Mechanisms of increased glucose-stimulated insulin secretion during pregnancy

2017 Fiscal Year Final Research Report

• Project/Area Number: 26460396
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Pathological medical chemistry
• Research Institution: Kyorin University
• Principal Investigator: Ohara-Imaizumi Mica 杏林大学, 医学部, 教授 (40201941)
• Co-Investigator(Renkei-kenkyūsha): AOYAGI Kyota 杏林大学, 医学部, 講師 (50453527) ; NAGAMATSU Shinya 杏林大学, 医学部, 教授 (80231489) ; OKAMURA Tadashi 独立行政法人 国立国際医療センター, 研究所, 室長 (00333790)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: インスリン分泌 / 膵β細胞 / 妊娠糖尿病

Outline of Final Research Achievements

In preparation for the metabolic demands of pregnancy, β cells in the maternal pancreatic islets increase both in number and in glucose-stimulated insulin secretion per cell. Mechanisms have been proposed for the increased β cell mass, but not for the increased glucose-stimulated insulin secretion. Here we show using knockout mice for P2X7-purinoreceptor and CDKAL1, a type 2 diabetes susceptibility gene that (i) ATP, acting in a paracrine/autocrine manner through P2X7 plays an essential role in the increased glucose-stimulated insulin secretion of pregnancy; (ii) the decreased expression of CDKAL1 is associated with reduced glucose-stimulated insulin secretion during pregnancy.

Free Research Field

細胞生物学