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2018 Fiscal Year Final Research Report

Development of specific ELISA for short-form GIP and elucidation of its secretion in human

Research Project

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Project/Area Number 16K19527
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Metabolomics
Research InstitutionAsahikawa Medical College

Principal Investigator

Takeda Yasutaka  旭川医科大学, 大学病院, 医員 (90431402)

Project Period (FY) 2016-04-01 – 2019-03-31
KeywordsGIP (1-30) / インクレチン / ELISA / 糖代謝
Outline of Final Research Achievements

The secretion of short-form gastric inhibitory polypeptide (GIP) (1-30) in human remains unclear. We developed an ELISA specific for GIP (1-30) and measured GIP (1-30) secretion during oral glucose tolerance test and cookie meal test in non-diabetics and type 2 diabetics. After both glucose and cookie load, GIP (1-30) blood levels increased. Interestingly, the increases of GIP (1-30) were much lower than those of GIP (1-42). Similarly to known incretins, the DPP-4 inhibitor increased blood GIP (1-30) levels.

Free Research Field

代謝・内分泌

Academic Significance and Societal Importance of the Research Achievements

本研究においてGIP (1-30)のELISA系を確立し、さらにヒトにおけるGIP (1-30)の分泌動態を世界に先駆けて明らかにした。GIP (1-30)が経口での糖の摂取や糖・蛋白質・脂質混成食の摂取により分泌が促進されること、即ち経口でのこれらの負荷がGIP (1-30)の分泌刺激となることや、GIP (1-42)とは末梢血中濃度が大きく異なること、既知のインクレチンと同様にDPP-4阻害薬によって分泌が増加することを見出した。以上の知見は、糖代謝における新たな調節因子としてのGIP (1-30)の役割の一端を明らかにするもので、糖尿病の病態や病因の解明の一助となる可能性を有する。

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Published: 2020-03-30  

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