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. 2018 Apr 12;10(4):473. doi: 10.3390/nu10040473

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© 2018 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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GPR40 signaling affects fatty acid β-oxidation in β-cells. (a) Ketone body β- hydroxybutyrate (BHB) production in INS1E β-cells in the presence of C8, C10 or C8:C10 40:60 mixture. (b) Inhibition of GPR40 signaling by the antagonist, GW1100 (GW), (c) the phospholipase C-β (PLCβ) inhibitor, U73122 (U7) and nifedipine (Nif) prevent BHB production from medium chain fatty acids (MCFA) in INS1E β-cells unlike the IP3 receptor inhibitor xantospongin (Xant). (d) Inhibition of GPR40 signaling by GW increased complete β-oxidation of palmitate. Data are presented as means + SEM of three independent experiments, * p < 0.05, ** p < 0.01 relative to control.

GPR40 signaling affects fatty acid β-oxidation in β-cells. (a) Ketone body β- hydroxybutyrate (BHB) production in INS1E β-cells in the presence of C8, C10 or C8:C10 40:60 mixture. (b) Inhibition of GPR40 signaling by the antagonist, GW1100 (GW), (c) the phospholipase C-β (PLCβ) inhibitor, U73122 (U7) and nifedipine (Nif) prevent BHB production from medium chain fatty acids (MCFA) in INS1E β-cells unlike the IP3 receptor inhibitor xantospongin (Xant). (d) Inhibition of GPR40 signaling by GW increased complete β-oxidation of palmitate. Data are presented as means + SEM of three independent experiments, * p < 0.05, ** p < 0.01 relative to control.