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July 20, 2004AJP Endocrinology and Metabolism198 citations

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

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Population

Isolated heart muscles

Design

Preclinical

Key result

Inhibition of NOS reduced AICAR-stimulated glucose uptake by 21-25% (P<0.05), indicating the NO-guanylate cyclase pathway partially mediates AMPK-stimulated glucose uptake in heart muscle.

Authors

JLJi LiXHXiaoyue HuPSPradeepa Selvakumar

Discussion

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Overview

In vitro AMPK-NO pathway data in cardiac muscle are hypothesis-generating; prospective in vivo studies needed before clinical relevance.

Structured PICO

P
Population
Isolated heart muscles
I
Intervention
Incubation with 1 mM 5-amino-4-imidazole-1-beta-carboxamide ribofuranoside (AICAR), NO donors, NOS inhibitors (N(omega)-nitro-l-arginine and N(omega)-methyl-l-arginine), and guanylate cyclase inhibitors (ODQ and LY-83583)
O
Outcome
Glucose uptake and GLUT4 translocation to the cell surfacesurrogate

The NO-guanylate cyclase pathway contributes to, but is not the sole mediator of, AMPK stimulation of glucose uptake and GLUT4 translocation in heart muscle.

Main Result

p-value: p=<0.05

Cite This Study

Li et al. (2004) studied this question. AICAR was evaluated on glucose uptake and GLUT4 translocation (p=<0.05). Inhibition of NOS reduced AICAR-stimulated glucose uptake by 21-25% (P<0.05), indicating the NO-guanylate cyclase pathway partially mediates AMPK-stimulated glucose uptake in heart muscle.

synapsesocial.com/papers/6a6181dc6b7099fe363f5eb4https://doi.org/10.1152/ajpendo.00234.2004
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