Rats were made diabetic by the administration of either alloxan or anti-insulin serum (AIS), and the capacity of hepatic polysome preparations from these animals to incorporate aniino acid into protein in an in vitro incubating system was compared to that of similar preparations from normal animals. Hepatic polysomes from rats with either form of experimental diabetes were characterized by a marked reduction in their ability to carry out in vitro protein synthesis. Prior washing with 0.5 M NH4CI accentuated the abtivity difference between normal and diabetic ribosomes, suggesting that the decrease in amino acid incorporation of diabetic ribosomes was not related to loss of “initiation” factors. In contrast, normal monosomes (polysomes stripped of natural messenger RNA) were no more active than monosomes from diabetic animals when protein synthesis was directed by polyuridylic acid, and this relationship was independent of the concentration of either polyuridylic acid or MgCI2 in the incubation medium. These results are consistent with the thesis that the decrease in hepatic ribosomal protein synthesis that results from experimental diabetes mellitus is related to a concomitant decrease in the amount or availability of messenger RNA.

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