AMP-activated protein kinase (AMPK) {beta}1{beta}2 muscle null mice reveal an essential role for AMPK in maintaining mitochondrial content and glucose uptake during exercise

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Standard

AMP-activated protein kinase (AMPK) {beta}1{beta}2 muscle null mice reveal an essential role for AMPK in maintaining mitochondrial content and glucose uptake during exercise. / O'Neill, Hayley M; Maarbjerg, Stine Just; Crane, Justin D; Jeppesen, Jacob; Jørgensen, Sebastian B; Schertzer, Jonathan D; Shyroka, Olga; Kiens, Bente; van Denderen, Bryce J; Tarnopolsky, Mark A; Kemp, Bruce E; Richter, Erik A.; Steinberg, Gregory R.

I: Proceedings of the National Academy of Sciences of the United States of America, Bind 108, Nr. 38, 2011, s. 16092-16097.

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Harvard

O'Neill, HM, Maarbjerg, SJ, Crane, JD, Jeppesen, J, Jørgensen, SB, Schertzer, JD, Shyroka, O, Kiens, B, van Denderen, BJ, Tarnopolsky, MA, Kemp, BE, Richter, EA & Steinberg, GR 2011, 'AMP-activated protein kinase (AMPK) {beta}1{beta}2 muscle null mice reveal an essential role for AMPK in maintaining mitochondrial content and glucose uptake during exercise', Proceedings of the National Academy of Sciences of the United States of America, bind 108, nr. 38, s. 16092-16097. https://doi.org/10.1073/pnas.1105062108

APA

O'Neill, H. M., Maarbjerg, S. J., Crane, J. D., Jeppesen, J., Jørgensen, S. B., Schertzer, J. D., Shyroka, O., Kiens, B., van Denderen, B. J., Tarnopolsky, M. A., Kemp, B. E., Richter, E. A., & Steinberg, G. R. (2011). AMP-activated protein kinase (AMPK) {beta}1{beta}2 muscle null mice reveal an essential role for AMPK in maintaining mitochondrial content and glucose uptake during exercise. Proceedings of the National Academy of Sciences of the United States of America, 108(38), 16092-16097. https://doi.org/10.1073/pnas.1105062108

Vancouver

O'Neill HM, Maarbjerg SJ, Crane JD, Jeppesen J, Jørgensen SB, Schertzer JD o.a. AMP-activated protein kinase (AMPK) {beta}1{beta}2 muscle null mice reveal an essential role for AMPK in maintaining mitochondrial content and glucose uptake during exercise. Proceedings of the National Academy of Sciences of the United States of America. 2011;108(38):16092-16097. https://doi.org/10.1073/pnas.1105062108

Author

O'Neill, Hayley M ; Maarbjerg, Stine Just ; Crane, Justin D ; Jeppesen, Jacob ; Jørgensen, Sebastian B ; Schertzer, Jonathan D ; Shyroka, Olga ; Kiens, Bente ; van Denderen, Bryce J ; Tarnopolsky, Mark A ; Kemp, Bruce E ; Richter, Erik A. ; Steinberg, Gregory R. / AMP-activated protein kinase (AMPK) {beta}1{beta}2 muscle null mice reveal an essential role for AMPK in maintaining mitochondrial content and glucose uptake during exercise. I: Proceedings of the National Academy of Sciences of the United States of America. 2011 ; Bind 108, Nr. 38. s. 16092-16097.

Bibtex

@article{359a9a336a8d4753bdaf21a1fcd2f62d,
title = "AMP-activated protein kinase (AMPK) {beta}1{beta}2 muscle null mice reveal an essential role for AMPK in maintaining mitochondrial content and glucose uptake during exercise",
abstract = "AMP-activated protein kinase (AMPK) {\ss}1 or {\ss}2 subunits are required for assembling of AMPK heterotrimers and are important for regulating enzyme activity and cellular localization. In skeletal muscle, a2{\ss}2¿3-containing heterotrimers predominate. However, compensatory up-regulation and redundancy of AMPK subunits in whole-body AMPK a2, {\ss}2, and ¿3 null mice has made it difficult to determine the physiological importance of AMPK in regulating muscle metabolism, because these models have normal mitochondrial content, contraction-stimulated glucose uptake, and insulin sensitivity. In the current study, we generated mice lacking both AMPK {\ss}1 and {\ss}2 isoforms in skeletal muscle ({\ss}1{\ss}2M-KO). {\ss}1{\ss}2M-KO mice are physically inactive and have a drastically impaired capacity for treadmill running that is associated with reductions in skeletal muscle mitochondrial content but not a fiber-type switch. Interestingly, young {\ss}1{\ss}2M-KO mice fed a control chow diet are not obese or insulin resistant but do have impaired contraction-stimulated glucose uptake. These data demonstrate an obligatory role for skeletal muscle AMPK in maintaining mitochondrial capacity and contraction-stimulated glucose uptake, findings that were not apparent in mice with single mutations or deletions in muscle a, {\ss}, or ¿ subunits.",
author = "O'Neill, {Hayley M} and Maarbjerg, {Stine Just} and Crane, {Justin D} and Jacob Jeppesen and J{\o}rgensen, {Sebastian B} and Schertzer, {Jonathan D} and Olga Shyroka and Bente Kiens and {van Denderen}, {Bryce J} and Tarnopolsky, {Mark A} and Kemp, {Bruce E} and Richter, {Erik A.} and Steinberg, {Gregory R}",
note = "CURIS 2011 5200 093",
year = "2011",
doi = "10.1073/pnas.1105062108",
language = "English",
volume = "108",
pages = "16092--16097",
journal = "Proceedings of the National Academy of Sciences of the United States of America",
issn = "0027-8424",
publisher = "The National Academy of Sciences of the United States of America",
number = "38",

