Dossier: Diabetes: Basic Research and Clinical Approach Effects of a statin group drug, pravastatin, on the insulin resistance in patients with metabolic syndrome Feyzullah Güçlü a , Bilgin Özmen b, *, Zeliha Hekimsoy b , Cengiz Kirmaz a a Department of Internal Medicine, Faculty of Medicine, Celal Bayar University, Manisa, Turkey b Division of Endocrinology of Internal Medicine, Faculty of Medicine, Celal Bayar University, Manisa, Turkey Received 4 May 2004 Available online 13 October 2004 Abstract Background. – In West of Scotland Coronary Prevention Study (WOSCOPS), development of type 2 diabetes mellitus (DM) was found to decrease by 30% in pravastatin-treated patients. In the study, it is suggested that pleiotropic effects of pravastatin may be responsible too as well as its lipid lowering effect. Objective. – The aim of this study was to assess the effects of pravastatin treatment on the insulin resistance in patients with metabolic syndrome with impaired glucose tolerance (IGT), by Homeostasis Model Assessment (HOMA) test, insulin sensitivity indices and glucose half activation time (glucose t1/2). Methods. – Study population consisted of 25 women who were diagnosed with metabolic syndrome. At baseline and 10 weeks after the 20 mg/daily tablet pravastatin treatment, waist/hip circumference, body weight and arterial blood pressure measurements, plasma glucose, total cholesterol, triglyceride, high density lipoprotein (HDL)-cholesterol, transaminases, glycosylated haemoglobin (A1C) and insulin level measurements were obtained along with HOMA test and insulin tolerance test after 12 h of fasting. Insulin sensitivity indices and glucose t1/2 were assessed. Results. – After the treatment, a statistically significant decrease was observed in arterial blood pressure values (P < 0.0001). While plasma total cholesterol, low density lipoprotein (LDL)-cholesterol, and triglyceride levels were found to decrease significantly and HDL-cholesterol levels increased significantly, a decrease in baseline insulin levels, an increase in insulin sensitivity levels were observed along with an decrease in glucose t1/2. Related to the improvement in aforementioned parameters, statistically significant decreases were noted in HOMA, postprandial and fasting glucose levels and A1C values (P < 0.0001). Conclusion. – Our study suggests that using pravastatin in the dyslipidemia treatment of metabolic syndrome with IGT may be an effective approach by its advantageous effects on insulin resistance. Based on this result, it is possible to say that this can be a risk lowering treatment approach for the development of type 2 DM. © 2004 Elsevier SAS. All rights reserved. Keywords: Insulin resistance; Metabolic syndrome; Pravastatin; Hyperlipidemia; HOMA-IR 1. Introduction Metabolic syndrome patients are at increased risk for devel- oping cardiovascular morbidity and mortality [1]. The increas- ing prevalence of the metabolic syndrome in various asymp- tomatic populations has been well documented, however, limited information is available about the prevalence in mani- fest atherosclerotic vascular disease patients [2]. Metabolic syndrome is a disorder in which insulin resis- tance is the main component of the pathogenetic mechanism. In 1988, Reaven [3], upon observing the more than coinci- dental existence of obesity, diabetes, hypertension, hyperlipi- demia and atherosclerotic coronary diseases concomittantly in a single patient, suggested that these are caused by a single metabolic disorder. On the basis of this conclusion, he defined the “insulin resistance syndrome” (syndrome X) which con- sists of insulin resistance, hyperinsulinemia, obesity, glucose intolerance, hypertriglyceridemia, reduced high density lipo- protein (HDL)-cholesterol level, hypertension and coronary arterial diseases, prothrombotic state (e.g., high fibrinogen or * Corresponding author. Plevne Bulvarı No. 14, D. 9, Alsancak, I ˙ zmir 35220, Turkey. E-mail address: bilozmen@yahoo.com (B. Özmen). Biomedicine & Pharmacotherapy 58 (2004) 614–618 http://france.elsevier.com/direct/BIOPHA/ 0753-3322/$ - see front matter © 2004 Elsevier SAS. All rights reserved. doi:10.1016/j.biopha.2004.09.005