Rac1 in muscle is dispensable for improved insulin action after exercise in mice

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Standard

Rac1 in muscle is dispensable for improved insulin action after exercise in mice. / Sylow, Lykke; Møller, Lisbeth Liliendal Valbjørn; D'Hulst, Gommaar; Schjerling, Peter; Jensen, Thomas Elbenhardt; Richter, Erik A.

I: Endocrinology, Bind 157, Nr. 8, 2016, s. 3009-3015.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Sylow, L, Møller, LLV, D'Hulst, G, Schjerling, P, Jensen, TE & Richter, EA 2016, 'Rac1 in muscle is dispensable for improved insulin action after exercise in mice', Endocrinology, bind 157, nr. 8, s. 3009-3015. https://doi.org/10.1210/en.2016-1220

APA

Sylow, L., Møller, L. L. V., D'Hulst, G., Schjerling, P., Jensen, T. E., & Richter, E. A. (2016). Rac1 in muscle is dispensable for improved insulin action after exercise in mice. Endocrinology, 157(8), 3009-3015. https://doi.org/10.1210/en.2016-1220

Vancouver

Sylow L, Møller LLV, D'Hulst G, Schjerling P, Jensen TE, Richter EA. Rac1 in muscle is dispensable for improved insulin action after exercise in mice. Endocrinology. 2016;157(8):3009-3015. https://doi.org/10.1210/en.2016-1220

Author

Sylow, Lykke ; Møller, Lisbeth Liliendal Valbjørn ; D'Hulst, Gommaar ; Schjerling, Peter ; Jensen, Thomas Elbenhardt ; Richter, Erik A. / Rac1 in muscle is dispensable for improved insulin action after exercise in mice. I: Endocrinology. 2016 ; Bind 157, Nr. 8. s. 3009-3015.

Bibtex

@article{27be6e50dfd84dccb95ff1e025a5d024,
title = "Rac1 in muscle is dispensable for improved insulin action after exercise in mice",
abstract = "Exercise has a potent insulin-sensitivity enhancing effect on skeletal muscle but the intracellular mechanisms that mediate this effect are not well understood. In muscle, Rac1 regulates both insulin- and contraction-stimulated glucose transport and is dysregulated in insulin resistant muscle. However, whether Rac1 is involved in mediating enhanced insulin sensitivity after an acute bout of exercise is unresolved. To address this question we investigated post exercise whole body (insulin tolerance test) as well as muscle (insulin-stimulated 2DG transport in isolated soleus muscle) insulin sensitivity in inducible muscle-specific Rac1 knockout (mKO) and wildtype littermate (WT) mice. Prior exercise enhanced whole body insulin sensitivity by 40% in WT mice and rescued the insulin intolerance in Rac1 mKO mice by improving whole body insulin sensitivity by 230%. In agreement, prior exercise significantly improved insulin sensitivity by 20% in WT and by 40% in Rac1 mKO soleus muscles. These findings suggest that muscle Rac1 is dispensable for the insulin sensitizing effect of exercise. Moreover, insulin resistance in Rac1 mKO mice can be completely normalized by prior exercise explaining why insulin resistant patients can increase insulin action with exercise despite dysfunctional Rac1 activity in muscle.",
author = "Lykke Sylow and M{\o}ller, {Lisbeth Liliendal Valbj{\o}rn} and Gommaar D'Hulst and Peter Schjerling and Jensen, {Thomas Elbenhardt} and Richter, {Erik A.}",
note = "CURIS 2016 NEXS 158",
year = "2016",
doi = "10.1210/en.2016-1220",
language = "English",
volume = "157",
pages = "3009--3015",
journal = "Endocrinology",
issn = "0013-7227",
publisher = "Oxford University Press",
number = "8",

}

RIS

TY - JOUR

T1 - Rac1 in muscle is dispensable for improved insulin action after exercise in mice

AU - Sylow, Lykke

AU - Møller, Lisbeth Liliendal Valbjørn

AU - D'Hulst, Gommaar

AU - Schjerling, Peter

AU - Jensen, Thomas Elbenhardt

AU - Richter, Erik A.

N1 - CURIS 2016 NEXS 158

PY - 2016

Y1 - 2016

N2 - Exercise has a potent insulin-sensitivity enhancing effect on skeletal muscle but the intracellular mechanisms that mediate this effect are not well understood. In muscle, Rac1 regulates both insulin- and contraction-stimulated glucose transport and is dysregulated in insulin resistant muscle. However, whether Rac1 is involved in mediating enhanced insulin sensitivity after an acute bout of exercise is unresolved. To address this question we investigated post exercise whole body (insulin tolerance test) as well as muscle (insulin-stimulated 2DG transport in isolated soleus muscle) insulin sensitivity in inducible muscle-specific Rac1 knockout (mKO) and wildtype littermate (WT) mice. Prior exercise enhanced whole body insulin sensitivity by 40% in WT mice and rescued the insulin intolerance in Rac1 mKO mice by improving whole body insulin sensitivity by 230%. In agreement, prior exercise significantly improved insulin sensitivity by 20% in WT and by 40% in Rac1 mKO soleus muscles. These findings suggest that muscle Rac1 is dispensable for the insulin sensitizing effect of exercise. Moreover, insulin resistance in Rac1 mKO mice can be completely normalized by prior exercise explaining why insulin resistant patients can increase insulin action with exercise despite dysfunctional Rac1 activity in muscle.

AB - Exercise has a potent insulin-sensitivity enhancing effect on skeletal muscle but the intracellular mechanisms that mediate this effect are not well understood. In muscle, Rac1 regulates both insulin- and contraction-stimulated glucose transport and is dysregulated in insulin resistant muscle. However, whether Rac1 is involved in mediating enhanced insulin sensitivity after an acute bout of exercise is unresolved. To address this question we investigated post exercise whole body (insulin tolerance test) as well as muscle (insulin-stimulated 2DG transport in isolated soleus muscle) insulin sensitivity in inducible muscle-specific Rac1 knockout (mKO) and wildtype littermate (WT) mice. Prior exercise enhanced whole body insulin sensitivity by 40% in WT mice and rescued the insulin intolerance in Rac1 mKO mice by improving whole body insulin sensitivity by 230%. In agreement, prior exercise significantly improved insulin sensitivity by 20% in WT and by 40% in Rac1 mKO soleus muscles. These findings suggest that muscle Rac1 is dispensable for the insulin sensitizing effect of exercise. Moreover, insulin resistance in Rac1 mKO mice can be completely normalized by prior exercise explaining why insulin resistant patients can increase insulin action with exercise despite dysfunctional Rac1 activity in muscle.

U2 - 10.1210/en.2016-1220

DO - 10.1210/en.2016-1220

M3 - Journal article

C2 - 27285860

VL - 157

SP - 3009

EP - 3015

JO - Endocrinology

JF - Endocrinology

SN - 0013-7227

IS - 8

ER -

ID: 162461524