Local effect of burn on skeletal muscle insulin responsiveness

Abstract

Basal and insulin-stimulated glucose metabolism by skeletal muscle were studied 3 days after a 3-sec scald of one hindlimb of the rat. Soleus muscles from the burned and unburned limb of the burned rats, as well as from timed controls, were incubated with [U- 14C]glucose and 0, 0.1, 1.0, or 10.0 mU insulin/ml. Basal glucose uptake by soleus muscle from the burned limb was 144% ( P < 0.001) greater than that of the controls. The glucose uptake by muscle from the unburned limb did not differ from that of controls. Insulin increased glucose uptake in control and unburned muscles but had no effect in burned muscles. Basal lactic acid release by soleus muscle from the burned limb and the contralateral unburned limb of burned rats was 123% ( P < 0.001) and 24% ( P < 0.01) higher, respectively, than that of soleus muscle from control rats. Of the lactic acid released by muscles from control rats or the unburned limb of burned rats, 35% was derived from exogenous glucose. In contrast, 50–55% of the lactic acid released by muscles from the burned limb was derived from exogenous glucose reflecting a predominant conversion of glucose to lactic acid. Insulin had no effect on the rate of lactic acid release and did not change the proportion of glucose converted to lactic acid by any of the three muscle groups. The basal rate of glucose conversion to CO 2 by muscle from the burned limb was elevated 133% ( P < 0.01) and that by muscle from the unburned limb was not altered as compared to controls. Insulin did not stimulate the conversion of glucose to CO 2 by any of the three muscle groups, and in the presence of insulin the release of CO 2 by burned, unburned, and control muscle did not differ. The basal rate of glucose incorporation into glycogen was the same in all three muscle groups. Insulin stimulated glucose incorporation into glycogen to a similar degree in muscles from control rats and the unburned limb of burned rats. However, the stimulatory effect of insulin was completely absent in soleus muscle from the burned limb. It is concluded that thermal injury suppresses the insulin-induced augmentation of glucose uptake and glucose incorporation into glycogen in skeletal muscles in the region of the burn but does not alter insulin sensitivity of skeletal muscles in the unburned region.