Premium
Opposite effects of exercise and dexamethasone on skeletal muscle glucose uptake: Role of AMPK and CaMKII
Author(s) -
Amaral Sandra Lia,
Andrade Louzada Juliana Cavalcante,
Dionísio Thiago José,
Viscelli Bruno Alvares,
Dionísio Evandro José,
Bosqueiro José Roberto,
Martuscelli Aline Mio
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.806.19
Subject(s) - ampk , endocrinology , medicine , skeletal muscle , dexamethasone , insulin , glucose uptake , western blot , insulin resistance , protein kinase a , amp activated protein kinase , chemistry , phosphorylation , biochemistry , gene
Dexamethasone (Dexa) and exercise training (T) induce opposite effects in the skeletal muscle glucose uptake. This study investigated whether physical exercise is effective to attenuate the side effects induced by Dexa on insulin‐independent skeletal muscle glucose uptake. Rats underwent a training period where they were either submitted to a running protocol (8 weeks) or kept sedentary. After this T period, the animals underwent dexamethasone treatment (1 mg/kg per day, i.p. , 10 days), concomitant with training. An ipGTT was performed and the area under the glucose curve (AUC) was calculated. Western blot analysis was performed to identify AMPKα2 and CaMKII protein expression in the tibialis anterior (TA) muscle. The AUC was 39% higher for dexamethasone‐treated rats, which was attenuated by T. Dexa significantly reduced AMPKα2 (−49%) and CaMKII (−45%) protein expression in the TA muscle. On the other hand, T significantly increased about 30% both AMPKα2 and CaMKII protein expression. Training completely blocked the reduction of AMPKα2 and also inhibited by 15% the decrease of CaMKII protein expression. These results suggest that T prevented the reductions in AMPKα2 and CaMKII protein expression induced by Dexa in the skeletal muscle. Therefore T may be a good strategy to prevent Dexa‐induced peripheral insulin resistance by improving the insulin‐independent glucose uptake. Financial support: FAPESP