Clenbuterol exerts antidiabetic activity through metabolic reprogramming of skeletal muscle cells

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Standard

Clenbuterol exerts antidiabetic activity through metabolic reprogramming of skeletal muscle cells. / Meister, Jaroslawna; Bone, Derek B J; Knudsen, Jonas Roland; Barella, Luiz F; Velenosi, Thomas J; Akhmedov, Dmitry; Lee, Regina J; Cohen, Amanda H; Gavrilova, Oksana; Cui, Yinghong; Karsenty, Gerard; Chen, Min; Weinstein, Lee S; Kleinert, Maximilian; Berdeaux, Rebecca; Jensen, Thomas Elbenhardt; Richter, Erik A.; Wess, Jürgen.

I: Nature Communications, Bind 13, 22, 2022.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Meister, J, Bone, DBJ, Knudsen, JR, Barella, LF, Velenosi, TJ, Akhmedov, D, Lee, RJ, Cohen, AH, Gavrilova, O, Cui, Y, Karsenty, G, Chen, M, Weinstein, LS, Kleinert, M, Berdeaux, R, Jensen, TE, Richter, EA & Wess, J 2022, 'Clenbuterol exerts antidiabetic activity through metabolic reprogramming of skeletal muscle cells', Nature Communications, bind 13, 22. https://doi.org/10.1038/s41467-021-27540-w

APA

Meister, J., Bone, D. B. J., Knudsen, J. R., Barella, L. F., Velenosi, T. J., Akhmedov, D., Lee, R. J., Cohen, A. H., Gavrilova, O., Cui, Y., Karsenty, G., Chen, M., Weinstein, L. S., Kleinert, M., Berdeaux, R., Jensen, T. E., Richter, E. A., & Wess, J. (2022). Clenbuterol exerts antidiabetic activity through metabolic reprogramming of skeletal muscle cells. Nature Communications, 13, [22]. https://doi.org/10.1038/s41467-021-27540-w

Vancouver

Meister J, Bone DBJ, Knudsen JR, Barella LF, Velenosi TJ, Akhmedov D o.a. Clenbuterol exerts antidiabetic activity through metabolic reprogramming of skeletal muscle cells. Nature Communications. 2022;13. 22. https://doi.org/10.1038/s41467-021-27540-w

Author

Meister, Jaroslawna ; Bone, Derek B J ; Knudsen, Jonas Roland ; Barella, Luiz F ; Velenosi, Thomas J ; Akhmedov, Dmitry ; Lee, Regina J ; Cohen, Amanda H ; Gavrilova, Oksana ; Cui, Yinghong ; Karsenty, Gerard ; Chen, Min ; Weinstein, Lee S ; Kleinert, Maximilian ; Berdeaux, Rebecca ; Jensen, Thomas Elbenhardt ; Richter, Erik A. ; Wess, Jürgen. / Clenbuterol exerts antidiabetic activity through metabolic reprogramming of skeletal muscle cells. I: Nature Communications. 2022 ; Bind 13.

Bibtex

@article{753a52f04f0b480894a3ad165d3f4e28,

title = "Clenbuterol exerts antidiabetic activity through metabolic reprogramming of skeletal muscle cells",

abstract = "Activation of the sympathetic nervous system causes pronounced metabolic changes that are mediated by multiple adrenergic receptor subtypes. Systemic treatment with β2-adrenergic receptor agonists results in multiple beneficial metabolic effects, including improved glucose homeostasis. To elucidate the underlying cellular and molecular mechanisms, we chronically treated wild-type mice and several newly developed mutant mouse strains with clenbuterol, a selective β2-adrenergic receptor agonist. Clenbuterol administration caused pronounced improvements in glucose homeostasis and prevented the metabolic deficits in mouse models of β-cell dysfunction and insulin resistance. Studies with skeletal muscle-specific mutant mice demonstrated that these metabolic improvements required activation of skeletal muscle β2-adrenergic receptors and the stimulatory G protein, Gs. Unbiased transcriptomic and metabolomic analyses showed that chronic β2-adrenergic receptor stimulation caused metabolic reprogramming of skeletal muscle characterized by enhanced glucose utilization. These findings strongly suggest that agents targeting skeletal muscle metabolism by modulating β2-adrenergic receptor-dependent signaling pathways may prove beneficial as antidiabetic drugs.",

