Decreased turnover of soluble liver proteins in mice with alloxan-induced diabetes.

Mice with alloxan-induced diabetes were used as a model to assess whether the synthesis and/or degradation of soluble liver proteins in general is affected in vivo by the diabetic state. Protein turnover was measured 2-3 wk after diabetes was induced. Degradation of liver cytosol proteins was decreased in diabetic mice as measured by the loss of protein radiolabeled with [14C]bicarbonate. The incorporation of radiolabeled amino acids into protein was also decreased in diabetic mice. When [3H]leucine was administered as the precursor for protein synthesis, the radiospecific activity of leucine derived from leucyl-tRNA in livers was similar in control and diabetic mice. Thus, the rate of protein synthesis appears to be decreased. There was no indication that diabetes affected the turnover of long- or short-lived proteins differentially. The activities of several cellular proteinases were unaffected or slightly decreased in livers of diabetic mice. These data indicate that protein turnover is decreased in this chronic form of diabetes.