Inhibition of contraction-, hypoxia-, and AICAR-stimulated, but not insulin-stimulated, muscle glucose transport by araA
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We used araA to evaluate the hypothesis that AMPK activation is involved in the stimulation of muscle glucose transport by contractions and hypoxia. After 1 week of adaptation period to the laboratory environment, 65 male Wistar rats were fasted for 12 hr. Rats were anesthetized and the epitrochlearis muscles were removed to measure glucose transport rate in muscle. To evaluate the rate of contraction (tetanic, 100Hz-10s, 10min), hypoxia (95% N2, 5% CO2, 80min), AICAR (2mM, 60min), insulin (2mU/ml, 60min) stimulated glucose transport activity after araA treat, we use 5 processing steps (Recovery, preincubation, stimulation, rinse, incubation). After rinse, muscles were incubated with two tracer (14C-mannitol, 3H-3-o-methylglucose) for 10 min, and radioactivity was measured with scintillation counter. Preincubation of muscles with 2 mM araA inhibited the stimulation of glucose transport induced by AICAR, contractions, or hypoxia by ~65%. Insulin-stimulated muscle glucose transport was not inhibited by araA. These findings provide support for the hypothesis that activation of AMPK is involved in the stimulation of muscle glucose transport by contractions and hypoxia. They clearly show that it is possible to inhibit the stimulation of glucose transport by contractions and hypoxia without affecting insulin-stimulated glucose transport in skeletal muscle.
Abstract
We used araA to evaluate the hypothesis that AMPK activation is involved in the stimulation of muscle glucose transport by contractions and hypoxia. After 1 week of adaptation period to the laboratory environment, 65 male Wistar rats were fasted for 12 hr. Rats were anesthetized and the epitrochlearis muscles were removed to measure glucose transport rate in muscle. To evaluate the rate of contraction (tetanic, 100Hz-10s, 10min), hypoxia (95% N2, 5% CO2, 80min), AICAR (2mM, 60min), insulin (2mU/ml, 60min) stimulated glucose transport activity after araA treat, we use 5 processing steps (Recovery, preincubation, stimulation, rinse, incubation). After rinse, muscles were incubated with two tracer (14C-mannitol, 3H-3-o-methylglucose) for 10 min, and radioactivity was measured with scintillation counter. Preincubation of muscles with 2 mM araA inhibited the stimulation of glucose transport induced by AICAR, contractions, or hypoxia by ~65%. Insulin-stimulated muscle glucose transport was not inhibited by araA. These findings provide support for the hypothesis that activation of AMPK is involved in the stimulation of muscle glucose transport by contractions and hypoxia. They clearly show that it is possible to inhibit the stimulation of glucose transport by contractions and hypoxia without affecting insulin-stimulated glucose transport in skeletal muscle.
참고문헌 (25)
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