Role of the nitric oxide pathway in AMPK-mediated glucose uptake and GLUT4 translocation in heart muscle

J Li; X Y Hu; P Selvakumar; R R Russell; S W Cushman; G D Holman; L H Young

doi:10.1152/ajpendo.00234.2004

Role of the nitric oxide pathway in AMPK-mediated glucose uptake and GLUT4 translocation in heart muscle

J Li, X Y Hu, P Selvakumar, R R Russell, S W Cushman, G D Holman, L H Young

Department of Life Sciences

Research output: Contribution to journal › Article › peer-review

164 Citations (SciVal)

Abstract

AMP-activated protein kinase (AMPK) is a serine-threonine kinase that regulates cellular metabolism and has an essential role in activating glucose transport during hypoxia and ischemia. The mechanisms responsible for AMPK stimulation of glucose transport are uncertain, but may involve interaction with other signaling pathways or direct effects on GLUT vesicular trafficking. One potential downstream mediator of AMPK signaling is the nitric oxide pathway. The aim of this study was to examine the extent to which AMPK mediates glucose transport through activation of the nitric oxide (NO)-signaling pathway in isolated heart muscles. Incubation with 1 mM 5-amino-4-imidazole-1-beta-carboxamide ribofuranoside (AICAR) activated AMPK (P

Original language	English
Pages (from-to)	E834-E841
Journal	American Journal of Physiology: Endocrinology and Metabolism
Volume	287
Issue number	5
DOIs	https://doi.org/10.1152/ajpendo.00234.2004
Publication status	Published - 2004

Access to Document

10.1152/ajpendo.00234.2004

Cite this

@article{ab6f7943f0de46ebb530ee37531c59ec,

title = "Role of the nitric oxide pathway in AMPK-mediated glucose uptake and GLUT4 translocation in heart muscle",

abstract = "AMP-activated protein kinase (AMPK) is a serine-threonine kinase that regulates cellular metabolism and has an essential role in activating glucose transport during hypoxia and ischemia. The mechanisms responsible for AMPK stimulation of glucose transport are uncertain, but may involve interaction with other signaling pathways or direct effects on GLUT vesicular trafficking. One potential downstream mediator of AMPK signaling is the nitric oxide pathway. The aim of this study was to examine the extent to which AMPK mediates glucose transport through activation of the nitric oxide (NO)-signaling pathway in isolated heart muscles. Incubation with 1 mM 5-amino-4-imidazole-1-beta-carboxamide ribofuranoside (AICAR) activated AMPK (P",

author = "J Li and Hu, {X Y} and P Selvakumar and Russell, {R R} and Cushman, {S W} and Holman, {G D} and Young, {L H}",

note = "ID number: ISI:000224382400007",

year = "2004",

doi = "10.1152/ajpendo.00234.2004",

language = "English",

volume = "287",

pages = "E834--E841",

journal = "American Journal of Physiology: Endocrinology and Metabolism",

issn = "0193-1849",

publisher = "American Physiological Society",

number = "5",

}

TY - JOUR

T1 - Role of the nitric oxide pathway in AMPK-mediated glucose uptake and GLUT4 translocation in heart muscle

AU - Li, J

AU - Hu, X Y

AU - Selvakumar, P

AU - Russell, R R

AU - Cushman, S W

AU - Holman, G D

AU - Young, L H

N1 - ID number: ISI:000224382400007

PY - 2004

Y1 - 2004

N2 - AMP-activated protein kinase (AMPK) is a serine-threonine kinase that regulates cellular metabolism and has an essential role in activating glucose transport during hypoxia and ischemia. The mechanisms responsible for AMPK stimulation of glucose transport are uncertain, but may involve interaction with other signaling pathways or direct effects on GLUT vesicular trafficking. One potential downstream mediator of AMPK signaling is the nitric oxide pathway. The aim of this study was to examine the extent to which AMPK mediates glucose transport through activation of the nitric oxide (NO)-signaling pathway in isolated heart muscles. Incubation with 1 mM 5-amino-4-imidazole-1-beta-carboxamide ribofuranoside (AICAR) activated AMPK (P

AB - AMP-activated protein kinase (AMPK) is a serine-threonine kinase that regulates cellular metabolism and has an essential role in activating glucose transport during hypoxia and ischemia. The mechanisms responsible for AMPK stimulation of glucose transport are uncertain, but may involve interaction with other signaling pathways or direct effects on GLUT vesicular trafficking. One potential downstream mediator of AMPK signaling is the nitric oxide pathway. The aim of this study was to examine the extent to which AMPK mediates glucose transport through activation of the nitric oxide (NO)-signaling pathway in isolated heart muscles. Incubation with 1 mM 5-amino-4-imidazole-1-beta-carboxamide ribofuranoside (AICAR) activated AMPK (P

U2 - 10.1152/ajpendo.00234.2004

DO - 10.1152/ajpendo.00234.2004

M3 - Article

SN - 0193-1849

VL - 287

SP - E834-E841

JO - American Journal of Physiology: Endocrinology and Metabolism

JF - American Journal of Physiology: Endocrinology and Metabolism

IS - 5

ER -

Role of the nitric oxide pathway in AMPK-mediated glucose uptake and GLUT4 translocation in heart muscle

Abstract

Access to Document

Fingerprint

Cite this