Resolution of Ch25h mechanism at pancreatic beta cells in fulminant type 1 diabetes

2019 Fiscal Year Final Research Report

• Project/Area Number: 18K16230
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 54040:Metabolism and endocrinology-related
• Research Institution: Osaka University
• Principal Investigator: Hosokawa Yoshiya 大阪大学, 医学部附属病院, 特任助教(常勤) (10814569)
• Project Period (FY): 2018-04-01 – 2020-03-31
• Keywords: MIN6 / iPS細胞 / 25HC / ch25h

Outline of Final Research Achievements

The caspase-3 activity was significantly lower in both 25HC and cytokine treatment pancreatic cells included INSULIN positive cells induced from fulminant type 1 diabetes iPSCs than in only cytokine treatment.The proportion of cleaved caspase-3-positive cells among the induced INSULIN-positive cells was significantly lower in both 25HC and cytokine treatment fulminant type 1 diabetes iPSCs than in only cytokine treatment.
Plasma 25HC levels could be detected by GC-MS/MS and the measurement system of plasma 25HC levels from minutes amounts of blood sample could be in sight.

Free Research Field

内分泌・代謝

Academic Significance and Societal Importance of the Research Achievements

今回の研究により劇症1型糖尿病における膵β細胞のアポトーシスにch25hが関与していることが示唆され、他の1型糖尿病をふくめ膵β細胞傷害を抑制することでの糖尿病治療薬への応用が考えられる。また血中25HC測定系の樹立は劇症1型糖尿病の新規バイオマーカーとなりうる可能性が考えられる。