• A-FABP;
  • atorvastatin;
  • cholesterol;
  • hyperlipidaemia;
  • metabolic syndrome;
  • treatment


Background  Adipocyte-fatty acid binding protein (A-FABP) is a circulating protein expressed in adipocytes and macrophages. Several recent studies demonstrated that A-FABP might be involved in the pathogenesis of metabolic syndrome, particularly in dyslipidaemia, insulin resistance and atherosclerosis. The aim of this study was to investigate the influence of atorvastatin treatment (20 mg day−1 for 3 months) on serum A-FABP value in subjects with hyperlipidaemia.

Materials and methods  Anthropometric and serum analyses were performed for body mass index, A-FABP, triglycerides, total cholesterol, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, uric acid, alanine aminotransferase (ALT), aspartate aminotransferase (AST), high sensitive C-reactive protein (hs-CRP), creatine kinase (CK) and glucose on 26 subjects (BMI 30·3 ± 6·0, mean age 62 ± 10 years) with hyperlipidaemia who met the criteria: total cholesterol > 5·2 mmol L−1, LDL cholesterol > 3·3 mmol L−1 and triglycerides < 3 mmol L−1.

Results  After the 3-month therapy, a significant reduction in total cholesterol (P < 0·001), LDL cholesterol (P < 0·001), glucose (P < 0·001), A-FABP (from 44·6 ± 26·2 to 38·6 ± 19·3 g L−1, P < 0·01), uric acid (P < 0·05), AST (P < 0·05) and triglycerides (P < 0·05) values was observed. No difference was found in BMI, CK, ALT, hs-CRP, or HDL cholesterol values. A significant difference in the serum A-FABP value before and after the therapy remains after the correction for total cholesterol value (P < 0·001). A positive correlation between serum A-FABP and glucose was found (P < 0·05).

Conclusions  In conclusion, our study confirmed in vivo that atorvastatin reduces serum A-FABP by a pleiotropic mechanism and supports the hypothesis that A-FABP is involved in atherosclerotic actions.