2022 Fiscal Year Final Research Report
Elucidation of pancreatic beta-cell mass regulation mechanism by glucokinase
| Project/Area Number |
19K08992
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 54040:Metabolism and endocrinology-related
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| Research Institution | Hokkaido University |
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Principal Investigator |
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| Project Period (FY) |
2019-04-01 – 2023-03-31
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| Keywords | グルコキナーゼ / 膵β細胞 |
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| Outline of Final Research Achievements |
One of the pathophysiological features of type 2 diabetes is the progressive decrease in pancreatic beta-cell mass. Therefore, prevention of the progressive decrease in beta-cell mass and maintenance of beta-cell mass are considered as therapeutics in type 2 diabetes. We aimed to elucidate the beta-cell mass regulation mechanism by glucokinase. As a result, administration of a glucokinase activator to a mouse model of obese diabetes did not increase insulin secretion and beta-cell mass. On the other hand, glucokinase inactivation improved glucose tolerance by maintaining beta-cell function and mass.
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| Free Research Field |
糖尿病内分泌代謝内科学
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| Academic Significance and Societal Importance of the Research Achievements |
グルコキナーゼ活性の抑制は、糖尿病病態下で認められる過剰な糖代謝を適正化するという膵β細胞overworkの軽減、すなわち「Beta cell rest」という概念に一致しており、膵β細胞を刺激してインスリンを分泌させることで血糖を低下させるという従来の方法と逆の発想による2型糖尿病治療へのアプローチであり、極めて創造性、新規性は高い。さらに本研究は、トランスレーショナルリサーチとして、将来的な臨床試験を含めた2型糖尿病の臨床応用に展開できることが大いに期待される。
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