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Presents a study that examined the use of an animal model of glucocorticoid-induced hypertension in rats in studying insulin resistance in the metabolic syndrome. Analysis of changes in blood glucose; Examination of the histological patterns of hepatocytes; Effect of the metformin drug on the insulin sensibility of rats.

Background Experimental evidence indicates that statins might have direct vascular effects independently from low-density lipoprotein (LDL) cholesterol reduction and we reported that the reduction in urinary albumin excretion rate during Simvastatin treatment in type 2 diabetic patients was not correlated with LDL-cholesterol decrease. However in humans there are no data regarding possible additional effects of Simvastatin on blood pressure and urinary albumin excretion beyond its capacity to lower serum cholesterol. Patients and methods Twenty-six microalbuminuric hypertensive type 2 diabetic patients (diastolic blood pressure — after four months wash-out from the previous antihypertensive therapy — consistently > 90 and < 100 mmHg; plasma LDL-cholesterol > 3.9 and < 6.5 mmol L-1) were enrolled in the study. In random order, these patients received Simvastatin (20 mg day-1) or Cholestyramine (6 g three times a day) for a period of 10 months and after three months of wash-out (cross-over) the sequence was reversed for an additional 10 months. Blood pressure, lipid parameters, glycated haemoglobin and urinary albumin excretion were measured during the study. Additionally, in eight patients, urinary glycosaminoglycan excretion (GAG) was also measured during the study. Results Simvastatin and Cholestyramine were equally effective in reducing total and LDL cholesterol. Only during Simvastatin treatment a significant reduction in diastolic blood pressure and both 24 h urinary albumin and GAG excretion rates were observed, while no significant changes were seen with Cholestyramine treatment. Conclusions Our results clearly show for the first time that the reduction of blood pressure, together with 24 h urinary albumin excretion rate — two established cardiovascular risk factors, obtained during Simvastatin therapy in hypertensive type 2 diabetic patients — is in large part independent from the reduction of LDL Cholesterol. [ABSTRACT FROM AUTHOR]

The plasma lipid changes commonly observed in patients with diabetic nephropathy may play a major role in determining the increased cardiovascular risk in these patients. Contrasting results have been reported on the patterns of lipids and lipoproteins in diabetic subjects with microalbuminuria. We examined 20 patients with type 1 (insulin-dependent) diabetes who had a urinary albumin excretion >30 mg/24 h (11 males and 9 females, age range 16-45 years, mean diabetes duration 11.7 years) and 20 type 1 diabetic patients without microalbuminuria matched for sex, age, diabetes duration, daily insulin requirement and degree of metabolic control. In all patients we measured plasma total cholesterol, highdensity lipoprotein (HDL)-cholesterol, triglycerides, apolipoproteins A and B and lipoprotein (a) [Lp(a)]. No significant differences were found for any parameter between subjects with a urinary albumin excretion <20 mg/ 24 h and microalbuminuric patients. Moreover in nondiabetic controls the levels of plasma Lp(a) and of the other parameters measured were not significantly different from those of the two diabetic groups. Our results suggest that in type 1 diabetic patients with fairly good glycaemic control microalbuminuria is not associated with significant changes in the lipoprotein pattern. [ABSTRACT FROM AUTHOR]

Progressive capillary occlusion often leads to severe retinopathy within 15-20 years of the onset of Type 1 (insulin-dependent) diabetes mellitus. Lipoprotein (a), a complex formed by apolipoprotein (a), apo B-100 and lipids, is considered an independent, genetically determined, predictor of cardiovascular disease. It may have antifibrinolytic properties in view of its similarity to plasminogen. To test the hypothesis that circulating lipoprotein (a) is associated with the process that leads to clinically active diabetic retinopathy, we measured the circulating levels of apolipoprotein (a) (which are strictly correlated with those of lipoprotein (a)) in two groups of patients with Type 1 diabetes of at least 15 years duration: 25 with active retinopathy and 27 without clinically detectable retinal lesions. Thirty-eight healthy subjects of the same age and sex served as controls. Serum apolipoprotein (a) was higher in the patients with active retinopathy (36(2-193) U/dl, geometric mean and range) than in those without clinically detectable retinal lesion (17(1-160)) and the control subjects (14(0-115)), p < 0.01 in both cases. The distribution of apolipoprotein (a) levels was skewed to the left, as expected, in the patients without clinically evident retinal lesions and the control groups, but there was a bimodal trend of distribution among those with active retinopathy. The levels of glycated haemoglobin were similar in the two groups of diabetic patients, and no significant differences were found for total and HDL cholesterol, triglycerides or apolipoproteins A1 and B between them and the control subjects. These preliminary results suggest that serum apolipoprotein (a) is elevated in patients with active retinopathy. The role of this lipoprotein as a predictor or a pathogenic effector of diabetic retinopathy, or both deserves further investigation. [ABSTRACT FROM AUTHOR]