| 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 |
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| Review Section |
Basic Section 54040:Metabolism and endocrinology-related
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| Research Institution | Gunma University |
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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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| Project Status |
Completed (Fiscal Year 2023)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2022: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2021: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | グルカゴン / 脂肪肝 / 肥満 / 糖尿病 / 生活習慣病 |
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| Outline of Research at the Start |
グルカゴンは膵α細胞から分泌されるが、その分泌機構は十分に解明されていない。申請者は既にグルコーストランスポーターSGLT-1が膵α細胞に発現していることを報告した。本研究は膵α細胞SGLT-1によるグルカゴン分泌制御に着目した臨床応用を目的とする。
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| 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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| 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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