The role of endothelial leptin receptor in lifestyle-related diseases.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25461396
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Endocrinology
• Research Institution: Keio University
• Principal Investigator: KANDA Takeshi 慶應義塾大学, 保健管理センター, 講師 (80317114)
• Co-Investigator(Kenkyū-buntansha): KOMATSU Motoaki 慶應義塾大学, 医学部腎臓内分泌代謝科, 助教 (70528687)
• Co-Investigator(Renkei-kenkyūsha): ITOH Hiroshi 慶應義塾大学, 医学部腎臓内分泌代謝科, 教授 (40252457) ; WAKINO Shu 慶應義塾大学, 医学部腎臓内分泌代謝科, 准教授 (50265823)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: レプチン / 内皮細胞

Outline of Final Research Achievements

Obesity is a major contributor of lifestyle-related diseases. The key hormone that regulates body weight is leptin, which is secreted mainly by white adipocytes and decreases adiposity by both reducing food intake and increase in energy expenditure through brown adipocyte activation. To examine the direct effect of leptin, we studied ob/ob mouse. We performed labeled oral fat load test mixed with 3H-triolein. Leptin decreased RI uptake in inguinal and epididymal white adipose tissue (WAT) and leptin increased RI uptake in brown adipose tissue (BAT). Endothelial cell is known to be leptin target organs and plays an important role in lipid uptake and obesity. We investigated the role of endothelial leptin signaling by using endothelial leptin receptor KO mouse (EC-ObR KO). The net uptake of labeled FFA was decreased in BAT in EC-ObR KO. These data suggest that leptin inhibits lipid uptake through endothelial Ob-R and endothelial cells shift fat distribution toward brown adipose tissue.

Free Research Field

内分泌