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Impact of β-adrenergic signaling in PGC-1α-mediated adaptations in mouse skeletal muscle

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Impact of β-adrenergic signaling in PGC-1α-mediated adaptations in mouse skeletal muscle. / Brandt, Nina; Nielsen, Lene; Buch, Bjørg Thiellesen; Gudiksen, Anders; Ringholm Jørgensen, Stine; Hellsten, Ylva; Bangsbo, Jens; Pilegaard, Henriette.

In: American Journal of Physiology: Endocrinology and Metabolism, Vol. 314, No. 1, 01.01.2018, p. E1-E20.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Brandt, N, Nielsen, L, Buch, BT, Gudiksen, A, Ringholm Jørgensen, S, Hellsten, Y, Bangsbo, J & Pilegaard, H 2018, 'Impact of β-adrenergic signaling in PGC-1α-mediated adaptations in mouse skeletal muscle', American Journal of Physiology: Endocrinology and Metabolism, vol. 314, no. 1, pp. E1-E20. https://doi.org/10.1152/ajpendo.00082.2017

APA

Brandt, N., Nielsen, L., Buch, B. T., Gudiksen, A., Ringholm Jørgensen, S., Hellsten, Y., ... Pilegaard, H. (2018). Impact of β-adrenergic signaling in PGC-1α-mediated adaptations in mouse skeletal muscle. American Journal of Physiology: Endocrinology and Metabolism, 314(1), E1-E20. https://doi.org/10.1152/ajpendo.00082.2017

Vancouver

Brandt N, Nielsen L, Buch BT, Gudiksen A, Ringholm Jørgensen S, Hellsten Y et al. Impact of β-adrenergic signaling in PGC-1α-mediated adaptations in mouse skeletal muscle. American Journal of Physiology: Endocrinology and Metabolism. 2018 Jan 1;314(1):E1-E20. https://doi.org/10.1152/ajpendo.00082.2017

Author

Brandt, Nina ; Nielsen, Lene ; Buch, Bjørg Thiellesen ; Gudiksen, Anders ; Ringholm Jørgensen, Stine ; Hellsten, Ylva ; Bangsbo, Jens ; Pilegaard, Henriette. / Impact of β-adrenergic signaling in PGC-1α-mediated adaptations in mouse skeletal muscle. In: American Journal of Physiology: Endocrinology and Metabolism. 2018 ; Vol. 314, No. 1. pp. E1-E20.

Bibtex

@article{0f436a7000ca41a3be9b2f936966dcf0,
title = "Impact of β-adrenergic signaling in PGC-1α-mediated adaptations in mouse skeletal muscle",
abstract = "PGC-1α has been suggested to regulate exercise training-induced metabolic adaptations and autophagy in skeletal muscle. The factors regulating PGC-1α are however not fully resolved. The aim was to investigate the impact of β-adrenergic signaling in PGC-1α mediated metabolic adaptations in skeletal muscle with exercise training. Muscle was obtained from muscle specific PGC-1α knockout (MKO) mice and LOX/LOX 1) 3h after a single exercise bout with or without prior injection of propranolol or 3h after a single injection of clenbuterol and 2) after 5 weeks of wheel running exercise training with or without propranolol treatment or after 5 weeks of clenbuterol treatment. A single clenbuterol injection and an acute exercise bout increased similarly the mRNA content of both N-Terminal and full-length PGC-1α isoforms and prior propranolol treatment reduced the exercise-induced increase of all isoforms. Furthermore, a single clenbuterol injection elicited a PGC-1α-dependent increase in Cyt c and VEGF mRNA, whereas prolonged clenbuterol treatment increased fiber size but reduced capillary density. Exercise training increased the protein content of OXPHOS, LC3I, and Parkin in a PGC-1α-dependent manner without effect of propranolol, while an exercise training-induced increase in Akt2 and p62 protein required PGC-1α and was blunted by prolonged propranolol treatment. This suggests that β-adrenergic signaling is not required for PGC-1α mediated exercise training-induced adaptations in mitochondrial proteins, but contributes to exercise training mediated adaptations in insulin signaling and autophagy regulation through PGC-1α. Furthermore, changes observed with acute stimulation of compounds like clenbuterol and propranolol may not lead to corresponding adaptations with prolonged treatment.",
keywords = "Skeletal muscle, PGC-1α, PGC-1α isoforms, Exercise, Training, Autophagy, β-adrenergic signaling, Clenbuterol, Propranolol",
author = "Nina Brandt and Lene Nielsen and Buch, {Bj{\o}rg Thiellesen} and Anders Gudiksen and {Ringholm J{\o}rgensen}, Stine and Ylva Hellsten and Jens Bangsbo and Henriette Pilegaard",
note = "CURIS 2018 NEXS 083",
year = "2018",
month = "1",
day = "1",
doi = "10.1152/ajpendo.00082.2017",
language = "English",
volume = "314",
pages = "E1--E20",
journal = "American Journal of Physiology: Endocrinology and Metabolism",
issn = "0193-1849",
publisher = "American Physiological Society",
number = "1",

