Title : Folic acid supplementation during high-fat diet feeding restores AMPK activation via an AMP-LKB1-dependent mechanism.

Pub. Date : 2015 Nov 15

PMID : 26400185






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1 Folic acid supplementation during high-fat diet feeding restores AMPK activation via an AMP-LKB1-dependent mechanism. Folic Acid protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens
2 The aim of the present study was to investigate the effect of folic acid on hepatic AMPK during high-fat diet feeding and the mechanisms involved. Folic Acid protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens
3 Folic acid supplementation restored AMPK phosphorylation (activation) and reduced blood glucose and hepatic cholesterol levels. Folic Acid protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens
4 Activation of AMPK by folic acid was mediated through an elevation of its allosteric activator AMP and activation of its upstream kinase, namely, liver kinase B1 (LKB1) in the liver. Folic Acid protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens
5 Consistent with in vivo findings, 5-methyltetrahydrofolate (bioactive form of folate) restored phosphorylation (activation) of both AMPK and LKB1 in palmitic acid-treated HepG2 cells. Folic Acid protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens
6 Activation of AMPK by folic acid might be responsible for AMPK-dependent phosphorylation of HMG-CoA reductase, leading to reduced hepatic cholesterol synthesis during high-fat diet feeding. Folic Acid protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens
7 Activation of AMPK by folic acid might be responsible for AMPK-dependent phosphorylation of HMG-CoA reductase, leading to reduced hepatic cholesterol synthesis during high-fat diet feeding. Folic Acid protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens
8 These results suggest that folic acid supplementation may improve cholesterol and glucose metabolism by restoration of AMPK activation in the liver. Folic Acid protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens