This study suggests that transferred or cocultured MSs from mld-SZ mice exert a functional immune aggression against beta cells at a very early stage, before donor mice develop impaired insulin secretion and hyperglycemia.

The hypoglycemic salicylate action has been related to an increased insulin secretion (Micossi, Pontiroli, Baron, Tamayo, Lengel, Bevilacqua, Raggi, Norbiato and Foa 1978). In this report we describe the effects of salicylate on the dynamics of glucose-induced insulin secretion, in the isolated perfused rat pancreas. Material and MethodsMale Wistar rats, weighing 200-300 g, were used, and in all cases were fasted overnight prior to each perfusion. Sodium salicylate 50 mg/100 g of body weight was injected subcutaneously, 90 min.

The influence of high blood sugar levels on lipid metabolism and urea production in the "diabetic liver" (DL) have been studied in isolated rat liver perfusion. For comparativc purposes DL were pcrfused with norm

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We studied the effect of the ionophere A 23187 and of phosphodiesterase inhibitors and activators (Theophylline, Pentoxiphylline and Imidazol) on insulin secretion and on the pool of free tubulin in rat pancreas in the presence of somatostatin and diazoxide. The results suggest that: 1. The inhibitory effect of somatostatin on insulin secretion does not seem to be related mainly to an inhibition of cAMP production. The decrease in calcium translocation induced by somatostatin could inhibit the cAMP participation in the mechanism of hormonal secretion. 2. Somatostatin seems to inhibit the movement of calcium towards the cytoplasm from outside and from within the cell. Diazoxide seems to inhibit only the entrance of calcium from outside the cell but does not seem to inhibit the entrance determined by theophylline and pentoxiphylline from intracellular compartments. 3. Arginine glucose stimulation in the presence of A 23187induced calcium translocation is able to determine insulin secretion although cAMP degradation is increased by imidazol. 4. Somatostatin and diazoxide inhibit pancreatic tubulin polymerization; however, the effect seem to be indirect and related to the inhibition of calcium translocation determined by both substances.