}

RIS

TY - JOUR

T1 - Impact of β-adrenergic signaling in PGC-1α-mediated adaptations in mouse skeletal muscle

AU - Brandt, Nina

AU - Nielsen, Lene

AU - Buch, Bjørg Thiellesen

AU - Gudiksen, Anders

AU - Ringholm Jørgensen, Stine

AU - Hellsten, Ylva

AU - Bangsbo, Jens

AU - Pilegaard, Henriette

N1 - CURIS 2018 NEXS 083

PY - 2018/1/1

Y1 - 2018/1/1

N2 - PGC-1α has been suggested to regulate exercise training-induced metabolic adaptations and autophagy in skeletal muscle. The factors regulating PGC-1α are however not fully resolved. The aim was to investigate the impact of β-adrenergic signaling in PGC-1α mediated metabolic adaptations in skeletal muscle with exercise training. Muscle was obtained from muscle specific PGC-1α knockout (MKO) mice and LOX/LOX 1) 3h after a single exercise bout with or without prior injection of propranolol or 3h after a single injection of clenbuterol and 2) after 5 weeks of wheel running exercise training with or without propranolol treatment or after 5 weeks of clenbuterol treatment. A single clenbuterol injection and an acute exercise bout increased similarly the mRNA content of both N-Terminal and full-length PGC-1α isoforms and prior propranolol treatment reduced the exercise-induced increase of all isoforms. Furthermore, a single clenbuterol injection elicited a PGC-1α-dependent increase in Cyt c and VEGF mRNA, whereas prolonged clenbuterol treatment increased fiber size but reduced capillary density. Exercise training increased the protein content of OXPHOS, LC3I, and Parkin in a PGC-1α-dependent manner without effect of propranolol, while an exercise training-induced increase in Akt2 and p62 protein required PGC-1α and was blunted by prolonged propranolol treatment. This suggests that β-adrenergic signaling is not required for PGC-1α mediated exercise training-induced adaptations in mitochondrial proteins, but contributes to exercise training mediated adaptations in insulin signaling and autophagy regulation through PGC-1α. Furthermore, changes observed with acute stimulation of compounds like clenbuterol and propranolol may not lead to corresponding adaptations with prolonged treatment.

AB - PGC-1α has been suggested to regulate exercise training-induced metabolic adaptations and autophagy in skeletal muscle. The factors regulating PGC-1α are however not fully resolved. The aim was to investigate the impact of β-adrenergic signaling in PGC-1α mediated metabolic adaptations in skeletal muscle with exercise training. Muscle was obtained from muscle specific PGC-1α knockout (MKO) mice and LOX/LOX 1) 3h after a single exercise bout with or without prior injection of propranolol or 3h after a single injection of clenbuterol and 2) after 5 weeks of wheel running exercise training with or without propranolol treatment or after 5 weeks of clenbuterol treatment. A single clenbuterol injection and an acute exercise bout increased similarly the mRNA content of both N-Terminal and full-length PGC-1α isoforms and prior propranolol treatment reduced the exercise-induced increase of all isoforms. Furthermore, a single clenbuterol injection elicited a PGC-1α-dependent increase in Cyt c and VEGF mRNA, whereas prolonged clenbuterol treatment increased fiber size but reduced capillary density. Exercise training increased the protein content of OXPHOS, LC3I, and Parkin in a PGC-1α-dependent manner without effect of propranolol, while an exercise training-induced increase in Akt2 and p62 protein required PGC-1α and was blunted by prolonged propranolol treatment. This suggests that β-adrenergic signaling is not required for PGC-1α mediated exercise training-induced adaptations in mitochondrial proteins, but contributes to exercise training mediated adaptations in insulin signaling and autophagy regulation through PGC-1α. Furthermore, changes observed with acute stimulation of compounds like clenbuterol and propranolol may not lead to corresponding adaptations with prolonged treatment.

KW - Skeletal muscle

KW - PGC-1α

KW - PGC-1α isoforms

KW - Exercise

KW - Training

KW - Autophagy

KW - β-adrenergic signaling

KW - Clenbuterol

KW - Propranolol

U2 - 10.1152/ajpendo.00082.2017

DO - 10.1152/ajpendo.00082.2017

M3 - Journal article

C2 - 28874356

VL - 314

SP - E1-E20

JO - American Journal of Physiology: Endocrinology and Metabolism

JF - American Journal of Physiology: Endocrinology and Metabolism

SN - 0193-1849

IS - 1

ER -

ID: 183009609