Increased phosphorylation of Akt substrate of 160 kDa (AS160) is essential to trigger the full increase in insulin-stimulated glucose transport in skeletal muscle. The primary aim of this study was to characterize the time course for reversal of insulin-stimulated AS160 phosphorylation in rat skeletal muscle after insulin removal. The time courses for reversal of insulin effects both upstream (Akt phosphorylation) and downstream (glucose uptake) of AS160 were also determined. Epitrochlearis muscles were incubated in vitro using three protocols which differed with regard to insulin exposure: No Insulin (never exposed to insulin), Transient Insulin (30 min with 1.8 nmol/l insulin, then incubation without insulin for 10, 20 or 40 min), or Sustained Insulin (continuously incubated with 1.8 nmol/l insulin). After removal of muscles from insulin, Akt and AS160 phosphorylation reversed rapidly, each with a half-time of <10 min and essentially full reversal by 20 min. Glucose uptake reversed more slowly (half time between 10 and 20 min with essentially full reversal by 40 min). Removal of muscles from insulin resulted in a rapid reversal of the increase in AS160 phosphorylation which preceded the reversal of the increase in glucose uptake, consistent with AS160 phosphorylation being essential for maintenance of insulin-stimulated glucose uptake., N. Sharma, E. B. Arias, G. D. Cartee., and Obsahuje bibliografii a bibliografické odkazy
Bradykinin can enhance skeletal muscle glucose uptake (GU), and exercise increases both br adykinin production and muscle insulin sensitivity, but bradykinin’s relationship with post-exercise insulin action is uncertain. Our primary aim was to determine if the B2 receptor of bradykinin (B2R) is essential for the post- exercise increase in GU by insulin-stimulated mouse soleus muscles. Wildtype (WT) and B2 R knockout (B2RKO) mice were sedentary or performed 60 minutes of treadmill exercise. Isolated soleus muscles were incubated with [ 3 H]-2-deoxyglucose ±insulin (60 or 100 μ U/ml). GU tended to be greater for WT vs. B2RKO soleus with 60 μ U/ml insulin (P=0.166) and was significantly greater for muscles with 100 μ U/ml insulin (P<0.05). Both genotypes had significant exercise-induced reductions (P<0.05) in glycemia and insulinemia, and the decrements for glucose (~14 %) and insulin (~55 %) were similar between genotypes. GU tended to be greater for exercised vs. sedentary soleus with 60 μ U/ml insulin (P=0.063) and wa s significantly greater for muscles with 100 μ U/ml insulin (P<0.05). There were no significant interactions between genotype and exercise for blood glucose, plasma insulin or GU. These results indicate that the B2R is not essential for the exerci se-induced decrements in blood glucose or plasma insulin or for the post-exercise increase in GU by insulin-stimulated mouse soleus muscle., G. G. Schweitzer ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy