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Role of AMPKalpha2 in basal, training-, and AICAR-induced GLUT4, hexokinase II, and mitochondrial protein expression in mouse muscle.
Am J Physiol Endocrinol Metab. 2007 Jan; 292(1):E331-9.AJ

Abstract

We investigated the role of AMPKalpha2in basal, exercise training-, and AICAR-induced protein expression of GLUT4, hexokinase II (HKII), mitochondrial markers, and AMPK subunits. This was conducted in red (RG) and white gastrocnemius (WG) muscle from wild-type (WT) and alpha2-knockout (KO) mice after 28 days of activity wheel running or daily AICAR injection. Additional experiments were conducted to measure acute activation of AMPK by exercise and AICAR. At basal, mitochondrial markers were reduced by approximately 20% in alpha2-KO muscles compared with WT. In both muscle types, AMPKalpha2 activity was increased in response to both stimuli, whereas AMPKalpha1 activity was increased only in response to exercise. Furthermore, AMPK signaling was estimated to be 60-70% lower in alpha2-KO compared with WT muscles. In WG, AICAR treatment increased HKII, GLUT4, cytochrome c, COX-1, and CS, and the alpha2-KO abolished the AICAR-induced increases, whereas no AICAR responses were observed in RG. Exercise training increased GLUT4, HKII, COX-1, CS, and HAD protein in WG, but the alpha2-KO did not affect training-induced increases. Furthermore, AMPKalpha1, -alpha2, -beta1, -beta2, and -gamma3 subunits were reduced in RG, but not in WG, by 30-60% in response to exercise training. In conclusion, the alpha2-KO was associated with an approximately 20% reduction in mitochondrial markers in both muscle types and abolished AICAR-induced increases in protein expression in WG. However, the alpha2-KO did not reduce training-induced increases in HKII, GLUT4, COX-1, HAD, or CS protein in WG, suggesting that AMPKalpha2 may not be essential for metabolic adaptations of skeletal muscles to exercise training.

Authors+Show Affiliations

Dept. of Human Physiology, Copenhagen Muscle Research Centre, Inst. of Exercise and Sport Sciences, 13-Universitetsparken, Univ. of Copenhagen, DK-2100 Copenhagen, Denmark. SBJorgensen@ifi.ku.dkNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

16954334

Citation

Jørgensen, Sebastian B., et al. "Role of AMPKalpha2 in Basal, Training-, and AICAR-induced GLUT4, Hexokinase II, and Mitochondrial Protein Expression in Mouse Muscle." American Journal of Physiology. Endocrinology and Metabolism, vol. 292, no. 1, 2007, pp. E331-9.
Jørgensen SB, Treebak JT, Viollet B, et al. Role of AMPKalpha2 in basal, training-, and AICAR-induced GLUT4, hexokinase II, and mitochondrial protein expression in mouse muscle. Am J Physiol Endocrinol Metab. 2007;292(1):E331-9.
Jørgensen, S. B., Treebak, J. T., Viollet, B., Schjerling, P., Vaulont, S., Wojtaszewski, J. F., & Richter, E. A. (2007). Role of AMPKalpha2 in basal, training-, and AICAR-induced GLUT4, hexokinase II, and mitochondrial protein expression in mouse muscle. American Journal of Physiology. Endocrinology and Metabolism, 292(1), E331-9.
Jørgensen SB, et al. Role of AMPKalpha2 in Basal, Training-, and AICAR-induced GLUT4, Hexokinase II, and Mitochondrial Protein Expression in Mouse Muscle. Am J Physiol Endocrinol Metab. 2007;292(1):E331-9. PubMed PMID: 16954334.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of AMPKalpha2 in basal, training-, and AICAR-induced GLUT4, hexokinase II, and mitochondrial protein expression in mouse muscle. AU - Jørgensen,Sebastian B, AU - Treebak,Jonas T, AU - Viollet,Benoit, AU - Schjerling,Peter, AU - Vaulont,Sophie, AU - Wojtaszewski,Jørgen F P, AU - Richter,Erik A, Y1 - 2006/09/05/ PY - 2006/9/7/pubmed PY - 2007/2/17/medline PY - 2006/9/7/entrez SP - E331 EP - 9 JF - American journal of physiology. Endocrinology and metabolism JO - Am. J. Physiol. Endocrinol. Metab. VL - 292 IS - 1 N2 - We investigated the role of AMPKalpha2in basal, exercise training-, and AICAR-induced protein expression of GLUT4, hexokinase II (HKII), mitochondrial markers, and AMPK subunits. This was conducted in red (RG) and white gastrocnemius (WG) muscle from wild-type (WT) and alpha2-knockout (KO) mice after 28 days of activity wheel running or daily AICAR injection. Additional experiments were conducted to measure acute activation of AMPK by exercise and AICAR. At basal, mitochondrial markers were reduced by approximately 20% in alpha2-KO muscles compared with WT. In both muscle types, AMPKalpha2 activity was increased in response to both stimuli, whereas AMPKalpha1 activity was increased only in response to exercise. Furthermore, AMPK signaling was estimated to be 60-70% lower in alpha2-KO compared with WT muscles. In WG, AICAR treatment increased HKII, GLUT4, cytochrome c, COX-1, and CS, and the alpha2-KO abolished the AICAR-induced increases, whereas no AICAR responses were observed in RG. Exercise training increased GLUT4, HKII, COX-1, CS, and HAD protein in WG, but the alpha2-KO did not affect training-induced increases. Furthermore, AMPKalpha1, -alpha2, -beta1, -beta2, and -gamma3 subunits were reduced in RG, but not in WG, by 30-60% in response to exercise training. In conclusion, the alpha2-KO was associated with an approximately 20% reduction in mitochondrial markers in both muscle types and abolished AICAR-induced increases in protein expression in WG. However, the alpha2-KO did not reduce training-induced increases in HKII, GLUT4, COX-1, HAD, or CS protein in WG, suggesting that AMPKalpha2 may not be essential for metabolic adaptations of skeletal muscles to exercise training. SN - 0193-1849 UR - https://www.unboundmedicine.com/medline/citation/16954334/Role_of_AMPKalpha2_in_basal_training__and_AICAR_induced_GLUT4_hexokinase_II_and_mitochondrial_protein_expression_in_mouse_muscle_ L2 - http://www.physiology.org/doi/full/10.1152/ajpendo.00243.2006?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -