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- Fujii, N., et al.
(författare)
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Exercise induces isoform-specific increase in 5'AMP-activated protein kinase activity in human skeletal muscle
- 2000
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Ingår i: Biochemical and Biophysical Research Communications - BBRC. - San Diego, CA, USA : Academic Press. - 0006-291X .- 1090-2104. ; 273:3, s. 1150-1155
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Tidskriftsartikel (refereegranskat)abstract
- The 5'AMP-activated protein kinase (AMPK) is stimulated by contractile activity in rat skeletal muscle. AMPK has emerged as an important signaling intermediary in the regulation of cell metabolism being linked to exercise-induced changes in muscle glucose and fatty acid metabolism. In the present study, we determined the effects of exercise on isoform-specific AMPK activity (alpha1 and alpha2) in human skeletal muscle. Needle biopsies of vastus lateralis muscle were obtained from seven healthy subjects at rest, after 20 and 60 min of cycle ergometer exercise at 70% of VO(2)max, and 30 min following the 60 min exercise bout. In comparison to the resting state, AMPK alpha2 activity significantly increased at 20 and 60 min of exercise, and remained at a higher level with 30 min of recovery. AMPK alpha1 activity tended to slightly decrease with 20 min of exercise at 70%VO(2)max; however, the change was not statistically significant. AMPK alpha1 activities were at basal levels at 60 min of exercise and 30 min of recovery. On a separate day, the same subjects exercised for 20 min at 50% of VO(2)max. Exercise at this intensity did not change alpha2 activity, and similar to exercise at 70% of VO(2)max, there was no significant change in alpha1 activity. In conclusion, exercise at a higher intensity for only 20 min leads to increases in AMPK alpha2 activity but not alpha1 activity. These results suggest that the alpha2-containing AMPK complex, rather than alpha1, may be involved in the metabolic responses to exercise in human skeletal muscle.
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| 2. |
- Musi, N., et al.
(författare)
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AMP-activated protein kinase (AMPK) is activated in muscle of subjects with type 2 diabetes during exercise
- 2001
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Ingår i: Diabetes. - Alexandria, VA, USA : American Diabetes Association Inc.. - 0012-1797 .- 1939-327X. ; 50:5, s. 921-927
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Tidskriftsartikel (refereegranskat)abstract
- Insulin-stimulated GLUT4 translocation is impaired in people with type 2 diabetes. In contrast, exercise results in a normal increase in GLUT4 translocation and glucose uptake in these patients. Several groups have recently hypothesized that exercise increases glucose uptake via an insulin-independent mechanism mediated by the activation of AMP-activated protein kinase (AMPK). If this hypothesis is correct, people with type 2 diabetes should have normal AMPK activation in response to exercise. Seven subjects with type 2 diabetes and eight matched control subjects exercised on a cycle ergometer for 45 min at 70% of maximum workload. Biopsies of vastus lateralis muscle were taken before exercise, after 20 and 45 min of exercise, and at 30 min postexercise. Blood glucose concentrations decreased from 7.6 to 4.77 mmol/l with 45 min of exercise in the diabetic group and did not change in the control group. Exercise significantly increased AMPK α2 activity 2.7-fold over basal at 20 min in both groups and remained elevated throughout the protocol, but there was no effect of exercise on AMPK α1 activity. Subjects with type 2 diabetes had similar protein expression of AMPK α1, α2, and β1 in muscle compared with control subjects. AMPK α2 was shown to represent approximately two-thirds of the total a mRNA in the muscle from both groups. In conclusion, people with type 2 diabetes have normal exercise-induced AMPK α2 activity and normal expression of the α1, α2 and β1 isoforms. Pharmacological activation of AMPK may be an attractive target for the treatment of type 2 diabetes.
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