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

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

6 Citations (Scopus)

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.

Original language	English
Journal	Cell Metabolism
Volume	27
Issue number	2
Pages (from-to)	273-275
Number of pages	3
ISSN	1550-4131
DOIs	https://doi.org/10.1016/j.cmet.2018.01.006
Publication status	Published - 2018

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10.1016/j.cmet.2018.01.006

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title = "The HETE Is on FFAR1 and Pancreatic Islet Cells",

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.",

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AU - Lückmann, Michael

AU - Frimurer, Thomas M

AU - Schwartz, Thue W

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AB - 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.

KW - Journal Article

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DO - 10.1016/j.cmet.2018.01.006

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JO - Cell Metabolism

JF - Cell Metabolism

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The HETE Is on FFAR1 and Pancreatic Islet Cells

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