The role of Semaphorin signaling in pathogenesis of obesity and fatty liver -possible implication of gastrointestinal biota.

2015 Fiscal Year Final Research Report

• Project/Area Number: 26670362
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: General internal medicine(including psychosomatic medicine)
• Research Institution: Chiba University
• Principal Investigator: Yokote Koutaro 千葉大学, 医学(系)研究科(研究院), 教授 (20312944)
• Co-Investigator(Kenkyū-buntansha): TAKEMOTO Minoru 千葉大学, 大学院医学研究院, 准教授 (60447307)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: セマフォリン / 腸内細菌 / 耐糖能 / 肥満 / 脂肪肝

Outline of Final Research Achievements

We previously identified a novel secretary Semaphorin, Semaphorin3G (Sema3G), that is expressed in vascular endothelial cells. We then evaluated the roles of Sema3G in gut microbiota and its implication in pathogenesis of the life-style related diseases including obesity and fatty liver disease. Metagenome analysis showed that Sema3G KO gut microbiota included more Bcteroides and less Firmicutes. In addition, Sema3G KO showed more Cyanobacteria and less Verrucomicrobia. Metabolic analysis revealed that Sema3G KO mice showed better glucose tolerance, better insulin sensitivity, and the fatty liver was less severe compared to wild type mice after high fat diet.

Free Research Field

老年医学