author = "Jaroslawna Meister and Bone, {Derek B J} and Knudsen, {Jonas Roland} and Barella, {Luiz F} and Velenosi, {Thomas J} and Dmitry Akhmedov and Lee, {Regina J} and Cohen, {Amanda H} and Oksana Gavrilova and Yinghong Cui and Gerard Karsenty and Min Chen and Weinstein, {Lee S} and Maximilian Kleinert and Rebecca Berdeaux and Jensen, {Thomas Elbenhardt} and Richter, {Erik A.} and J{\"u}rgen Wess",

note = "{\textcopyright} 2022. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.",

year = "2022",

doi = "10.1038/s41467-021-27540-w",

language = "English",

volume = "13",

journal = "Nature Communications",

issn = "2041-1723",

publisher = "nature publishing group",

}

RIS

TY - JOUR

T1 - Clenbuterol exerts antidiabetic activity through metabolic reprogramming of skeletal muscle cells

AU - Meister, Jaroslawna

AU - Bone, Derek B J

AU - Knudsen, Jonas Roland

AU - Barella, Luiz F

AU - Velenosi, Thomas J

AU - Akhmedov, Dmitry

AU - Lee, Regina J

AU - Cohen, Amanda H

AU - Gavrilova, Oksana

AU - Cui, Yinghong

AU - Karsenty, Gerard

AU - Chen, Min

AU - Weinstein, Lee S

AU - Kleinert, Maximilian

AU - Berdeaux, Rebecca

AU - Jensen, Thomas Elbenhardt

AU - Richter, Erik A.

AU - Wess, Jürgen

PY - 2022

Y1 - 2022

N2 - Activation of the sympathetic nervous system causes pronounced metabolic changes that are mediated by multiple adrenergic receptor subtypes. Systemic treatment with β2-adrenergic receptor agonists results in multiple beneficial metabolic effects, including improved glucose homeostasis. To elucidate the underlying cellular and molecular mechanisms, we chronically treated wild-type mice and several newly developed mutant mouse strains with clenbuterol, a selective β2-adrenergic receptor agonist. Clenbuterol administration caused pronounced improvements in glucose homeostasis and prevented the metabolic deficits in mouse models of β-cell dysfunction and insulin resistance. Studies with skeletal muscle-specific mutant mice demonstrated that these metabolic improvements required activation of skeletal muscle β2-adrenergic receptors and the stimulatory G protein, Gs. Unbiased transcriptomic and metabolomic analyses showed that chronic β2-adrenergic receptor stimulation caused metabolic reprogramming of skeletal muscle characterized by enhanced glucose utilization. These findings strongly suggest that agents targeting skeletal muscle metabolism by modulating β2-adrenergic receptor-dependent signaling pathways may prove beneficial as antidiabetic drugs.

AB - Activation of the sympathetic nervous system causes pronounced metabolic changes that are mediated by multiple adrenergic receptor subtypes. Systemic treatment with β2-adrenergic receptor agonists results in multiple beneficial metabolic effects, including improved glucose homeostasis. To elucidate the underlying cellular and molecular mechanisms, we chronically treated wild-type mice and several newly developed mutant mouse strains with clenbuterol, a selective β2-adrenergic receptor agonist. Clenbuterol administration caused pronounced improvements in glucose homeostasis and prevented the metabolic deficits in mouse models of β-cell dysfunction and insulin resistance. Studies with skeletal muscle-specific mutant mice demonstrated that these metabolic improvements required activation of skeletal muscle β2-adrenergic receptors and the stimulatory G protein, Gs. Unbiased transcriptomic and metabolomic analyses showed that chronic β2-adrenergic receptor stimulation caused metabolic reprogramming of skeletal muscle characterized by enhanced glucose utilization. These findings strongly suggest that agents targeting skeletal muscle metabolism by modulating β2-adrenergic receptor-dependent signaling pathways may prove beneficial as antidiabetic drugs.

U2 - 10.1038/s41467-021-27540-w

DO - 10.1038/s41467-021-27540-w

M3 - Journal article

C2 - 35013148

VL - 13

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

M1 - 22

ER -

ID: 289308321

Institut for Idræt og Ernæring