Hypertension is hugely underdiagnosed in apnoeic patients unknown to be hypertensive. Use of 24-h blood pressure monitoring allowed the diagnosis of twice as much hypertension than did clinical measurement. Even at the beginning of their history of hypertension, apnoeic patients exhibited chronic adaptations of their cardiovascular system, as shown by early changes in baroreflex sensitivity and an increased prevalence of left ventricular hypertrophy.

Recently there has been growing interest in the effects of antioxidants on insulin activity. In the present study, we investigated the effect of metformin on free radical activity and insulin sensitivity in high fructose-fed rats, a diet that leads to insulin resistance. The animals were divided into four groups (n = 16 per group; experiment duration = 6 weeks): the control (C) group received a standard diet; the control metformin (CM) group was fed a control diet and received metformin (200 mg x kg(-1) x day(-1) in water); the fructose control (FT) group was fed a diet in which fructose composed 56.8% of the total carbohydrates; and the fructose metformin (FM) group received high-fructose diet and metformin (200 mg x kg(-1) x day(-1) in water). The glucose clamp technique was used to determine insulin sensitivity in eight animals per group. Metabolic and oxidative stress parameters were measured in the remaining rats. In the FT rats, insulin resistance, lower red cell CuZn superoxide dismutase activity and lower blood reduced glutathione were observed. Metformin treatment improved both the insulin activity and the antioxidant defense system. In the CM group, metformin had no effect on metabolic parameters, but improved red cell antioxidant enzyme activities and the blood GSH level, which suggests that it has an antioxidant activity independent of its effect on insulin activity.

The purpose of this study was to investigate the effects of vitamin E in rats fed a high fructose diet which leads to insulin resistance, on some components of the free radical defense system and on insulin sensitivity. The rats (postweaning, 50 g) were divided into three groups: the control group (C, n = 16), which received a purified diet containing 60 g/100 g carbohydrates, the high fructose-fed group (FT, n = 16),fed a diet in which 56.8% of the carbohydrate as fructose, and a high fructose and vitamin E-fed group (FVE, n = 16), fed the FT diet supplemented with 3.4 g vitamin E/kg diet (vs. 0.17 g/kg in C and FT groups). The duration of the treatment was 6 wk. Insulin sensitivity was determined in half of the rats in each group using the euglycemic hyperinsulinic glucose clamp technique. The remaining rats were investigated for plasma glucose, insulin, triglyceride and fructosamine concentrations and for components of the free radical defense system. The FT group had a significantly lower insulin sensitivity than the C group. Basal glycemia was not different among the groups. In comparison with the C group, the FT group had a greater lipid peroxidation, as indicated by the higher concentrations of plasma thiobarbituric acid reactive substances (TBARS) and blood disulfide glutathione (GSSG) and the lower Cu-Zn superoxide dismutase (Cu-Zn SOD) activity. These markers approached the values of the controls after addition of vitamin E. Moreover, the FVE group had a higher insulin sensitivity than the FT group, but it remained lower than in the C group. These results show that a high fructose diet in rats leads to insulin resistance and a defect in the free radical defense system. Vitamin E supplementation improves insulin sensitivity in fructose-fed rats.

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