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2018 Fiscal Year Final Research Report

the role of endothelial cells on adipocyte metabolism

Research Project

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Project/Area Number 16K09812
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Endocrinology
Research InstitutionKeio University

Principal Investigator

Kanda Takeshi  慶應義塾大学, 腎臓内分泌代謝内科, 講師 (80317114)

Research Collaborator ITOH Hiroshi  
WAKINO Shu  
Project Period (FY) 2016-04-01 – 2019-03-31
Keywordsグレリン / 血管内皮細胞 / 肥満
Outline of Final Research Achievements

Endothelial cells are known to regulate adiposity by lipid uptake from the blood circulation to white adipocytes. However, the mechanism underlying the regulation of endothelial transport by systemic energy balance remains unclear. Ghrelin, a gastric peptide, conveys nutritional information and increases adiposity mainly through the central nervous system. The deficiency of its receptor, growth hormone secretagogue-receptor (GHSR), leads to reduced adiposity after high fat intake.
This study demonstrated that endothelial GHSR plays an important role in endothelial function and controls lipid metabolism in response to ghrelin. The findings also suggest that the endothelium regulates white adipocyte metabolism.

Free Research Field

内分泌

Academic Significance and Societal Importance of the Research Achievements

肥満症を基盤として耐糖能異常、高中性脂肪血症、低HDL血症、高血圧が集積し動脈硬化の高リスク群を形成することから、肥満症ならびに脂肪蓄積の病態解明は心血管イベントを阻止する上で極めて重要である。肥満症では耐糖能異常・脂質代謝異常を介して血管内皮障害が引き起こされ、血管拡張不全や接着分子発現亢進により動脈硬化の発症に寄与すると従来は考えられてきた。本研究により血管内皮細胞はグレリンを介して体内の負エネルギーバランス時に脂質を吸収することが明らかとなり、新たな内皮細胞の機能が明らかとなった。

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Published: 2020-03-30  

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