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The effects of apelin treatment on skeletal muscle mitochondrial content.

Abstract

Adipose tissue is recognized as a key player in the regulation of whole body metabolism. Apelin, is a recently identified adipokine that when given to mice results in increases in skeletal muscle uncoupling protein 3 (UCP3) content. Similarly, acute apelin treatment has been shown to increase the activity of 5'-AMP-activated protein kinase (AMPK), a reputed mediator of skeletal muscle mitochondrial biogenesis. Given these findings, we sought to determine the effects of apelin on skeletal muscle mitochondrial content. Male Wistar rats were given daily intraperitoneal injections of apelin-13 (100 nmol/kg) for 2 wk. We made the novel observation that the activities of citrate synthase, cytochrome c oxidase, and beta-hydroxyacyl coA dehydrogenase (betaHAD) were increased in triceps but not heart and soleus muscles from apelin-treated rats. When confirming these results we found that both nuclear and mitochondrial-encoded subunits of the respiratory chain were increased in triceps from apelin-treated rats. Similarly, apelin treatment increased the protein content of components of the mitochondrial import and assembly pathway. The increases in mitochondrial marker proteins were associated with increases in proliferator-activated receptor-gamma coactivator-1 (PGC-1beta) but not PGC-1alpha or Pgc-1-related co-activator (PRC) mRNA expression. Chronic and acute apelin treatment did not increase the protein content and/or phosphorylation status of AMPK and its downstream substrate acetyl-CoA carboxylase. These findings are the first to demonstrate that apelin treatment can induce skeletal muscle mitochondrial content. Given the lack of an effect of apelin on AMPK signaling and PGC-1alpha mRNA expression, these results suggest that apelin increases skeletal muscle mitochondrial content through a mechanism that is distinct from that of more robust physiological stressors.

Authors+Show Affiliations

Alberta Diabetes Institute, University of Alberta, Edmonton, Alberta, Canada T6G 2E1.No affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

19793954

Citation

Frier, Bruce C., et al. "The Effects of Apelin Treatment On Skeletal Muscle Mitochondrial Content." American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, vol. 297, no. 6, 2009, pp. R1761-8.
Frier BC, Williams DB, Wright DC. The effects of apelin treatment on skeletal muscle mitochondrial content. Am J Physiol Regul Integr Comp Physiol. 2009;297(6):R1761-8.
Frier, B. C., Williams, D. B., & Wright, D. C. (2009). The effects of apelin treatment on skeletal muscle mitochondrial content. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, 297(6), pp. R1761-8. doi:10.1152/ajpregu.00422.2009.
Frier BC, Williams DB, Wright DC. The Effects of Apelin Treatment On Skeletal Muscle Mitochondrial Content. Am J Physiol Regul Integr Comp Physiol. 2009;297(6):R1761-8. PubMed PMID: 19793954.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The effects of apelin treatment on skeletal muscle mitochondrial content. AU - Frier,Bruce C, AU - Williams,Deon B, AU - Wright,David C, Y1 - 2009/09/30/ PY - 2009/10/2/entrez PY - 2009/10/2/pubmed PY - 2009/12/16/medline SP - R1761 EP - 8 JF - American journal of physiology. Regulatory, integrative and comparative physiology JO - Am. J. Physiol. Regul. Integr. Comp. Physiol. VL - 297 IS - 6 N2 - Adipose tissue is recognized as a key player in the regulation of whole body metabolism. Apelin, is a recently identified adipokine that when given to mice results in increases in skeletal muscle uncoupling protein 3 (UCP3) content. Similarly, acute apelin treatment has been shown to increase the activity of 5'-AMP-activated protein kinase (AMPK), a reputed mediator of skeletal muscle mitochondrial biogenesis. Given these findings, we sought to determine the effects of apelin on skeletal muscle mitochondrial content. Male Wistar rats were given daily intraperitoneal injections of apelin-13 (100 nmol/kg) for 2 wk. We made the novel observation that the activities of citrate synthase, cytochrome c oxidase, and beta-hydroxyacyl coA dehydrogenase (betaHAD) were increased in triceps but not heart and soleus muscles from apelin-treated rats. When confirming these results we found that both nuclear and mitochondrial-encoded subunits of the respiratory chain were increased in triceps from apelin-treated rats. Similarly, apelin treatment increased the protein content of components of the mitochondrial import and assembly pathway. The increases in mitochondrial marker proteins were associated with increases in proliferator-activated receptor-gamma coactivator-1 (PGC-1beta) but not PGC-1alpha or Pgc-1-related co-activator (PRC) mRNA expression. Chronic and acute apelin treatment did not increase the protein content and/or phosphorylation status of AMPK and its downstream substrate acetyl-CoA carboxylase. These findings are the first to demonstrate that apelin treatment can induce skeletal muscle mitochondrial content. Given the lack of an effect of apelin on AMPK signaling and PGC-1alpha mRNA expression, these results suggest that apelin increases skeletal muscle mitochondrial content through a mechanism that is distinct from that of more robust physiological stressors. SN - 1522-1490 UR - https://www.unboundmedicine.com/medline/citation/19793954/The_effects_of_apelin_treatment_on_skeletal_muscle_mitochondrial_content_ L2 - http://www.physiology.org/doi/full/10.1152/ajpregu.00422.2009?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -