Mice deficient for the lipid sensor Gpr120 develop obesity and both impaired fasting glucose and glucose intolerance under a high-fat diet.

In humans, a loss-of-function mutation in /GPR120/ was shown to markedly contribute to obesity. Here, the authors investigate the effect of the same mutation in type 2 diabetes and glucose-related traits. They identified a significant contribution of the mutation to increased fasting glucose levels and reduced pancreatic beta-cell function in

9,000 non-diabetic participants of French-European origin. This study tends to confirm a potential role of GPR120 in pancreatic islets in humans (besides gut and adipose tissue). (http://jmg.bmj.com/content/early/2015/05/29/jmedgenet-2015-103065 )