Related Experiment Video
Updated: May 22, 2026
09:21
BRET-based G Protein Biosensors for Measuring G Protein-Coupled Receptor Activity in Live Cells
Published on: November 7, 2025
Omega 3 fatty acids and GPR120
Da Young Oh1, Jerrold M Olefsky
1Department of Medicine, Division of Endocrinology and Metabolism, University of California, San Diego, La Jolla, CA 92093, USA.
Cell Metabolism
|May 8, 2012
Summary
Genetic variants in GPR120 increase obesity and metabolic syndrome risk. GPR120 knockout mice show obesity, inflammation, and insulin resistance, highlighting its role in metabolic diseases like diabetes.
Area of Science:
- Metabolic diseases
- Genetics
- Molecular biology
Background:
- Loss-of-function gene variants in GPR120 are linked to increased risk of obesity and metabolic syndrome.
- GPR120 plays a crucial role in metabolic regulation.
Purpose of the Study:
- To investigate the role of GPR120 signaling in the development of obesity, inflammation, and insulin resistance.
- To understand the implications of GPR120 dysfunction in metabolic syndrome and diabetes mellitus.
Main Methods:
- Analysis of human gene variants.
- Phenotypic characterization of GPR120 knockout (KO) mice.
Main Results:
- Human GPR120 variants are associated with higher risk for obesity and metabolic syndrome.
- GPR120 KO mice exhibit obesity, heightened inflammation, and insulin resistance.
Conclusions:
- GPR120 signaling is critical for maintaining metabolic homeostasis.
- Dysfunctional GPR120 signaling contributes to the pathogenesis of metabolic syndrome and type 2 diabetes.
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