Glucose availability but not changes in pancreatic hormones sensitizes hepatic AMPK activity during nutritional transition in rodents.


Journal

The Journal of biological chemistry
ISSN: 1083-351X
Titre abrégé: J Biol Chem
Pays: United States
ID NLM: 2985121R

Informations de publication

Date de publication:
01 05 2020
Historique:
received: 17 07 2019
revised: 10 03 2020
pubmed: 19 3 2020
medline: 29 12 2020
entrez: 19 3 2020
Statut: ppublish

Résumé

The cellular energy sensor AMP-activated protein kinase (AMPK) is a metabolic regulator that mediates adaptation to nutritional variations to maintain a proper energy balance in cells. We show here that suckling-weaning and fasting-refeeding transitions in rodents are associated with changes in AMPK activation and the cellular energy state in the liver. These nutritional transitions were characterized by a metabolic switch from lipid to glucose utilization, orchestrated by modifications in glucose levels and the glucagon/insulin ratio in the bloodstream. We therefore investigated the respective roles of glucose and pancreatic hormones on AMPK activation in mouse primary hepatocytes. We found that glucose starvation transiently activates AMPK, whereas changes in glucagon and insulin levels had no impact on AMPK. Challenge of hepatocytes with metformin-induced metabolic stress strengthened both AMPK activation and cellular energy depletion under limited-glucose conditions, whereas neither glucagon nor insulin altered AMPK activation. Although both insulin and glucagon induced AMPKα phosphorylation at its Ser

Identifiants

pubmed: 32184359
pii: S0021-9258(17)48219-6
doi: 10.1074/jbc.RA119.010244
pmc: PMC7196663
pii:
doi:

Substances chimiques

Pancreatic Hormones 0
AMP-Activated Protein Kinases EC 2.7.11.31
Glucose IY9XDZ35W2

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

5836-5849

Informations de copyright

© 2020 Huet et al.

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Auteurs

Camille Huet (C)

Université de Paris, Institut Cochin, CNRS, INSERM, F-75014 Paris, France.

Nadia Boudaba (N)

Université de Paris, Institut Cochin, CNRS, INSERM, F-75014 Paris, France.

Bruno Guigas (B)

Department of Parasitology, Leiden University Medical Center, 2333 ZA Leiden, Netherlands.

Benoit Viollet (B)

Université de Paris, Institut Cochin, CNRS, INSERM, F-75014 Paris, France.

Marc Foretz (M)

Université de Paris, Institut Cochin, CNRS, INSERM, F-75014 Paris, France. Electronic address: marc.foretz@inserm.fr.

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