AMPK-α2 is involved in exercise training-induced adaptations in insulin-stimulated metabolism in skeletal muscle following high-fat diet.

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: Marcia J Abbott, Lorraine P Turcotte
• Journal: Journal of applied physiology (Bethesda, Md. : 1985) (J Appl Physiol (1985)) Vol. 117 Issue 8 Pg. 869-79 (Oct 15 2014) ISSN: 1522-1601 [Electronic] United States
• PMID: 25103967 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2014 the American Physiological Society.

Chemical References

• Blood Glucose
• CD36 Antigens
• Insulin
• Palmitates
• Carnitine O-Palmitoyltransferase
• Citrate (si)-Synthase
• Mitogen-Activated Protein Kinase 9
• AMPK alpha2 subunit, mouse
• Mitogen-Activated Protein Kinase 8
• AMP-Activated Protein Kinases

Topics

• AMP-Activated Protein Kinases (metabolism)
• Adaptation, Physiological (physiology)
• Animals
• Blood Glucose (metabolism, physiology)
• CD36 Antigens (metabolism)
• Carnitine O-Palmitoyltransferase (metabolism)
• Citrate (si)-Synthase (metabolism)
• Diet, High-Fat (methods)
• Hindlimb (metabolism, physiology)
• Insulin (metabolism)
• Insulin Resistance (physiology)
• MAP Kinase Signaling System (physiology)
• Male
• Mice
• Mice, Inbred C57BL
• Mitogen-Activated Protein Kinase 8 (metabolism)
• Mitogen-Activated Protein Kinase 9 (metabolism)
• Muscle, Skeletal (metabolism, physiology)
• Obesity (metabolism, pathology)
• Oxidation-Reduction
• Palmitates (metabolism)
• Phosphorylation (physiology)
• Physical Conditioning, Animal (physiology)