2021 Fiscal Year Final Research Report
G12/13-dependent signaling of bioactive lipid receptors that regulate PPARgamma activity in adipocytes
| Project/Area Number |
19H03411
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Review Section |
Basic Section 48040:Medical biochemistry-related
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| Research Institution | Akita University |
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Principal Investigator |
Ishii Satoshi 秋田大学, 医学系研究科, 教授 (10300815)
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| Co-Investigator(Kenkyū-buntansha) |
安田 大恭 秋田大学, 医学系研究科, 講師 (70594951)
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| Project Period (FY) |
2019-04-01 – 2022-03-31
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| Keywords | シグナル伝達 / LPA / リゾフォスファチジン酸 |
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| Outline of Final Research Achievements |
Analysis of obese mice has shown that the fourth receptor (LPA4) for lysophosphatidic acid (LPA) functions as an aggravating factor for type 2 diabetes by coupling with G12/13 proteins in adipocytes. Thus, we compared the expression of LPA4 mRNA in human white adipose tissue between lean, diabetic obese, and non-diabetic obese individuals and found no significant differences among the three groups.
Like LPA4, LPA6 is a G12/13-coupled receptor and is expressed in adipocytes. Therefore, we conducted a study on the metabolic function of LPA6 using obese LPA6-KO mice and found no abnormalities in the metabolic parameters examined.
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| Free Research Field |
生化学
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| Academic Significance and Societal Importance of the Research Achievements |
肥満者の中には、代謝的に健康な肥満（MHO）と呼ばれるサブグループが存在し、これらの肥満者は健康な代謝を維持し、2型糖尿病などの肥満関連疾患の発症リスクの上昇を示さない。LPA4を介したMHOのメカニズムについての理解につながる研究を発展させることにより、新しい2型糖尿病の治療・診断方法の開発に寄与できる可能性がある。また、LPA4と受容体の機能が類似しているLPA6にも注目して今後検討することも有用であると考えられる。
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