Exploration of the role of glucagon in the crosstalk between glucose metabolism and amino acid metabolism
Project/Area Number |
15H04681
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Environmental physiology(including physical medicine and nutritional physiology)
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Research Institution | Nagoya University |
Principal Investigator |
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Research Collaborator |
ODA HIROAKI
SEINO YUSUKE
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Project Period (FY) |
2015-04-01 – 2019-03-31
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Project Status |
Completed (Fiscal Year 2018)
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Budget Amount *help |
¥14,950,000 (Direct Cost: ¥11,500,000、Indirect Cost: ¥3,450,000)
Fiscal Year 2017: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2016: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2015: ¥8,320,000 (Direct Cost: ¥6,400,000、Indirect Cost: ¥1,920,000)
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Keywords | グルカゴン / アミノ酸 / 糖新生 / 肝臓 / 糖尿病 / 膵臓ランゲルハンス島 / エネルギー代謝 / 蛋白質 / ニコチンアミド / FGF21 / ランゲルハンス島 / α細胞 / アミノ酸代謝 / 細胞増殖 / 細胞内シグナル伝達 |
Outline of Final Research Achievements |
Glucagon was originally reported as a hyperglycemic substance that is present in pancreatic extract in 1923, the year of the Nobel Prize in Physiology or Medicine given to discovery of insulin. Therefore, the major physiological role of glucagon has been considered to raise blood glucose levels. However, mice deficient in glucagon gene, which we have produced, are normoglycemic and displayed increased serum amino acid levels. Our effort has been made to explore mechanisms involved in glucagon-dependent regulation of amino acid metabolism. Several lines of data and evidence are indicating that “truly” specific and physiological role of glucagon is regulation of amino acid catabolism, especially conversion of amino acids to substrates available for gluconeogenesis.
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Academic Significance and Societal Importance of the Research Achievements |
グルカゴンは血糖値を上げるホルモンであると広く認知され、糖尿病においては血糖値を上昇させることにより病態を悪化させる「悪役」とも考えられてきた。しかしながら、我々が独自に作成したグルカゴンを欠損する動物モデルを詳細に解析した結果、グルカゴンは蛋白質の構成要素であるアミノ酸の血中濃度の維持に必要不可欠な役割を持つことが明らかとなった。生体におけるアミノ酸代謝の制御のしくみは未解明の部分が多く、我々の成果をさらに展開することにより、糖尿病学・栄養学のみならず生命科学全般に広く影響を及ぼす新しい知見がもたらされることが期待できる。
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Report
(4 results)
Research Products
(39 results)
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[Journal Article] Glucose-dependent insulinotropic polypeptide is required for moderate high fat diet, but not high carbohydrate diet-induced weight gain.2018
Author(s)
Maekawa R, Ogata H, Murase M, Harada N, Suzuki K, Joo E, Sankoda A, Iida A, Izumoto T, Tsunekawa S, Hamada Y, Oiso Y, Inagaki N, Arima H, Hayashi Y, Seino Y.
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Journal Title
Am J Physiol Endocrinol Metab.
Volume: 6
Issue: 6
Pages: 111-112
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] Endogenous GIP ameliorates impairment of insulin secretion in proglucagon-deficient mice under moderate beta cell damage induced by streptozotocin.2016
Author(s)
Iida A, Seino Y, Fukami A, Maekawa R, Yabe D, Shimizu S, Kinoshita K, Takagi Y, Izumoto T, Ogata H, Ishikawa K, Ozaki N, Tsunekawa S, Hamada Y, Oiso Y, Arima H, Hayashi Y.
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Journal Title
Diabetologia
Volume: x
Issue: 7
Pages: 1533-1541
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Journal Article] Fatty acid binding protein 5 (FABP5) regulates diet-induced obesity (DIO) via GIP secretion from enteroendocrine K-cells in response to fat ingestion.2015
Author(s)
Shibue, K., Yamane, S., Harada, N., Hamasaki, A., Suzuki, K., Joo, E., Iwasaki, K., Nasteska, D., Harada, T., Hayashi, Y., Adachi, Y., Owada, Y., Takayanagi, R. and Inagaki, N.
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Journal Title
Am J Physiol Endocrinol Metab
Volume: 308
Issue: 7
Pages: 583-591
DOI
Related Report
Peer Reviewed / Open Access
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[Presentation] GIPはグルカゴン遺伝子欠損マウスにおいて膵β細胞障害時の血糖値改善に関与する2015
Author(s)
飯田淳史, 清野祐介, 前川龍也, 丹羽靖浩, 細川香里, 泉元貴子, 木下佳大, 高木祐輔, 尾方秀忠, 尾崎信暁, 恒川 新, 濱田洋司, 林 良敬, 大磯ユタカ
Organizer
第58回日本糖尿病学会年次学術集会
Place of Presentation
長野
Year and Date
2015-05-21
Related Report
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