Molecular basis of the severe ectopic browning transition of adipocytes in novel mice with resistance against obesity and diabetes

2016 Fiscal Year Final Research Report

• Project/Area Number: 26461369
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Metabolomics
• Research Institution: Toho University
• Principal Investigator: JIANG Meizi 東邦大学, 医学部, 非常勤研究生 (00624066)
• Co-Investigator(Renkei-kenkyūsha): BUJO Hideaki 東邦大学, 医学部, 教授 (80291300)
• Research Collaborator: SHIMIZU Naomi 東邦大学, 医学部, 講師 (30375802) ; HIGASHI Morihiko 埼玉医科大学, 医学部, 准教授 (00323395) ; Antonio Vidal-Puig University of Cambridge, Addenbrooke's Hospital Metabolic Research Laboratories, 教授
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: LR11 / エネルギー消費 / 褐色細胞 / 機能獲得 / 肥満 / 糖尿病

Outline of Final Research Achievements

This study was aimed to clarify the mechanism underlying the regulation for the functional transition from white adipocytes to brown adipocytes, and to propose a novel modulation therapy for diabetes and obesity. Cell biological analyses showed that LR11 played an important role as an inhibitor in the functional acquisition of brown adipocytes. Intracellular signal analyses showed that, in the inhibition activity of soluble LR11 for the browning differentiation, LR11 was thought to at least in part inhibit the BMP7-induced signal cascade by the complex formation with the receptor BMPR. Taken together, LR11 was an inhibitor for the functional acquisition of brown adipocytes, and is possibly applied for the novel therapy for obesity and diabetes.

Free Research Field

代謝学