Effect of AMPK activation on mechanisms responsible for exercise-induced expression of monocarboxylate transporter

本研究的目的是验证一种假说，即信号分子AMPK会介导急性运动诱导的骨骼肌单羧酸转运蛋白MCT1和MCT4的表达。雄性SD大鼠进行一次高强度间歇游泳(HIS)或低强度长时间游泳运动(LIS)。运动肌肉中AMPK磷酸化水平随Lis和His的升高而增加。His和Lis瞬时上调MCT1和MCT4基因的表达。LIS后MCT1蛋白表达增加，HIS后MCT4蛋白表达增加，而MCT1蛋白表达无明显变化。0.5 mM 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside(AICAR)或1 mM咖啡因直接暴露于Eporochlearis可增加MCT1和MCT4mRNA的表达，但不增加MCT1和MCT4的蛋白表达。丹曲林可抑制1 mM咖啡因诱导的pAMPK，但对MCT1和MCT4的表达无明显影响。提示急性运动可通过调节骨骼肌MCT1和MCT4的表达途径上调MCT1和MCT4的表达。

The purpose of this study was to examine the hypothesis that signaling molecules AMPKwould mediate the acute exercise-induced expression of monocarboxylate transporters MCT1and MCT4 in skeletal muscle. The male SD rats were subjected to a bout of high-intensityintermittent swimming (HIS) or low-intensity prolonged swimming exercise (LIS). AMPKphosphorylation was increased in response to LIS and HIS in exercised muscle. MCT1 andMCT4 mRNA were transiently upregulated by HIS and LIS. MCT1 protein was increased afterLIS, but MCT4 protein was increased after HIS, while no changes in MCT1 protein wereobserved. Direct exposure of epitrochlearis to 0.5mM 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR) or 1mM caffeine increased both MCT1 and MCT4 mRNA but notMCT1 and MCT4 protein. When 1mM caffeine-induced pAMPK was inhibited by dantrolene,neither MCT1 nor MCT4 mRNA was increased. The present findings suggest that acute exercisemay upregulate MCT1 and MCT4 mRNA expression thrg-mediated pathway in skeletalmuscle.