Rats were made diabetic by the administration of alloxan, streptozotocin or anti-insulin serum, and the capacity of kidney ribosome preparations to incorporate labeled amino acid into protein in vitro was compared for diabetic and normal rats. Kidney ribosomes from diabetic rats always incorporated markedly more amino acid into protein than normal controls. These results are in contrast to the decrease in hepatic and muscle ribosomal protein synthesis that has previously been shown to accompany experimental diabetes in the rat. When polysomes were preincubated to “strip off” endogenous messenger RNA, and artificial messenger was added, the increased protein synthetic activity of diabetic ribosomes persisted. Consequently, it is concluded that the effect of insulin deficiency to increase the incorporation of amino acid into protein by kidney ribosomes is most likely due to a post-transcriptional change in protein synthesis.