Study of new glucagon secretion mechanism for clinical application

2020 Fiscal Year Final Research Report

• Project/Area Number: 19K23958
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Multi-year Fund
• Review Section: 0902:General internal medicine and related fields
• Research Institution: Gunma University
• Principal Investigator: Suga Takayoshi 群馬大学, 大学院医学系研究科, 助教 (40848686)
• Project Period (FY): 2019-08-30 – 2021-03-31
• Keywords: グルカゴン / 脂肪肝 / 肥満 / 糖尿病

Outline of Final Research Achievements

The mechanism of glucagon secretion from pancreatic α cells has not been fully elucidated. We recently reported that sodium-glucose cotransporter (SGLT) -1 is expressed in pancreatic α-cells. However, it was unclear whether this pancreatic α-cell SGLT-1 actually regulates endogenous glucagon secretion in vivo. In this study, we found that SGLT-specific substrate significantly increased plasma glucagon concentration in mice compared to control, which indicated that pancreatic α-cell SGLT-1 regulates glucagon secretion in vivo.

Free Research Field

消化器病学

Academic Significance and Societal Importance of the Research Achievements

本研究において膵α細胞SGLT-1が生体内においても実際に内因性グルカゴン分泌を制御している可能性が示唆された。糖尿病ではグルカゴンの分泌異常が知られているが、そのメカニズムを解明する上で、膵α細胞SGLT-1の観点から有用な情報を提供できる可能性がある点が、本研究の意義である。