Cell-derived microparticles are supposed to be involved in endothelial dysfunction and atherogenesis. This study aimed to evaluate circulating microparticles in diabetic subjects with erectile dysfunction (ED) and their relation with endothelial dysfunction. Thirty diabetic men with ED and 20 age-matched control subjects without ED were assessed for circulating microparticles and endothelial dysfunction. Flow cytometry was used to assess microparticles by quantification of circulating endothelial (EMP, CD31 þ /CD42b À ) and platelet (PMP, CD31 þ /CD42b þ ) microparticles in peripheral blood. Endothelium-dependent flow-mediated dilation (FMD) was evaluated in the right brachial artery after reactive hyperemia. Compared with non-diabetic subjects, diabetic men presented significantly higher numbers of EMP (P ¼ 0.001), and reduced FMD (P ¼ 0.01), with a significant inverse correlation between the number of circulating EMP and the International Index of Erectile Function (IIEF) score (r ¼ À0.457, P ¼ 0.01). Multivariate analysis correcting for age, anthropometric indices, glucose and lipid parameters, FMD and PMP identified EMP as the only independent predictor for IIEF score (P ¼ 0.03). EMP are elevated in impotent diabetic subjects and independently involved in the pathogenesis of ED.

Summary. In 14 normal subjects, treatment with acetylsalicylic acid (ASA, 3.2 g daily for 3 days) a well known inhibitor of prostaglandin synthesis, caused a slight but significant decrease (p < 0.05) in basal plasma glucose levels; by contrast, basal insulin rose from 5 _+1 to 8 +1 ~tU/ml (p < 0.01) after ASA. Pretreatment with ASA augmented the early insulin response to a standard IV glucose tolerance test (25 g) in 7 normal subjects (p<0.05 at 2 min; p < 0.02 at 5 min; p < 0.01 at 10 min). No significant changes were detected in the rate of glucose utilization. 7 additional subjects received a standard arginine test without and with ASA pretreatment. Arginine stimulated insulin levels were increased after ASA (p<0.01 at 15 min; p<0.05 at 30 min; p < 0.05 at 45 rain), whereas glucose values were lower than under basal conditions at all times, with significant differences at 105 (p<0.02) and 120 (p <0.05) min. A possible role of prostaglandins upon the insulin responses to glucose and arginine is discussed.

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In this study we evaluated the influence of changes in serum calcium concentration upon somatostatin-mediated inhibition of insulin secretion in man. For this purpose, we investigated the effect of somatostatin in a group of subjects with hypoparathyroidism before and after correction of hypocalcemia and in normal subjects made hypercalcemic by exogenous calcium administration. In the presence of hypocalcemia, somatostatin caused an almost total inhibition of glucose-induced insulin secretion. In addition, somatostatin significantly decreased glucose tolerance in those hypocalcemic patients who exhibited normal tolerance under basal conditions [glucose utilization (kG), 1.44 +/- 0.13 before vs. 0.68 +/- 0.14 during somatostatin; P < 0.02]. Glucose tolerance was unaltered in those subjects who had a decreased glucose tolerance under basal conditions (kG, 1.01 +/- 0.1 before vs. 0.88 +/- 0.16 during somatostatin; P = NS). Under normocalcemic conditions, the insulin response to glucose and glucose tolerance were significantly greater than values measured during hypocalcemia. However, somatostatin blunted the insulin response to glucose and significantly decreased glucose utilization. These inhibitory effects of somatostatin upon insulin secretion and glucose tolerance were not reversed by a concurrent infusion of calcium (serum calcium, 6.9 +/- 0.3 meq/liter) in a group of normal subjects. Our data confirm the reduced insulin secretion and glucose tolerance in hypoparathyroidism and demonstrate that the suppressive effect of somatostatin upon glucose-stimulated insulin secretion is independent of changes in serum calcium concentration over a wide range.

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