Forskning
Udskriv Udskriv
Switch language
Region Hovedstaden - en del af Københavns Universitetshospital
Udgivet

Rac1 in Muscle Is Dispensable for Improved Insulin Action After Exercise in Mice

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

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. 3009-15. 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), 3009-15. https://doi.org/10.1210/en.2016-1220

CBE

MLA

Vancouver

Author

Sylow, Lykke ; Møller, Lisbeth L V ; D'Hulst, Gommaar ; Schjerling, Peter ; Jensen, Thomas E ; Richter, Erik A. / Rac1 in Muscle Is Dispensable for Improved Insulin Action After Exercise in Mice. I: Endocrinology. 2016 ; Bind 157, Nr. 8. s. 3009-15.

Bibtex

@article{2737c81a4ebe49a5b27f89b74c87af84,
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, Ras-related C3 botulinum toxin substrate 1 (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 after exercise whole-body (insulin tolerance test) as well as muscle (insulin-stimulated 2-deoxyglucose transport in isolated soleus muscle) insulin sensitivity in inducible muscle-specific Rac1 knockout (mKO) and wild-type (WT) littermate mice. Previous 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, previous 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 previous exercise explaining why insulin resistant patients can increase insulin action with exercise despite dysfunctional Rac1 activity in muscle.",
keywords = "Journal Article",
author = "Lykke Sylow and M{\o}ller, {Lisbeth L V} and Gommaar D'Hulst and Peter Schjerling and Jensen, {Thomas E} and Richter, {Erik A}",
year = "2016",
month = "8",
doi = "10.1210/en.2016-1220",
language = "English",
volume = "157",
pages = "3009--15",
journal = "Endocrinology",
issn = "0013-7227",
publisher = "The/Endocrine Society",
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 L V

AU - D'Hulst, Gommaar

AU - Schjerling, Peter

AU - Jensen, Thomas E

AU - Richter, Erik A

PY - 2016/8

Y1 - 2016/8

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, Ras-related C3 botulinum toxin substrate 1 (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 after exercise whole-body (insulin tolerance test) as well as muscle (insulin-stimulated 2-deoxyglucose transport in isolated soleus muscle) insulin sensitivity in inducible muscle-specific Rac1 knockout (mKO) and wild-type (WT) littermate mice. Previous 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, previous 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 previous 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, Ras-related C3 botulinum toxin substrate 1 (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 after exercise whole-body (insulin tolerance test) as well as muscle (insulin-stimulated 2-deoxyglucose transport in isolated soleus muscle) insulin sensitivity in inducible muscle-specific Rac1 knockout (mKO) and wild-type (WT) littermate mice. Previous 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, previous 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 previous exercise explaining why insulin resistant patients can increase insulin action with exercise despite dysfunctional Rac1 activity in muscle.

KW - Journal Article

U2 - 10.1210/en.2016-1220

DO - 10.1210/en.2016-1220

M3 - Journal article

VL - 157

SP - 3009

EP - 3015

JO - Endocrinology

JF - Endocrinology

SN - 0013-7227

IS - 8

ER -

ID: 49639644