Oxidative and inflammatory status and HDL functions of obese pre and post menopausal women

Objectıve: Obesity and age related vascular changes coupled with the effect of estrogen withdrawal increases predisposition to atherosclerosis in postmenopausal women. But the functions of high density lipoprotein (HDL) were not well established in postmenopausal women. In the present study, we mainly aimed to evaluate the changes in the functions of HDL and aimed to measure, lipid peroxidation, lipid profile and homocysteine levels as a supporting evidence in pre and postmenopausal obese women as a result of estrogen depletion. Material and Methods: This study included 20 premenopausal, 22 postmenopausal 42 obese (BMI>30 kg/m2) and 26 premenopausal non-obese. These twenty six premenopausal women with normal BMI (20<BMI<25 kg/m2) were recruited to serve as the control group. Markers of cardiovascular disease (CVD), namely high sensitive C-reactive protein (hsCRP), homocysteine and lipoprotein(a) (Lp(a)) were measured. Glucose, lipid parameters and Malondialdehyde (MDA), antiinflammatory HDL levels were also measured. Functional properties of HDL were determined by the change in fluorescence intensity resulting from oxidation of DCFH (Dichloroflorescein) by LDL in the presence of patient HDL in cell free serum. Results: Lipid profiles were impaired in both pre and postmenopausal obese women. CVD markers and glucose levels increased in post menopausal women. But hsCRP levels were also increased in premenopausal compared to control group. MDA, the product of lipid peroxidation was increased in both pre and postmenopausal women. Antiinflammatory characteristics of HDL were only impaired in postmenopausal women. Conclusion: Postmenopausal obese women have lost their antiinflammatory HDL functions. This situation can be a significant indicator of endothelial dysfunction and cardiovascular disease in postmenopausal women. But the increase in oxidative stress was observed in all of the obese patients regardless of estrogen withdrawal.