Insulin-induced membrane permeability to glucose in human muscles at rest and following exercise

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Insulin-induced membrane permeability to glucose in human muscles at rest and following exercise. / McConell, Glenn Kevin; Sjøberg, Kim Anker; Ceutz, Frederik; Gliemann, Lasse; Nyberg, Michael Permin; Hellsten, Ylva; Frøsig, Christian; Kiens, Bente; Wojtaszewski, Jørgen; Richter, Erik A.

In: Journal of Physiology, Vol. 598, No. 2, 2020, p. 303-315.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

McConell, GK, Sjøberg, KA, Ceutz, F, Gliemann, L, Nyberg, MP, Hellsten, Y, Frøsig, C, Kiens, B, Wojtaszewski, J & Richter, EA 2020, 'Insulin-induced membrane permeability to glucose in human muscles at rest and following exercise', Journal of Physiology, vol. 598, no. 2, pp. 303-315. https://doi.org/10.1113/JP278600

APA

McConell, G. K., Sjøberg, K. A., Ceutz, F., Gliemann, L., Nyberg, M. P., Hellsten, Y., ... Richter, E. A. (2020). Insulin-induced membrane permeability to glucose in human muscles at rest and following exercise. Journal of Physiology, 598(2), 303-315. https://doi.org/10.1113/JP278600

Vancouver

McConell GK, Sjøberg KA, Ceutz F, Gliemann L, Nyberg MP, Hellsten Y et al. Insulin-induced membrane permeability to glucose in human muscles at rest and following exercise. Journal of Physiology. 2020;598(2):303-315. https://doi.org/10.1113/JP278600

Author

McConell, Glenn Kevin ; Sjøberg, Kim Anker ; Ceutz, Frederik ; Gliemann, Lasse ; Nyberg, Michael Permin ; Hellsten, Ylva ; Frøsig, Christian ; Kiens, Bente ; Wojtaszewski, Jørgen ; Richter, Erik A. / Insulin-induced membrane permeability to glucose in human muscles at rest and following exercise. In: Journal of Physiology. 2020 ; Vol. 598, No. 2. pp. 303-315.

Bibtex

@article{d2ee9840399948ca864c2301dd1204c1,
title = "Insulin-induced membrane permeability to glucose in human muscles at rest and following exercise",
abstract = "Increased insulin action is an important component of the health benefits of exercise, but the regulation of insulin action in vivo is complex and not fully elucidated. Increases in skeletal muscle insulin-stimulated GLUT4 translocation are inconsistent and mostly cannot explain the increases in insulin action in humans. Here we used leg glucose uptake (LGU) and interstitial muscle glucose concentration to calculate insulin-induced muscle membrane permeability to glucose, a variable not previously possible to quantify in humans. Muscle membrane permeability to glucose, measured 4 h after one-legged knee-extensor exercise, increased ∼17-fold during a submaximal euglycaemic hyperinsulinaemic clamp in rested muscle (R) and ∼36-fold in exercised muscle (EX). Femoral arterial infusion of L-NMMA or ATP decreased and increased, respectively, leg blood flow (LBF) in both legs but did not affect membrane glucose permeability. Decreasing LBF reduced interstitial glucose concentrations to ∼2 mM in the exercised but only to ∼3.5 mM in non-exercised muscle and abrogated the augmented effect of insulin on LGU in the EX leg. Increasing LBF by ATP infusion increased LGU in both legs with uptake higher in the EX leg. We conclude that it is possible to measure functional muscle membrane permeability to glucose in humans and it increases twice as much in exercised vs. rested muscle during submaximal insulin stimulation. We also show that muscle perfusion is an important regulator of muscle glucose uptake when membrane permeability to glucose is high and we show that the capillary wall can be a significant barrier for glucose transport.",
keywords = "Faculty of Science, Insulin sensitivity, Microdialysis, Glucose uptake",
author = "McConell, {Glenn Kevin} and Sj{\o}berg, {Kim Anker} and Frederik Ceutz and Lasse Gliemann and Nyberg, {Michael Permin} and Ylva Hellsten and Christian Fr{\o}sig and Bente Kiens and J{\o}rgen Wojtaszewski and Richter, {Erik A.}",
note = "This article is protected by copyright. All rights reserved.",
year = "2020",
doi = "10.1113/JP278600",
language = "English",
volume = "598",
pages = "303--315",
journal = "The Journal of Physiology",
issn = "0022-3751",
publisher = "Wiley-Blackwell",
number = "2",

