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AMPK-α2 is involved in exercise training-induced adaptations in insulin-stimulated metabolism in skeletal muscle following high-fat diet.
J Appl Physiol (1985) 2014; 117(8):869-79JA

Abstract

AMP-activated protein kinase (AMPK) has been studied extensively and postulated to be a target for the treatment and/or prevention of metabolic disorders such as insulin resistance. Exercise training has been deemed a beneficial treatment for obesity and insulin resistance. Furthermore, exercise is a feasible method to combat high-fat diet (HFD)-induced alterations in insulin sensitivity. The purpose of this study was to determine whether AMPK-α2 activity is required to gain beneficial effects of exercise training with high-fat feeding. Wild-type (WT) and AMPK-α2 dominant-negative (DN) male mice were fed standard diet (SD), underwent voluntary wheel running (TR), fed HFD, or trained with HFD (TR + HFD). By week 6, TR, irrespective of genotype, decreased blood glucose and increased citrate synthase activity in both diet groups and decreased insulin levels in HFD groups. Hindlimb perfusions were performed, and, in WT mice with SD, TR increased insulin-mediated palmitate uptake (76.7%) and oxidation (>2-fold). These training-induced changes were not observed in the DN mice. With HFD, TR decreased palmitate oxidation (61-64%) in both WT and DN and increased palmitate uptake (112%) in the WT with no effects on palmitate uptake in the DN. With SD, TR increased ERK1/2 and JNK1/2 phosphorylation, regardless of genotype. With HFD, TR reduced JNK1/2 phosphorylation, regardless of genotype, carnitine palmitoyltransferase 1 expression in WT, and CD36 expression in both DN and WT. These data suggest that low AMPK-α2 signaling disrupts, in part, the exercise training-induced adaptations in insulin-stimulated metabolism in skeletal muscle following HFD.

Authors+Show Affiliations

Department of Biological Sciences, Human and Evolutionary Biology Section, Dana and David Dornsife College of Arts, Letters, and Sciences, University of Southern California, Los Angeles, California; and Crean College of Health and Behavioral Sciences, Chapman University, Orange, California.Department of Biological Sciences, Human and Evolutionary Biology Section, Dana and David Dornsife College of Arts, Letters, and Sciences, University of Southern California, Los Angeles, California; and turcotte@usc.edu.

Pub Type(s)

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

Language

eng

PubMed ID

25103967

Citation

Abbott, Marcia J., and Lorraine P. Turcotte. "AMPK-α2 Is Involved in Exercise Training-induced Adaptations in Insulin-stimulated Metabolism in Skeletal Muscle Following High-fat Diet." Journal of Applied Physiology (Bethesda, Md. : 1985), vol. 117, no. 8, 2014, pp. 869-79.
Abbott MJ, Turcotte LP. AMPK-α2 is involved in exercise training-induced adaptations in insulin-stimulated metabolism in skeletal muscle following high-fat diet. J Appl Physiol. 2014;117(8):869-79.
Abbott, M. J., & Turcotte, L. P. (2014). AMPK-α2 is involved in exercise training-induced adaptations in insulin-stimulated metabolism in skeletal muscle following high-fat diet. Journal of Applied Physiology (Bethesda, Md. : 1985), 117(8), pp. 869-79. doi:10.1152/japplphysiol.01380.2013.
Abbott MJ, Turcotte LP. AMPK-α2 Is Involved in Exercise Training-induced Adaptations in Insulin-stimulated Metabolism in Skeletal Muscle Following High-fat Diet. J Appl Physiol. 2014 Oct 15;117(8):869-79. PubMed PMID: 25103967.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - AMPK-α2 is involved in exercise training-induced adaptations in insulin-stimulated metabolism in skeletal muscle following high-fat diet. AU - Abbott,Marcia J, AU - Turcotte,Lorraine P, Y1 - 2014/08/07/ PY - 2014/8/9/entrez PY - 2014/8/12/pubmed PY - 2015/10/31/medline KW - AMPK KW - exercise training KW - fatty acid metabolism KW - glucose uptake KW - insulin resistance SP - 869 EP - 79 JF - Journal of applied physiology (Bethesda, Md. : 1985) JO - J. Appl. Physiol. VL - 117 IS - 8 N2 - AMP-activated protein kinase (AMPK) has been studied extensively and postulated to be a target for the treatment and/or prevention of metabolic disorders such as insulin resistance. Exercise training has been deemed a beneficial treatment for obesity and insulin resistance. Furthermore, exercise is a feasible method to combat high-fat diet (HFD)-induced alterations in insulin sensitivity. The purpose of this study was to determine whether AMPK-α2 activity is required to gain beneficial effects of exercise training with high-fat feeding. Wild-type (WT) and AMPK-α2 dominant-negative (DN) male mice were fed standard diet (SD), underwent voluntary wheel running (TR), fed HFD, or trained with HFD (TR + HFD). By week 6, TR, irrespective of genotype, decreased blood glucose and increased citrate synthase activity in both diet groups and decreased insulin levels in HFD groups. Hindlimb perfusions were performed, and, in WT mice with SD, TR increased insulin-mediated palmitate uptake (76.7%) and oxidation (>2-fold). These training-induced changes were not observed in the DN mice. With HFD, TR decreased palmitate oxidation (61-64%) in both WT and DN and increased palmitate uptake (112%) in the WT with no effects on palmitate uptake in the DN. With SD, TR increased ERK1/2 and JNK1/2 phosphorylation, regardless of genotype. With HFD, TR reduced JNK1/2 phosphorylation, regardless of genotype, carnitine palmitoyltransferase 1 expression in WT, and CD36 expression in both DN and WT. These data suggest that low AMPK-α2 signaling disrupts, in part, the exercise training-induced adaptations in insulin-stimulated metabolism in skeletal muscle following HFD. SN - 1522-1601 UR - https://www.unboundmedicine.com/medline/citation/25103967/AMPK_α2_is_involved_in_exercise_training_induced_adaptations_in_insulin_stimulated_metabolism_in_skeletal_muscle_following_high_fat_diet_ L2 - http://www.physiology.org/doi/full/10.1152/japplphysiol.01380.2013?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -