| First Author | Fentz J | Year | 2015 |
| Journal | FASEB J | Volume | 29 |
| Issue | 5 | Pages | 1725-38 |
| PubMed ID | 25609422 | Mgi Jnum | J:220997 |
| Mgi Id | MGI:5637632 | Doi | 10.1096/fj.14-266650 |
| Citation | Fentz J, et al. (2015) AMPKalpha is critical for enhancing skeletal muscle fatty acid utilization during in vivo exercise in mice. FASEB J 29(5):1725-38 |
| abstractText | The importance of AMPK in regulation of fatty acid (FA) oxidation in skeletal muscle with contraction/exercise is unresolved. Using a mouse model lacking both AMPKalpha1 and -alpha2 in skeletal muscle specifically (mdKO), we hypothesized that FA utilization would be impaired in skeletal muscle. AMPKalpha mdKO mice displayed normal respiratory exchange ratio (RER) when fed chow or a high-fat diet, or with prolonged fasting. However, in vivo treadmill exercise at the same relative intensity induced a higher RER in AMPKalpha mdKO mice compared to wild-type (WT = 0.81 +/- 0.01 (sem); mdKO = 0.87 +/- 0.02 (sem); P < 0.01), indicating a decreased utilization of FA. Further, ex vivo contraction-induced FA oxidation was impaired in AMPKalpha mdKO muscle, suggesting that the increased RER during exercise originated from decreased skeletal muscle FA oxidation. A decreased muscle protein expression of CD36 (cluster of differentiation 36) and FABPpm (plasma membrane fatty acid binding protein) (by approximately 17-40%), together with fully abolished TBC1D1 (tre-2/USP6, BUB2, cdc16 domain family member 1) Ser(237) phosphorylation during contraction/exercise in AMPKalpha mdKO mice, may impair FA transport capacity and FA transport protein translocation to sarcolemma, respectively. AMPKalpha is thus required for normal FA metabolism during exercise and muscle contraction.-Fentz, J., Kjobsted, R., Birk, J. B., Jordy, A. B., Jeppesen, J., Thorsen, K., Schjerling, P., Kiens, B., Jessen, N., Viollet, B., Wojtaszewski, J. F. P. AMPKalpha is critical for enhancing skeletal muscle fatty acid utilization during in vivo exercise in mice. |
