It is well known that there is a large increase in protein catabolism and in the elimination of the urea nitrogen in diabetes. However, the molecular mechanisms of these increases, particularly in urea synthesis, are not known. We have, therefore, tried to clarify this by studying the levels of a number of enzymes and intermediates connected to the urea cycle and especially of those that affect the initial step, i.e., carbamylphosphate synthesis. As model we used the experimental production of diabetes in rats using streptozotocin, which simulates juvenile diabetes leading to an almost total absence of insulin.