Journal article
Dysfunction of lipid sensor GPR120 leads to obesity in both mouse and human
Abstract
Mice deficient in the lipid sensor GPR120 develop obesity, glucose intolerance and fatty liver when fed a high-fat diet, and a loss-of-function variant in the GPR120 gene strongly contributes to increased obesity in human.
Authors
Ichimura A; Hirasawa A; Poulain-Godefroy O; Bonnefond A; Hara T; Yengo L; Kimura I; Leloire A; Liu N; Iida K
Journal
Nature, Vol. 483, No. 7389, pp. 350–354
Publisher
Springer Nature
Publication Date
March 2012
DOI
10.1038/nature10798
ISSN
0028-0836
Fields of Research (FoR)
Medical Subject Headings (MeSH)
AdipocytesAdipogenesisAdipose TissueAnimalsCalcium SignalingCell DifferentiationDNA Mutational AnalysisDiet, High-FatEnergy MetabolismEuropeExonsFatty LiverGene Expression RegulationGlucagon-Like Peptide 1GlucoseGlucose IntoleranceHumansInsulinInsulin ResistanceLipogenesisLiverMacrophagesMiceMutationObesityReceptors, G-Protein-CoupledSignal TransductionWhite People