2023 Fiscal Year Final Research Report
Development of lifestyle-related disease treatment using a novel glucagon secretion mechanism
Project/Area Number |
21K16362
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Research Category |
Grant-in-Aid for Early-Career Scientists
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Allocation Type | Multi-year Fund |
Review Section |
Basic Section 54040:Metabolism and endocrinology-related
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Research Institution | Gunma University |
Principal Investigator |
Suga Takayoshi 群馬大学, 大学院医学系研究科, 研究員 (40848686)
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Project Period (FY) |
2021-04-01 – 2023-03-31
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Keywords | グルカゴン |
Outline of Final Research Achievements |
The mechanism of glucagon secretion from pancreatic α cells has not been fully elucidated. Previously, we reported that the sodium-glucose-coupled transporter (SGLT)-1, which co-transports glucose along with Na+ into cells, is expressed in pancreatic α-cells.However, it was unclear whether SGLT-1 in pancreatic α cells affected endogenous glucagon secretion in vivo.When SGLT-specific substrate was administered to mice, a significant increase in blood glucagon concentration was observed compared to control. Chronic administration of SGLT-specific substrates to mice resulted in weight loss. It has been suggested that promoting glucagon secretion may be applicable to obesity treatment.
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Free Research Field |
消化器病学
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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。またグルカゴンには抗肥満作用が知られており、膵α細胞SGLT-1を介した新たな生活習慣病治療に繋がる可能性が本研究の意義である。
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