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. 2020 Mar 3;11:215. doi: 10.3389/fphar.2020.00215

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Copyright © 2020 Mata-Torres, Andrade-Cetto, Espinoza-Hernández and Cárdenas-Vázquez.

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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Mechanisms of hepatic gluconeogenesis inhibition exerted by some identified compounds from evaluated plant extracts in this study. Active compounds could have two main ways to decrease HGO: (1) direct inhibition of gluconeogenic enzymes, for instance, inhibition of G6Pase system by CA and inhibition of PC by kaempferol; or (2) decreasing expression levels of gluconeogenic enzymes via Akt pathway (kaempferol, resveratrol and, epicatechin) or AMPK activation (CA and epicatechin). IRS, insulin receptor substrate; PI(4,5)P2, phosphatidylinositol 4,5-bisphosphate; PI(3,4,5)P3, phosphatidylinositol 3,4,5-triphosphate; PDK1, phosphoinositide-dependent kinase 1; PDK2, phosphoinositide-dependent kinase 2; Akt, protein kinase B; AMPK, AMP-activated protein kinase; G6P, glucose-6-phosphate; F-6-P, fructose-6-phosphate; F-1,6-bisP, fructose-1,6-bisphosphate; G6Pase, glucose-6-phosphatase.