Dysregulation of Adipocytokines and Pathogenesis of Obesity-Related Disorders

2014 Fiscal Year Final Research Report

• Project Area: Molecular Basis and Disorders of Control of Apetite and Fat Accumulation
• Project/Area Number: 22126008
• Research Category: Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)
• Allocation Type: Single-year Grants
• Review Section: Biological Sciences
• Research Institution: Osaka University
• Principal Investigator: FUNAHASHI Tohru 大阪大学, 医学(系)研究科(研究院), 寄附講座教授 (60243234)
• Co-Investigator(Kenkyū-buntansha): KISHIDA Ken 大阪大学, 大学院医学(系)研究科, 非常勤講師 (10437329) ; MAEDA Norikazu (30506308) ; NISHIZAWA Hitoshi 大阪大学, 大学院医学(系)研究科, 助教 (20379259)
• Project Period (FY): 2010-04-01 – 2015-03-31
• Keywords: 内科 / 糖尿病 / 循環器・高血圧

Outline of Final Research Achievements

Adipocytes overexpressed S100A8 in early phase of obesity. Anti-S100A8 antibody suppressed dynamic movement of macrophage in adipose tissue of obesity. Exogenous adiponectin accumulated mainly to stromal vascular fraction (SVF) of adipose tissue and aorta without ectopic expression. Adipose SVF adiponecitn increased in obesity. Adiponectin covered surface of endothelial cells in aorta, and was additionally detected on smooth muscle cells in atherosclerotic lesion. Binding of adiponectin to aorta required T-cadherin. Also, concentration of adiponectin binding to C1q was elevated in spite of hypoadiponectinemia in patients with acute coronary syndrome. These data suggest adiponectin belongs to a new category of endocrine factors. Type 2 diabetics with metabolic syndrome often had polyvascular lesions by ultrasonography and abnormalities of adipocytokines. Estimation of arteriosclerosis and visceral fat are potentially useful for the management of these patients.

Free Research Field

内分泌代謝学