Nitric oxide increases cyclic GMP levels, AMP-activated protein kinase (AMPK)alpha1-specific activity and glucose transport in human skeletal muscle

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Nitric oxide increases cyclic GMP levels, AMP-activated protein kinase (AMPK)alpha1-specific activity and glucose transport in human skeletal muscle. / Deshmukh, A S; Long, Y C; de Castro Barbosa, T; Karlsson, H K R; Glund, S; Zavadoski, W J; Gibbs, E M; Koistinen, H A; Wallberg-Henriksson, H; Zierath, J R.

In: Diabetologia, Vol. 53, No. 6, 06.2010, p. 1142-50.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Deshmukh, AS, Long, YC, de Castro Barbosa, T, Karlsson, HKR, Glund, S, Zavadoski, WJ, Gibbs, EM, Koistinen, HA, Wallberg-Henriksson, H & Zierath, JR 2010, 'Nitric oxide increases cyclic GMP levels, AMP-activated protein kinase (AMPK)alpha1-specific activity and glucose transport in human skeletal muscle', Diabetologia, vol. 53, no. 6, pp. 1142-50. https://doi.org/10.1007/s00125-010-1716-x

APA

Deshmukh, A. S., Long, Y. C., de Castro Barbosa, T., Karlsson, H. K. R., Glund, S., Zavadoski, W. J., ... Zierath, J. R. (2010). Nitric oxide increases cyclic GMP levels, AMP-activated protein kinase (AMPK)alpha1-specific activity and glucose transport in human skeletal muscle. Diabetologia, 53(6), 1142-50. https://doi.org/10.1007/s00125-010-1716-x

Vancouver

Deshmukh AS, Long YC, de Castro Barbosa T, Karlsson HKR, Glund S, Zavadoski WJ et al. Nitric oxide increases cyclic GMP levels, AMP-activated protein kinase (AMPK)alpha1-specific activity and glucose transport in human skeletal muscle. Diabetologia. 2010 Jun;53(6):1142-50. https://doi.org/10.1007/s00125-010-1716-x

Author

Deshmukh, A S ; Long, Y C ; de Castro Barbosa, T ; Karlsson, H K R ; Glund, S ; Zavadoski, W J ; Gibbs, E M ; Koistinen, H A ; Wallberg-Henriksson, H ; Zierath, J R. / Nitric oxide increases cyclic GMP levels, AMP-activated protein kinase (AMPK)alpha1-specific activity and glucose transport in human skeletal muscle. In: Diabetologia. 2010 ; Vol. 53, No. 6. pp. 1142-50.

Bibtex

@article{9f794c3480bf4b90b6bf3b9ad9b13d9e,
title = "Nitric oxide increases cyclic GMP levels, AMP-activated protein kinase (AMPK)alpha1-specific activity and glucose transport in human skeletal muscle",
abstract = "AIMS/HYPOTHESIS: We investigated the direct effect of a nitric oxide donor (spermine NONOate) on glucose transport in isolated human skeletal muscle and L6 skeletal muscle cells. We hypothesised that pharmacological treatment of human skeletal muscle with N-(2-aminoethyl)-N-(2-hydroxy-2-nitrosohydrazino)-1,2-ethylenediamine (spermine NONOate) would increase intracellular cyclic GMP (cGMP) levels and promote glucose transport.METHODS: Skeletal muscle strips were prepared from vastus lateralis muscle biopsies obtained from seven healthy men. Muscle strips were incubated in the absence or presence of 5 mmol/l spermine NONOate or 120 nmol/l insulin. The L6 muscle cells were treated with spermine NONOate (20 micromol/l) and incubated in the absence or presence of insulin (120 nmol/l). The direct effect of spermine NONOate and insulin on glucose transport, cGMP levels and signal transduction was determined.RESULTS: In human skeletal muscle, spermine NONOate increased glucose transport 2.4-fold (p < 0.05), concomitant with increased cGMP levels (80-fold, p < 0.001). Phosphorylation of components of the canonical insulin signalling cascade was unaltered by spermine NONOate exposure, implicating an insulin-independent signalling mechanism. Consistent with this, spermine NONOate increased AMP-activated protein kinase (AMPK)-alpha1-associated activity (1.7-fold, p < 0.05). In L6 muscle cells, spermine NONOate increased glucose uptake (p < 0.01) and glycogen synthesis (p < 0.001), an effect that was in addition to that of insulin. Spermine NONOate also elicited a concomitant increase in AMPK and acetyl-CoA carboxylase phosphorylation. In the presence of the guanylate cyclase inhibitor LY-83583 (10 micromol/l), spermine NONOate had no effect on glycogen synthesis and AMPK-alpha1 phosphorylation.CONCLUSIONS/INTERPRETATION: Pharmacological treatment of skeletal muscle with spermine NONOate increases glucose transport via insulin-independent signalling pathways involving increased intracellular cGMP levels and AMPK-alpha1-associated activity.",
keywords = "AMP-Activated Protein Kinases, Analysis of Variance, Biological Transport, Blotting, Western, Cells, Cultured, Cyclic GMP, Glucose, Humans, Insulin, Male, Middle Aged, Muscle, Skeletal, Nitric Oxide, Nitric Oxide Donors, Phosphorylation, Signal Transduction, Spermine, Journal Article, Research Support, Non-U.S. Gov't",
author = "Deshmukh, {A S} and Long, {Y C} and {de Castro Barbosa}, T and Karlsson, {H K R} and S Glund and Zavadoski, {W J} and Gibbs, {E M} and Koistinen, {H A} and H Wallberg-Henriksson and Zierath, {J R}",
year = "2010",
month = "6",
doi = "10.1007/s00125-010-1716-x",
language = "English",
volume = "53",
pages = "1142--50",
journal = "Diabetologia",
issn = "0012-186X",
publisher = "Springer",
number = "6",

