A role for AMP-activated protein kinase in contraction- and hypoxia-regulated glucose transport in skeletal muscle

Citation
J. Mu et al., A role for AMP-activated protein kinase in contraction- and hypoxia-regulated glucose transport in skeletal muscle, MOL CELL, 7(5), 2001, pp. 1085-1094
Citations number
49
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cell & Developmental Biology
Journal title
MOLECULAR CELL
ISSN journal
1097-2765 → ACNP
Volume
7
Issue
5
Year of publication
2001
Pages
1085 - 1094
Database
ISI
SICI code
1097-2765(200105)7:5<1085:ARFAPK>2.0.ZU;2-I
Abstract
Eukaryotic cells possess systems for sensing nutritional stress and inducin g compensatory mechanisms that minimize the consumption of ATP while utiliz ing alternative energy sources. Such stress can also be imposed by increase d energy needs, such as in skeletal muscle of exercising animals. In these studies, we consider the role of the metabolic sensor, AMP-activated protei n kinase (AMPK), in the regulation of glucose transport in skeletal muscle. Expression in mouse muscle of a dominant inhibitory mutant of AMPK complet ely blocked the ability of hypoxia or AICAR to activate hexose uptake, whil e only partially reducing contraction-stimulated hexose uptake. These data indicate that AMPK transmits a portion of the signal by which muscle contra ction increases glucose uptake, but other AMPK-independent pathways also co ntribute to the response.