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. 2019 Mar 26;10:176. doi: 10.3389/fendo.2019.00176

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Copyright © 2019 Hernández-Cáceres, Toledo-Valenzuela, Díaz-Castro, Ávalos, Burgos, Narro, Peña-Oyarzun, Espinoza-Caicedo, Cifuentes-Araneda, Navarro-Aguad, Riquelme, Troncoso, Criollo and Morselli.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Palmitic acid-mediated FFAR1 activation decreases autophagic flux and insulin sensitivity in hypothalamic neuronal cells (Graphical abstract). The FFAR1 antagonist GW1100 prevents autophagic flux inhibition and restores insulin sensitivity, as indicated by AKT phosphorylation levels, in cells exposed to PA. Downregulation of autophagy essential genes (ATG7 and Beclin 1 -BECN1-), as well as pharmacological inhibition of the autophagic flux by BafA1, reduces the increase in AKT and IR phosphorylation levels stimulated by insulin.