Skeletal muscle mitochondrial respiration in AMPKa2 kinase dead mice

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Skeletal muscle mitochondrial respiration in AMPKa2 kinase dead mice. / Larsen, Steen; Kristensen, Jonas Møller; Stride, Nis; Wojtaszewski, Jørgen; Helge, Jørn Wulff; Dela, Flemming.

I: Acta Physiologica (Print), Bind 205, Nr. 2, 2012, s. 314-320.

Publikation: Bidrag til tidsskriftTidsskriftartikel

Harvard

Larsen, S, Kristensen, JM, Stride, N, Wojtaszewski, J, Helge, JW & Dela, F 2012, 'Skeletal muscle mitochondrial respiration in AMPKa2 kinase dead mice', Acta Physiologica (Print), bind 205, nr. 2, s. 314-320. https://doi.org/10.1111/j.1748-1716.2011.02399.x

APA

Larsen, S., Kristensen, J. M., Stride, N., Wojtaszewski, J., Helge, J. W., & Dela, F. (2012). Skeletal muscle mitochondrial respiration in AMPKa2 kinase dead mice. Acta Physiologica (Print), 205(2), 314-320. https://doi.org/10.1111/j.1748-1716.2011.02399.x

Vancouver

Larsen S, Kristensen JM, Stride N, Wojtaszewski J, Helge JW, Dela F. Skeletal muscle mitochondrial respiration in AMPKa2 kinase dead mice. Acta Physiologica (Print). 2012;205(2):314-320. https://doi.org/10.1111/j.1748-1716.2011.02399.x

Author

Larsen, Steen ; Kristensen, Jonas Møller ; Stride, Nis ; Wojtaszewski, Jørgen ; Helge, Jørn Wulff ; Dela, Flemming. / Skeletal muscle mitochondrial respiration in AMPKa2 kinase dead mice. I: Acta Physiologica (Print). 2012 ; Bind 205, Nr. 2. s. 314-320.

Bibtex

@article{4b2878380df14a24b849948e284975c2,
title = "Skeletal muscle mitochondrial respiration in AMPKa2 kinase dead mice",
abstract = "AIM: To study if the phenotypical characteristics (exercise intolerance; reduced spontaneous activity) of the AMPKa2 kinase-dead (KD) mice can be explained by a reduced mitochondrial respiratory flux rates (JO(2) ) in skeletal muscle. Secondly, the effect of the maturation process on JO(2) was studied. METHODS: In tibialis anterior (almost exclusively type 2 fibers) muscle from young (12-17 weeks, n = 7) and mature (25-27 weeks, n = 12) KD and wild type (WT) (12-17 weeks, n = 9; 25-27 weeks, n = 11) littermates JO(2) was quantified in permeabilized fibers ex vivo by respirometry, using a substrate-uncoupler-inhibitor-titration (SUIT) protocol: malate, octanoyl-carnitine, ADP and glutamate (GMO(3) ), +succinate (GMOS(3) ), +uncoupler (U) and inhibitor (rotenone) of complex I respiration. Citrate synthase (CS) activity was measured as and index of mitochondrial content. RESULTS: CS activity was highest in young WT animals, and lower in KD animals compared with age-matched WT. JO(2) per mg tissue was lower (P",
author = "Steen Larsen and Kristensen, {Jonas M{\o}ller} and Nis Stride and J{\o}rgen Wojtaszewski and Helge, {J{\o}rn Wulff} and Flemming Dela",
note = "CURIS 2012 5200 018",
year = "2012",
doi = "10.1111/j.1748-1716.2011.02399.x",
language = "English",
volume = "205",
pages = "314--320",
journal = "Acta Physiologica (Print)",
issn = "1748-1708",
publisher = "Wiley-Blackwell",
number = "2",

}

RIS

TY - JOUR

T1 - Skeletal muscle mitochondrial respiration in AMPKa2 kinase dead mice

AU - Larsen, Steen

AU - Kristensen, Jonas Møller

AU - Stride, Nis

AU - Wojtaszewski, Jørgen

AU - Helge, Jørn Wulff

AU - Dela, Flemming

N1 - CURIS 2012 5200 018

PY - 2012

Y1 - 2012

N2 - AIM: To study if the phenotypical characteristics (exercise intolerance; reduced spontaneous activity) of the AMPKa2 kinase-dead (KD) mice can be explained by a reduced mitochondrial respiratory flux rates (JO(2) ) in skeletal muscle. Secondly, the effect of the maturation process on JO(2) was studied. METHODS: In tibialis anterior (almost exclusively type 2 fibers) muscle from young (12-17 weeks, n = 7) and mature (25-27 weeks, n = 12) KD and wild type (WT) (12-17 weeks, n = 9; 25-27 weeks, n = 11) littermates JO(2) was quantified in permeabilized fibers ex vivo by respirometry, using a substrate-uncoupler-inhibitor-titration (SUIT) protocol: malate, octanoyl-carnitine, ADP and glutamate (GMO(3) ), +succinate (GMOS(3) ), +uncoupler (U) and inhibitor (rotenone) of complex I respiration. Citrate synthase (CS) activity was measured as and index of mitochondrial content. RESULTS: CS activity was highest in young WT animals, and lower in KD animals compared with age-matched WT. JO(2) per mg tissue was lower (P

AB - AIM: To study if the phenotypical characteristics (exercise intolerance; reduced spontaneous activity) of the AMPKa2 kinase-dead (KD) mice can be explained by a reduced mitochondrial respiratory flux rates (JO(2) ) in skeletal muscle. Secondly, the effect of the maturation process on JO(2) was studied. METHODS: In tibialis anterior (almost exclusively type 2 fibers) muscle from young (12-17 weeks, n = 7) and mature (25-27 weeks, n = 12) KD and wild type (WT) (12-17 weeks, n = 9; 25-27 weeks, n = 11) littermates JO(2) was quantified in permeabilized fibers ex vivo by respirometry, using a substrate-uncoupler-inhibitor-titration (SUIT) protocol: malate, octanoyl-carnitine, ADP and glutamate (GMO(3) ), +succinate (GMOS(3) ), +uncoupler (U) and inhibitor (rotenone) of complex I respiration. Citrate synthase (CS) activity was measured as and index of mitochondrial content. RESULTS: CS activity was highest in young WT animals, and lower in KD animals compared with age-matched WT. JO(2) per mg tissue was lower (P

U2 - 10.1111/j.1748-1716.2011.02399.x

DO - 10.1111/j.1748-1716.2011.02399.x

M3 - Journal article

C2 - 22192354

VL - 205

SP - 314

EP - 320

JO - Acta Physiologica (Print)

JF - Acta Physiologica (Print)

SN - 1748-1708

IS - 2

ER -

ID: 36090126