Fasting and diabetes mellitus elicit opposite effects on agonist-stimulated prostacyclin synthesis by the rat aorta

The effects of prolonged fasting and experimental nonketonuric diabetes on rat aortic prostacyclin (PGI₂) synthesis were compared. Whereas fasting (for 48 hours or longer) resulted in a marked increase in trauma-, adrenaline-, and U46619-stimulated aortic PGI₂ synthesis, prolonged experimental (streptozotocin-induced) nonketonuric diabetes caused a marked decrease in aortic PGI₂ synthesis stimulated by the above agonists. Arachidonic acid (AA)-stimulated aortic PGI₂ synthesis in fasted and diabetic rats, however, was not different from that in controls. The reduction in adrenaline- and U46619-stimulated, but not AA-induced, PGI₂ synthesis in the diabetic rat suggests that the diminished production of PGI₂ in diabetes may be due to diminished phospholipase A₂ (or of the phospholipase C-diglyceride lipase system) activity, diminished AA stores, or both. The opposite effects of prolonged fasting and diabetes on aortic PGI₂ synthesis suggest that caution should be exercised when comparing the metabolic consequences of starvation with those of diabetes.