The HETE Is on FFAR1 and Pancreatic Islet Cells

Mette Trauelsen; Michael Lückmann; Thomas M Frimurer; Thue W Schwartz

doi:10.1016/j.cmet.2018.01.006

The HETE Is on FFAR1 and Pancreatic Islet Cells

Cell Metab. 2018 Feb 6;27(2):273-275. doi: 10.1016/j.cmet.2018.01.006.

Authors

Mette Trauelsen¹, Michael Lückmann¹, Thomas M Frimurer¹, Thue W Schwartz²

Affiliations

¹ Center for Basic Metabolic Research, University of Copenhagen, Denmark.
² Center for Basic Metabolic Research, University of Copenhagen, Denmark; Laboratory for Molecular Pharmacology, Department for Biomedical Research, Faculty of Health Sciences, University of Copenhagen, Denmark. Electronic address: tws@sund.ku.dk.

PMID: 29414682
DOI: 10.1016/j.cmet.2018.01.006

Abstract

It is known but generally unappreciated that the fatty acid receptor FFAR1 (GPR40) is responsible for a major part of glucose-induced insulin secretion. This puzzling fact is now explained by Tunaru et al. (2018), who demonstrate that glucose-induced 20-hydroxyeicosatetraenoic acid (20-HETE) amplifies insulin secretion through autocrine activation of FFAR1.

Publication types

Comment

MeSH terms

Glucose*
Hydroxyeicosatetraenoic Acids
Insulin Secretion
Insulin*
Islets of Langerhans
Receptors, G-Protein-Coupled

Substances

Hydroxyeicosatetraenoic Acids
Insulin
Receptors, G-Protein-Coupled
20-hydroxy-5,8,11,14-eicosatetraenoic acid
Glucose