}

RIS

TY - JOUR

T1 - AMP-activated protein kinase (AMPK) {beta}1{beta}2 muscle null mice reveal an essential role for AMPK in maintaining mitochondrial content and glucose uptake during exercise

AU - O'Neill, Hayley M

AU - Maarbjerg, Stine Just

AU - Crane, Justin D

AU - Jeppesen, Jacob

AU - Jørgensen, Sebastian B

AU - Schertzer, Jonathan D

AU - Shyroka, Olga

AU - Kiens, Bente

AU - van Denderen, Bryce J

AU - Tarnopolsky, Mark A

AU - Kemp, Bruce E

AU - Richter, Erik A.

AU - Steinberg, Gregory R

N1 - CURIS 2011 5200 093

PY - 2011

Y1 - 2011

N2 - AMP-activated protein kinase (AMPK) ß1 or ß2 subunits are required for assembling of AMPK heterotrimers and are important for regulating enzyme activity and cellular localization. In skeletal muscle, a2ß2¿3-containing heterotrimers predominate. However, compensatory up-regulation and redundancy of AMPK subunits in whole-body AMPK a2, ß2, and ¿3 null mice has made it difficult to determine the physiological importance of AMPK in regulating muscle metabolism, because these models have normal mitochondrial content, contraction-stimulated glucose uptake, and insulin sensitivity. In the current study, we generated mice lacking both AMPK ß1 and ß2 isoforms in skeletal muscle (ß1ß2M-KO). ß1ß2M-KO mice are physically inactive and have a drastically impaired capacity for treadmill running that is associated with reductions in skeletal muscle mitochondrial content but not a fiber-type switch. Interestingly, young ß1ß2M-KO mice fed a control chow diet are not obese or insulin resistant but do have impaired contraction-stimulated glucose uptake. These data demonstrate an obligatory role for skeletal muscle AMPK in maintaining mitochondrial capacity and contraction-stimulated glucose uptake, findings that were not apparent in mice with single mutations or deletions in muscle a, ß, or ¿ subunits.

AB - AMP-activated protein kinase (AMPK) ß1 or ß2 subunits are required for assembling of AMPK heterotrimers and are important for regulating enzyme activity and cellular localization. In skeletal muscle, a2ß2¿3-containing heterotrimers predominate. However, compensatory up-regulation and redundancy of AMPK subunits in whole-body AMPK a2, ß2, and ¿3 null mice has made it difficult to determine the physiological importance of AMPK in regulating muscle metabolism, because these models have normal mitochondrial content, contraction-stimulated glucose uptake, and insulin sensitivity. In the current study, we generated mice lacking both AMPK ß1 and ß2 isoforms in skeletal muscle (ß1ß2M-KO). ß1ß2M-KO mice are physically inactive and have a drastically impaired capacity for treadmill running that is associated with reductions in skeletal muscle mitochondrial content but not a fiber-type switch. Interestingly, young ß1ß2M-KO mice fed a control chow diet are not obese or insulin resistant but do have impaired contraction-stimulated glucose uptake. These data demonstrate an obligatory role for skeletal muscle AMPK in maintaining mitochondrial capacity and contraction-stimulated glucose uptake, findings that were not apparent in mice with single mutations or deletions in muscle a, ß, or ¿ subunits.

U2 - 10.1073/pnas.1105062108

DO - 10.1073/pnas.1105062108

M3 - Journal article

C2 - 21896769

VL - 108

SP - 16092

EP - 16097

JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

SN - 0027-8424

IS - 38

ER -

ID: 34409495