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Metabolism. 2016 Mar;65(3):8-17. doi: 10.1016/j.metabol.2015.10.003. Epub 2015 Nov 2.

Oleic acid stimulates glucagon-like peptide-1 release from enteroendocrine cells by modulating cell respiration and glycolysis.

Author information

1
Physiology and Behavior Laboratory, ETH Zürich, 8603 Schwerzenbach (Zürich), Switzerland.
2
Physiology and Behavior Laboratory, ETH Zürich, 8603 Schwerzenbach (Zürich), Switzerland. Electronic address: abdelhak-mansouri@ethz.ch.

Abstract

OBJECTIVE:

Glucagon-like peptide-1 (GLP-1) is a potent satiating and incretin hormone released by enteroendocrine L-cells in response to eating. Dietary fat, in particular monounsaturated fatty acids, such as oleic acid (OA), potently stimulates GLP-1 secretion from L-cells. It is, however, unclear whether the intracellular metabolic handling of OA is involved in this effect.

METHODS:

First we determined the optimal medium for the bioenergetics measurements. Then we examined the effect of OA on the metabolism of the immortalized enteroendocrine GLUTag cell model and assessed GLP-1 release in parallel. We measured oxygen consumption rate and extracellular acidification rate in response to OA and to different metabolic inhibitors with the Seahorse extracellular flux analyzer.

RESULTS:

OA increased cellular respiration and potently stimulated GLP-1 release. The fatty acid oxidation inhibitor etomoxir did neither reduce OA-induced respiration nor affect the OA-induced GLP-1 release. In contrast, inhibition of the respiratory chain or of downstream steps of aerobic glycolysis reduced the OA-induced GLP-1 release, and an inhibition of the first step of glycolysis by addition of 2-deoxy-d-glucose even abolished it.

CONCLUSION:

These findings indicate that an indirect stimulation of glycolysis is crucial for the OA-induced release of GLP-1.

KEYWORDS:

Extracellular acidification rate; GLP-1; GLUTag cells; Oxygen consumption rate; Seahorse extracellular flux analyzer

PMID:
26892511
DOI:
10.1016/j.metabol.2015.10.003
[Indexed for MEDLINE]

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