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Epinephrine and AICAR-induced PGC-1α mRNA expression is intact in skeletal muscle from rats fed a high-fat diet.
Am J Physiol Cell Physiol. 2012 Jun 15; 302(12):C1772-9.AJ

Abstract

Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) is a master regulator of mitochondrial biogenesis and is controlled, at least in part, through AMP-activated protein kinase and p38-dependent pathways. There is evidence demonstrating that activation of these kinases and induction of PGC-1α in skeletal muscle are regulated by catecholamines. The purpose of the present study was to determine if consumption of a high-fat diet (HFD) impairs epinephrine and 5-aminoimidazole-4-carboxamide-1β-d-ribofuranoside (AICAR) signaling and induction of PGC-1α in rat skeletal muscle. Male Wistar rats were fed chow or a HFD for 6 wk and then given a weight-adjusted bolus injection of epinephrine (20, 10, or 5 μg/100 g body wt sc) or saline, and triceps muscles were harvested 30 min (signaling) or 2 and 4 h (gene expression) postinjection. Despite blunted increases in p38 phosphorylation, the ability of epinephrine to induce PGC-1α was intact in skeletal muscle from HFD-fed rats and was associated with normal increases in activation of PKA and phosphorylation of cAMP response element-binding protein, reputed mediators of PGC-1α expression. The attenuated epinephrine-mediated increase in p38 phosphorylation was independent of increases in MAPK phosphatase 1. At 2 h following AICAR treatment (0.5 g/kg body wt sc), AMP-activated protein kinase and acetyl-CoA carboxylase phosphorylation were similar in skeletal muscle from chow- and HFD-fed rats. Surprisingly, AICAR-induced increases in PGC-1α mRNA levels were greater in skeletal muscle from HFD-fed rats. Our results demonstrate that the ability of epinephrine and AICAR to induce PGC-1α remains intact in skeletal muscle from HFD-fed rats. These results question the existence of reduced β-adrenergic responsiveness in diet-induced obesity and demonstrate that increases in p38 phosphorylation are not required for induction of PGC-1α in muscle from obese rats.

Authors+Show Affiliations

Department of Agriculture, Food, and Nutritional Science, University of Alberta, Edmonton, Canada.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22496244

Citation

Frier, Bruce C., et al. "Epinephrine and AICAR-induced PGC-1α mRNA Expression Is Intact in Skeletal Muscle From Rats Fed a High-fat Diet." American Journal of Physiology. Cell Physiology, vol. 302, no. 12, 2012, pp. C1772-9.
Frier BC, Wan Z, Williams DB, et al. Epinephrine and AICAR-induced PGC-1α mRNA expression is intact in skeletal muscle from rats fed a high-fat diet. Am J Physiol, Cell Physiol. 2012;302(12):C1772-9.
Frier, B. C., Wan, Z., Williams, D. B., Stefanson, A. L., & Wright, D. C. (2012). Epinephrine and AICAR-induced PGC-1α mRNA expression is intact in skeletal muscle from rats fed a high-fat diet. American Journal of Physiology. Cell Physiology, 302(12), C1772-9. https://doi.org/10.1152/ajpcell.00410.2011
Frier BC, et al. Epinephrine and AICAR-induced PGC-1α mRNA Expression Is Intact in Skeletal Muscle From Rats Fed a High-fat Diet. Am J Physiol, Cell Physiol. 2012 Jun 15;302(12):C1772-9. PubMed PMID: 22496244.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Epinephrine and AICAR-induced PGC-1α mRNA expression is intact in skeletal muscle from rats fed a high-fat diet. AU - Frier,Bruce C, AU - Wan,Zhongxiao, AU - Williams,Deon B, AU - Stefanson,Amanda L, AU - Wright,David C, Y1 - 2012/04/11/ PY - 2012/4/13/entrez PY - 2012/4/13/pubmed PY - 2012/8/24/medline SP - C1772 EP - 9 JF - American journal of physiology. Cell physiology JO - Am. J. Physiol., Cell Physiol. VL - 302 IS - 12 N2 - Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) is a master regulator of mitochondrial biogenesis and is controlled, at least in part, through AMP-activated protein kinase and p38-dependent pathways. There is evidence demonstrating that activation of these kinases and induction of PGC-1α in skeletal muscle are regulated by catecholamines. The purpose of the present study was to determine if consumption of a high-fat diet (HFD) impairs epinephrine and 5-aminoimidazole-4-carboxamide-1β-d-ribofuranoside (AICAR) signaling and induction of PGC-1α in rat skeletal muscle. Male Wistar rats were fed chow or a HFD for 6 wk and then given a weight-adjusted bolus injection of epinephrine (20, 10, or 5 μg/100 g body wt sc) or saline, and triceps muscles were harvested 30 min (signaling) or 2 and 4 h (gene expression) postinjection. Despite blunted increases in p38 phosphorylation, the ability of epinephrine to induce PGC-1α was intact in skeletal muscle from HFD-fed rats and was associated with normal increases in activation of PKA and phosphorylation of cAMP response element-binding protein, reputed mediators of PGC-1α expression. The attenuated epinephrine-mediated increase in p38 phosphorylation was independent of increases in MAPK phosphatase 1. At 2 h following AICAR treatment (0.5 g/kg body wt sc), AMP-activated protein kinase and acetyl-CoA carboxylase phosphorylation were similar in skeletal muscle from chow- and HFD-fed rats. Surprisingly, AICAR-induced increases in PGC-1α mRNA levels were greater in skeletal muscle from HFD-fed rats. Our results demonstrate that the ability of epinephrine and AICAR to induce PGC-1α remains intact in skeletal muscle from HFD-fed rats. These results question the existence of reduced β-adrenergic responsiveness in diet-induced obesity and demonstrate that increases in p38 phosphorylation are not required for induction of PGC-1α in muscle from obese rats. SN - 1522-1563 UR - https://www.unboundmedicine.com/medline/citation/22496244/Epinephrine_and_AICAR_induced_PGC_1α_mRNA_expression_is_intact_in_skeletal_muscle_from_rats_fed_a_high_fat_diet_ L2 - http://www.physiology.org/doi/full/10.1152/ajpcell.00410.2011?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -