Contribution of the low-frequency, loss-of-function p.R270H mutation in FFAR4 (GPR120) to increased fasting plasma glucose levels

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). (By Dr. Amélie Bonnefond, )

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