| Project/Area Number |
18K16196
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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 | Kyoto University |
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Principal Investigator |
SUZUKI Kazuyo 京都大学, 医学研究科, 特定助教 (90813866)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2020: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 代謝 / 肥満 / インクレチン / GIP / mTOR / 腸管ホルモン |
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| Outline of Final Research Achievements |
Incretins, gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1(GLP-1), are a group of peptide hormones that are secreted from enteroendocrine cells in response to meal ingestion and potentiate glucose-dependent insulin secretion from pancreatic β-cells. GIP, also called glucose-dependent insulinotropic polypeptide, secreted from enteroendorine K-cells located mainly in duodenum and upper small intestine. In this study, we tried to elucidate whether mTOR signaling potentiates incretin secretions or not.
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| Academic Significance and Societal Importance of the Research Achievements |
GIPはインスリン分泌促進作用・脂肪組織へのエネルギー蓄積作用を有しており、特に脂肪摂取は腸管内分泌K細胞からのGIP分泌を増強する。GIPは脂質代謝調節上重要な催肥満ホルモンであると言え、K細胞GIP産生機序の解明は摂食を通した脂質代謝制御機構を明らかにし肥満症治療薬の創薬にもつながる。本研究課題で、マウス腸管内分泌腫瘍株STC-1を用いて、生物種を越えて存在し細胞内栄養状態を関知して代謝調節する主要なリン酸化伝達経路mammalian target of rapamycin (mTOR)シグナルのK細胞内GIP産生における関与を検討した。
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