OBJECTIVE: There is controversy about the effects of statins on insulin resistance and plasma adiponectin. The aim of this study was to investigate the effects of fluvastatin treatment on these parameters in a group of dyslipidaemic patients who had no confounding factors for insulin resistance or alterations in plasma adiponectin. DESIGN AND PATIENTS: Forty-nine patients [27 males, 22 females; mean age 47.2 +/- 10.3 years; body mass index (BMI) 29.64 +/- 3.2 kg/m2] with dyslipidaemia and 20 controls (six males, 14 females; mean age 45.3 +/- 9.31 years; BMI 30.07 +/- 4.04 kg/m2) were enrolled. All patients were treated initially with therapeutic lifestyle changes (TLC) for 6 weeks. Six out of 49 subjects were excluded from the study. Then, 24 out of 43 patients with high blood cholesterol despite TLC were allocated to fluvastatin 80 mg daily plus TLC, and the remaining 19 patients with normal cholesterol were subjected to TLC alone for additional 12 weeks. MEASUREMENTS: Plasma adiponectin, immunoreactive insulin levels, BMI, waist circumference, blood pressure, lipids, and glucose were determined. The insulin sensitivity index was quantified using the homeostasis model assessment (HOMA). RESULTS: TLC caused significant improvement in plasma insulin (P = 0.02) and elevation in plasma adiponectin (P = 0.02). Fluvastatin treatment decreased total cholesterol and low density lipoprotein (LDL)-cholesterol significantly (P = 0.01 and P = 0.02, respectively). No significant effect of fluvastatin was observed on plasma insulin or adiponectin or on the HOMA index. CONCLUSIONS: Fluvastatin does not improve plasma adiponectin levels and insulin sensitivity, despite its beneficial effects on lipid levels. Our data, however, were limited by the fact that a more accurate method of assessing insulin sensitivity, the euglycaemic-hyperinsulinaemic glucose clamp technique, was not used.
OBJECTIVE: There is controversy about the effects of statins on insulin resistance and plasma adiponectin. The aim of this study was to investigate the effects of fluvastatin treatment on these parameters in a group of dyslipidaemic patients who had no confounding factors for insulin resistance or alterations in plasma adiponectin. DESIGN AND PATIENTS: Forty-nine patients [27 males, 22 females; mean age 47.2 +/- 10.3 years; body mass index (BMI) 29.64 +/- 3.2 kg/m2] with dyslipidaemia and 20 controls (six males, 14 females; mean age 45.3 +/- 9.31 years; BMI 30.07 +/- 4.04 kg/m2) were enrolled. All patients were treated initially with therapeutic lifestyle changes (TLC) for 6 weeks. Six out of 49 subjects were excluded from the study. Then, 24 out of 43 patients with high blood cholesterol despite TLC were allocated to fluvastatin 80 mg daily plus TLC, and the remaining 19 patients with normal cholesterol were subjected to TLC alone for additional 12 weeks. MEASUREMENTS: Plasma adiponectin, immunoreactive insulin levels, BMI, waist circumference, blood pressure, lipids, and glucose were determined. The insulin sensitivity index was quantified using the homeostasis model assessment (HOMA). RESULTS: TLC caused significant improvement in plasma insulin (P = 0.02) and elevation in plasma adiponectin (P = 0.02). Fluvastatin treatment decreased total cholesterol and low density lipoprotein (LDL)-cholesterol significantly (P = 0.01 and P = 0.02, respectively). No significant effect of fluvastatin was observed on plasma insulin or adiponectin or on the HOMA index. CONCLUSIONS:Fluvastatin does not improve plasma adiponectin levels and insulin sensitivity, despite its beneficial effects on lipid levels. Our data, however, were limited by the fact that a more accurate method of assessing insulin sensitivity, the euglycaemic-hyperinsulinaemic glucose clamp technique, was not used.