2021 Fiscal Year Final Research Report
Preventive and therapeutic significance of CD52 in metabolic diseases with obesity
Project/Area Number |
19K08997
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 54040:Metabolism and endocrinology-related
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Research Institution | University of Toyama |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
和田 努 富山大学, 学術研究部薬学・和漢系, 講師 (00419334)
恒枝 宏史 富山大学, 学術研究部薬学・和漢系, 准教授 (20332661)
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Project Period (FY) |
2019-04-01 – 2022-03-31
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Keywords | 未病 / 2型糖尿病 / 肥満 / 慢性炎症 / エネルギー代謝 / SiglecG |
Outline of Final Research Achievements |
It is important to capture the condition before the onset of obesity as a cause of diabetes. By comprehensive mathematical analysis of gene fluctuation, CD52 is found as a "Mibyou”candidate factor involved in obesity. We examined the impact of CD52 on the obesity pathology. Expression of CD52 was specifically increased in the visceral fat of obese mice. TNFalpha and IL1beta expressions were increased in the liver of obese CD52-deficient mice. The expression of IFNgamma showed an increasing tendency in the visceral adipose tissue. Impaired glucose tolerance was observed in the CD52 knockout mice. Flow-cytometric analysis showed no changes in CD4- and CD8-positive T cells in the spleen and CD52 receptor Siglec-G in the macrophage of visceral adipose tissues. Thus, CD52 is the key factor involved in the suppression of obesity progression to keep adipose tissue healthy, and it exerts the effect by controlling chronic inflammation via mechanisms affecting the adipose-hepatic function.
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Free Research Field |
糖尿病・内分泌
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Academic Significance and Societal Importance of the Research Achievements |
病気の発症前状態である「未病」への対策は究極の予防医学であり、今後の医療に対する国家戦略と位置付けられている。本研究により、「未病肥満」の鍵因子CD52が、実際に2型糖尿病などの代謝疾患を未病状態で抑制 する生体防御因子であることが明らかとなり、本因子を標的とした未病状態からの介入の実現化に向けた研究が加速すると考えられる。また、本成果をプロトタイプとして、神経変性疾患やがんなど他の多彩な疾患の未病状態への介入法の開発研究に応用され、学際的波及効果は極めて高いと考えられる。
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