2016 Fiscal Year Final Research Report
ANGPTL8 function and development of coronary artery disease
| Project/Area Number |
26461359
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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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| Research Field |
Metabolomics
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
INAZU Akihiro 金沢大学, 保健学系, 教授 (80293348)
YAGI Kunimasa 金沢大学, 医学系, 准教授 (30293343)
OKAZAKI Satoko 金沢大学, 医薬保健学総合研究科, 特任助教 (80613744)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | ANGPTL8 / LPL / 冠動脈硬化症 |
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| Outline of Final Research Achievements |
Betatrophin (ANGPTL8), also known as “Lipasin” (lipoprotein lipase inhibitor), has been reported as a dual-regulator of glucose and lipid metabolism, even if it may not proliferate pancreatic beta cell in human. Functional variant R59W in betatrophin gene is common in Japanese, but little is known about long-term impact of this gene variant, and also about the effect of lipid-lowering drugs on this hormone.
Betatrophin R59W variant may be beneficial for healthy group, but was worsening genetic contributor of metabolic disorder in presence of metabolic burden especially low LPL activity. On the impact of R59W variant in 10 years follow up on glucose metabolism, betatrophin R59W variant was a susceptibility factor of future diabetes mellitus with low LPL activity. Strong statin treatments slightly decreased betatrophin levels, but effect sizes were minimal.
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| Free Research Field |
脂質代謝
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