}

RIS

TY - JOUR

T1 - Insulin-induced membrane permeability to glucose in human muscles at rest and following exercise

AU - McConell, Glenn Kevin

AU - Sjøberg, Kim Anker

AU - Ceutz, Frederik

AU - Gliemann, Lasse

AU - Nyberg, Michael Permin

AU - Hellsten, Ylva

AU - Frøsig, Christian

AU - Kiens, Bente

AU - Wojtaszewski, Jørgen

AU - Richter, Erik A.

N1 - This article is protected by copyright. All rights reserved.

PY - 2020

Y1 - 2020

N2 - Increased insulin action is an important component of the health benefits of exercise, but the regulation of insulin action in vivo is complex and not fully elucidated. Increases in skeletal muscle insulin-stimulated GLUT4 translocation are inconsistent and mostly cannot explain the increases in insulin action in humans. Here we used leg glucose uptake (LGU) and interstitial muscle glucose concentration to calculate insulin-induced muscle membrane permeability to glucose, a variable not previously possible to quantify in humans. Muscle membrane permeability to glucose, measured 4 h after one-legged knee-extensor exercise, increased ∼17-fold during a submaximal euglycaemic hyperinsulinaemic clamp in rested muscle (R) and ∼36-fold in exercised muscle (EX). Femoral arterial infusion of L-NMMA or ATP decreased and increased, respectively, leg blood flow (LBF) in both legs but did not affect membrane glucose permeability. Decreasing LBF reduced interstitial glucose concentrations to ∼2 mM in the exercised but only to ∼3.5 mM in non-exercised muscle and abrogated the augmented effect of insulin on LGU in the EX leg. Increasing LBF by ATP infusion increased LGU in both legs with uptake higher in the EX leg. We conclude that it is possible to measure functional muscle membrane permeability to glucose in humans and it increases twice as much in exercised vs. rested muscle during submaximal insulin stimulation. We also show that muscle perfusion is an important regulator of muscle glucose uptake when membrane permeability to glucose is high and we show that the capillary wall can be a significant barrier for glucose transport.

AB - Increased insulin action is an important component of the health benefits of exercise, but the regulation of insulin action in vivo is complex and not fully elucidated. Increases in skeletal muscle insulin-stimulated GLUT4 translocation are inconsistent and mostly cannot explain the increases in insulin action in humans. Here we used leg glucose uptake (LGU) and interstitial muscle glucose concentration to calculate insulin-induced muscle membrane permeability to glucose, a variable not previously possible to quantify in humans. Muscle membrane permeability to glucose, measured 4 h after one-legged knee-extensor exercise, increased ∼17-fold during a submaximal euglycaemic hyperinsulinaemic clamp in rested muscle (R) and ∼36-fold in exercised muscle (EX). Femoral arterial infusion of L-NMMA or ATP decreased and increased, respectively, leg blood flow (LBF) in both legs but did not affect membrane glucose permeability. Decreasing LBF reduced interstitial glucose concentrations to ∼2 mM in the exercised but only to ∼3.5 mM in non-exercised muscle and abrogated the augmented effect of insulin on LGU in the EX leg. Increasing LBF by ATP infusion increased LGU in both legs with uptake higher in the EX leg. We conclude that it is possible to measure functional muscle membrane permeability to glucose in humans and it increases twice as much in exercised vs. rested muscle during submaximal insulin stimulation. We also show that muscle perfusion is an important regulator of muscle glucose uptake when membrane permeability to glucose is high and we show that the capillary wall can be a significant barrier for glucose transport.

KW - Faculty of Science

KW - Insulin sensitivity

KW - Microdialysis

KW - Glucose uptake

U2 - 10.1113/JP278600

DO - 10.1113/JP278600

M3 - Journal article

C2 - 31696935

VL - 598

SP - 303

EP - 315

JO - The Journal of Physiology

JF - The Journal of Physiology

SN - 0022-3751

IS - 2

ER -

ID: 229899780