からのグルコースによるインスリン分泌応答が選択的に低下していることから、厳密なインスリン分泌応答の制御機構の解明や糖尿病におけるインスリン分泌障害のメカニズムを明らかにすることは糖尿病の治療につながる。今回の検討により、これまで明らかにされていなかった細胞膜上の小器官である一次繊毛の新たな役割が明らかとなったことから、インスリン分泌機構の研究分野に新たな研究アプローチが開けたものと確信する。