}

RIS

TY - JOUR

T1 - Nitric oxide increases cyclic GMP levels, AMP-activated protein kinase (AMPK)alpha1-specific activity and glucose transport in human skeletal muscle

AU - Deshmukh, A S

AU - Long, Y C

AU - de Castro Barbosa, T

AU - Karlsson, H K R

AU - Glund, S

AU - Zavadoski, W J

AU - Gibbs, E M

AU - Koistinen, H A

AU - Wallberg-Henriksson, H

AU - Zierath, J R

PY - 2010/6

Y1 - 2010/6

N2 - AIMS/HYPOTHESIS: We investigated the direct effect of a nitric oxide donor (spermine NONOate) on glucose transport in isolated human skeletal muscle and L6 skeletal muscle cells. We hypothesised that pharmacological treatment of human skeletal muscle with N-(2-aminoethyl)-N-(2-hydroxy-2-nitrosohydrazino)-1,2-ethylenediamine (spermine NONOate) would increase intracellular cyclic GMP (cGMP) levels and promote glucose transport.METHODS: Skeletal muscle strips were prepared from vastus lateralis muscle biopsies obtained from seven healthy men. Muscle strips were incubated in the absence or presence of 5 mmol/l spermine NONOate or 120 nmol/l insulin. The L6 muscle cells were treated with spermine NONOate (20 micromol/l) and incubated in the absence or presence of insulin (120 nmol/l). The direct effect of spermine NONOate and insulin on glucose transport, cGMP levels and signal transduction was determined.RESULTS: In human skeletal muscle, spermine NONOate increased glucose transport 2.4-fold (p < 0.05), concomitant with increased cGMP levels (80-fold, p < 0.001). Phosphorylation of components of the canonical insulin signalling cascade was unaltered by spermine NONOate exposure, implicating an insulin-independent signalling mechanism. Consistent with this, spermine NONOate increased AMP-activated protein kinase (AMPK)-alpha1-associated activity (1.7-fold, p < 0.05). In L6 muscle cells, spermine NONOate increased glucose uptake (p < 0.01) and glycogen synthesis (p < 0.001), an effect that was in addition to that of insulin. Spermine NONOate also elicited a concomitant increase in AMPK and acetyl-CoA carboxylase phosphorylation. In the presence of the guanylate cyclase inhibitor LY-83583 (10 micromol/l), spermine NONOate had no effect on glycogen synthesis and AMPK-alpha1 phosphorylation.CONCLUSIONS/INTERPRETATION: Pharmacological treatment of skeletal muscle with spermine NONOate increases glucose transport via insulin-independent signalling pathways involving increased intracellular cGMP levels and AMPK-alpha1-associated activity.

AB - AIMS/HYPOTHESIS: We investigated the direct effect of a nitric oxide donor (spermine NONOate) on glucose transport in isolated human skeletal muscle and L6 skeletal muscle cells. We hypothesised that pharmacological treatment of human skeletal muscle with N-(2-aminoethyl)-N-(2-hydroxy-2-nitrosohydrazino)-1,2-ethylenediamine (spermine NONOate) would increase intracellular cyclic GMP (cGMP) levels and promote glucose transport.METHODS: Skeletal muscle strips were prepared from vastus lateralis muscle biopsies obtained from seven healthy men. Muscle strips were incubated in the absence or presence of 5 mmol/l spermine NONOate or 120 nmol/l insulin. The L6 muscle cells were treated with spermine NONOate (20 micromol/l) and incubated in the absence or presence of insulin (120 nmol/l). The direct effect of spermine NONOate and insulin on glucose transport, cGMP levels and signal transduction was determined.RESULTS: In human skeletal muscle, spermine NONOate increased glucose transport 2.4-fold (p < 0.05), concomitant with increased cGMP levels (80-fold, p < 0.001). Phosphorylation of components of the canonical insulin signalling cascade was unaltered by spermine NONOate exposure, implicating an insulin-independent signalling mechanism. Consistent with this, spermine NONOate increased AMP-activated protein kinase (AMPK)-alpha1-associated activity (1.7-fold, p < 0.05). In L6 muscle cells, spermine NONOate increased glucose uptake (p < 0.01) and glycogen synthesis (p < 0.001), an effect that was in addition to that of insulin. Spermine NONOate also elicited a concomitant increase in AMPK and acetyl-CoA carboxylase phosphorylation. In the presence of the guanylate cyclase inhibitor LY-83583 (10 micromol/l), spermine NONOate had no effect on glycogen synthesis and AMPK-alpha1 phosphorylation.CONCLUSIONS/INTERPRETATION: Pharmacological treatment of skeletal muscle with spermine NONOate increases glucose transport via insulin-independent signalling pathways involving increased intracellular cGMP levels and AMPK-alpha1-associated activity.

KW - AMP-Activated Protein Kinases

KW - Analysis of Variance

KW - Biological Transport

KW - Blotting, Western

KW - Cells, Cultured

KW - Cyclic GMP

KW - Glucose

KW - Humans

KW - Insulin

KW - Male

KW - Middle Aged

KW - Muscle, Skeletal

KW - Nitric Oxide

KW - Nitric Oxide Donors

KW - Phosphorylation

KW - Signal Transduction

KW - Spermine

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1007/s00125-010-1716-x

DO - 10.1007/s00125-010-1716-x

M3 - Journal article

C2 - 20349036

VL - 53

SP - 1142

EP - 1150

JO - Diabetologia

JF - Diabetologia

SN - 0012-186X

IS - 6

ER -

ID: 170597608