Abstract
The insulin sensitivity of protein synthesis and glucose incorporation into glycogen by the soleus and epitrochlearis muscles from fed rats and 24 h-starved rats was determined in vitro during the 1st and 2nd h of incubation after isolation of incubation were 2-fold higher than in the 2nd h and were not increased by insulin. Rates of protein synthesis during the 1st h in the presence of 6000 .mu. units of insulin/ml were increased in soleus, but not in epitrochlearis muscles from starved rats. Rates of protein synthesis in both muscles from fed and starved rats were increased significantly by insulin during the 2nd h. High concentrations of insulin caused a marked stimulation of the rates of glucose incorporation by both muscles from fed and starved rats in both the 1st and 2nd h of incubation. The insulin sensitivity of glucose incorporation during the 2nd h, defined as the concentration of insulin causing half-maximal stimulation, was increased 10-fold for both muscle types from starved rats (soleus, 65 .mu.units/ml; epitrochlearis, 45 .mu.units/ml) relative to muscles from fed rats (soleus, 600 .mu.units/ml; epitrochlearis, 500 .mu.units/ml). The insulin sensitivity of protein synthesis in the 2nd was greater for soleus muscles from starved rats (65 .mu.units/ml) than from fed rats (500 .mu.units/ml). In contrast, the insulin sensitivity of protein synthesis in epitrochlearis muscles from starved rats was significantly decreased (225 .mu.units/ml) compared with fed rats (25 .mu.units/ml). Maximal rates achieved by high concentrations of insulin were not different from those in the same muscle from fed rats. Protein synthesis, in distinction to glucose utilization, may be resistant to insulin stimulation during periods of acute starvation in muscles with fiber compositions similar to the epitrochlearis, but not in muscles with fiber compositions similar to the soleus. Partial reversal of the resistance observed in vitro for epitrochlearis muscles from starved rats may be due to the loss of factors which suppress the effect of insulin in vivo.