In order to investigate whether the hyperaggregability of platelets in diabetic and starved rats was due to an increase in the inherent capability of these platelets to synthesize thromboxane A2, we assessed the total thromboxane A2 synthesizing capacity of platelets in rats with streptozotocin-induced diabetes and rats which have been semistarved (nine days) or fasted for various periods (24-72 h). Fasting for 48 h or more and semistarvation resulted in highly significant increases in thromboxane A2 synthesizing capacity. Experimental diabetes, however, resulted in a marked diminution in thromboxane A2 synthesizing capacity. This decrease in thromboxane A2 synthesizing capacity was prevented in diabetic rats treated with insulin. We conclude that while the hyperaggregability of starvation is associated with an increase in thromboxane A2 synthesizing capacity, that of diabetes is associated with a fall in this capacity. The decrease of this capacity in diabetic animals can be prevented by insulin treatment. Total thromboxane A2 synthesizing capacity is therefore not a major determinant of either platelet hyperaggregability or of agonist induced platelet thromboxane A2 release.