Adiponectin, leptin and lipid profiles evaluation in oral contraceptive pill consumers

The aim of this study was to evaluate serum lipid profiles, leptin and adiponectin levels in women with a normal menstrual cycle receiving low-dose (LD) combined oral contraceptive pill (COC) (levonorgestrel 0.15 mg, ethinyl-estradiol 0.03 mg). Serum adiponectin and leptin concentrations were measured by enzyme-linked immunosorbent assay (ELISA), and spectrophotometric assay was used for serum lipid and lipoprotein profiles assay in 50 healthy women with normal menstrual cycles who served as the control group and 50 women taking COCs. Unpaired test and Chi-square test were used for comparison of variables between oral contraceptive users and non-oral contraceptive users. Serum adiponectin and leptin levels were changed in COC consumers. The data obtained for adiponectin in COC consumers (6.6 +/- A 4.06 mu g/ml) were significantly lower (-27.4%, = 0.004) than control group (9.1 +/- A 5.09 mu g/ml). The difference between the serum leptin concentration of the control group (11.5 +/- A 6.9 ng/ml) and women receiving COCs (14.1 +/- A 6.7 ng/ml) was not significant (+18.4%, = 0.083). There was nonsignificant difference between HDL levels of subjects taking COC (44.02 +/- A 10.7 mg/dl) and control group (49.4 +/- A 14.3 mg/dl). The LDL levels of COC consumer (131.40 +/- A 66.40 mg/dl) was significantly higher ( = 0.002) than controls (102.30 +/- A 44.0 mg/dl). The serum cholesterol concentration of women receiving COC (193.2 +/- A 70.4 mg/dl) was significantly higher ( = 0.05) than controls (172.8 +/- A 49.6 mg/dl). The age of COC consumption and the duration of intake of COCs beyond 36 months had no significant effect on the adiponectin and leptin concentrations. LD COC uptake results in a significant decrease in serum adiponectin concentration, nonsignificant increase in leptin levels and a more atherogenic lipid profile by significantly increasing LDL and nonsignificantly decreasing HDL concentrations. These findings suggested that COC may reduce or stimulate the adiponectin and leptin concentrations, respectively. This might be due to an effect of these pills on adipocyte maturation via inhibition or stimulation of the synthesis of new adiponectin and leptin molecules or may be a result of the increased frequency of a particular allele of the adiponectin and leptin. It is suggested that these alterations in adiponectin and leptin concentrations and lipid profiles may be related to their probable effects in response to various pathological and physiological properties of COC or its metabolites. It seems that probably free radicals produced during metabolism of COCs change the amounts of adipokines and atherogenic lipids.