Our data suggest that mild to moderate elevations of plasma homocysteine levels in healthy subjects activate coagulation, modify the adhesive properties of endothelium, and impair the vascular responses to L-arginine. Pretreatment with antioxidant vitamin E and ascorbic acid blocks the effects of hyperhomocysteinemia, suggesting an oxidative mechanism.

Erectile dysfunction (ED) is a common complication and an important cause of decreased quality of life in men with diabetes. These patients present a risk of ED three-fold higher than the general population; the prevalence of ED increases with age, but in diabetic men it can occur 10 to 15 years earlier regardless of their insulin dependency status [1].The causes of ED in diabetic patients can be multifactorial, involving mainly vascular, neurological and Diabetologia (2001) AbstractAims/hypothesis. The aim of this study was to evaluate the relation between erectile dysfunction and endothelial functions, coagulation activation, peripheral and autonomic neuropathy in men with Type II (non-insulin-dependent) diabetes mellitus. Methods. We studied 30 Type II diabetic patients with symptomatic erectile dysfunction and 30 potent diabetic patients matched for age and disease. Endothelial functions were assessed with the l-arginine test, plasma thrombomodulin and cell adhesion molecules circulating concentrations. Haemostasis was evaluated with markers of thrombin activation and fibrinolysis. Quantitative sensory testing (vibratory, warming, and heat-pain thresholds), cardiovascular reflex tests and 24-h blood pressure monitoring were used to assess peripheral or autonomic neuropathy. Results. Mean erectile score and HbA 1 c were 10.5 5.8 and 8.3 1.6 % in patients with erectile dysfunction, and 24.0 0.7 and 6.8 1.4 % in those without erectile dysfunction, respectively (p < 0.001); there was a significant relation between HbA 1 c and erectile function score in patients with erectile dysfunction (r = ±0.45, p = 0.02). The decrease in blood pressure and platelet aggregation in response to l-arginine was lower (p < 0.05±0.02) in patients with erectile dysfunction, whereas soluble thrombomodulin, P-selectin and intercellular cell ahhesion molecule-1 concentrations were higher (p < 0.05±0.02). Indices of coagulation activation (F1 + 2 and d-dimers) and reduced fibrinolysis (PAI-1) were also found to be higher in erectile dysfunction patients. Heat-pain and warm perception thresholds, as well as cardiovascular reflex tests, were most commonly abnormal in patients with erectile dysfunction (p < 0.05). In multivariate analysis, HbA 1 c , MBP response to l-arginine, P-selectin, indices of coagulation, and quantitative sensory testing were independent predictors of erectile function score. Conclusion/interpretation. Erectile dysfunction in diabetic men correlates with endothelial dysfunction. A reduced nitric oxide activity might provide a unifying explanation. [Diabetologia (2001

Low-to-high frequency ratio (LF/HF) is an indirect index of sympathovagal balance derived by heart rate spectral analysis. We investigated the effect of glucose ingestion on LF/HF in 17 healthy, normotensive young subjects (9 male, 8 female) with a wide body fat content range (body fat = 29 +/- 5.9%; range = 19-42%) and a normal thyroid hormone status. Before and after an oral glucose tolerance test (OGTT), the Holter technique and indirect calorimetry allowed us to determine heart rate and substrate oxidation in all subjects. At baseline, LF/HF correlated with body fat (r = 0.60, P < 0.005), waist-to-hip ratio (r = 0.57, P < 0.01), fasting plasma insulin (r = 0.55, P < 0.04), leptin (r = 0.56, P < 0.01), and norepinephrine (r = 0.58, P < 0.009) concentrations. Age-, body fat-, content-, and fat-free mass-adjusted respiratory quotient (r = 0.59, P < 0.007) and basal metabolic rate (r = 0.61, P < 0.001) were also correlated with basal LF/HF. Along with OGTT plasma glucose, insulin and norepinephrine concentrations and basal LF/HF significantly rose at 60 min and then declined throughout the test. Area under the curve (AUC) for LF/HF correlated with body fat (r = -0.66, P < 0.004), fasting plasma leptin concentration (r = -0.57, P < 0.01), glucose induced thermogenesis (r = 0.62, P < 0.001), glucose uptake (r = 0.59, P < 0.007), and AUC for plasma norepinephrine concentration (r = 0.63, P < 0.001). Water instead of glucose ingestion does not significantly affect LF/HF (n = 8). In conclusion, our study supports the hypothesis that glucose ingestion affects LF/HF and that such change is related to the amount of body fat.

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