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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.

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Physiology and Behavior Laboratory, ETH Zürich, 8603 Schwerzenbach (Zürich), Switzerland.
Physiology and Behavior Laboratory, ETH Zürich, 8603 Schwerzenbach (Zürich), Switzerland. Electronic address:



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.


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.


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.


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


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

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