Polycystic ovary syndrome (PCOS) is an endocrine disorder in women. Omentin-1 and vaspin are secretary adipokines that are produced by the visceral adipose tissue. These levels change in obese women with PCOS. The aim of this study is to investigate whether omentin and vaspin levels change in nonobese PCOS subjects. This study is a cross-sectional case control study in which 39 women with PCOS were picked out for this study. The inclusion criteria were based on the Rotterdam 2003 diagnostic criteria. The control group consisted of 39 women with normal pelvic sonographic reports having regular menstruation and showing no signs of infertility. The fasting plasma glucose (FPG), triglyceride (TG), Chol, and high-density lipoprotein cholesterol (HDL-C), insulin, testosterone, omentin and vaspin were measured by the enzymatic methods. The differences within these groups were calculated by the un-paired t-test and the Mann-Whitney test. The results from this study show a significant increase in the amount of insulin, testosterone, homeostasis model assessments for insulin resistance, TG and lower HDL in the patient group. No significant differences were seen in omentin, vaspin, FPG, Cho, low-density lipoprotein, very low-density lipoprotein cholesterol, blood urea nitrogen, Cr and homeostasis model assessments for B cell function levels between groups. Results show that PCOS is not a determinant of decreased omentin and vaspin plasma levels and those high androgen level and insulin resistances are warning signs of PCOS.

As the prevalence of lipoprotein abnormalities in adolescents is increasing dramatically, the identification of relevant risk factors is a major public health challenge. The aim of this study was to investigate whether a family history of diabetes could be a risk factor for lipid abnormalities in healthy individuals. This study is a cross-sectional case control study. 179 men and women were studied in two equal-member groups (with diabetic parents' background and without any diabetic sibling). Both groups matched in body mass index (BMI), age and sex. The serum concentration of oxidized-low density lipoprotein (LDL), Apo B100 and insulin were measured by enzyme linked immunosorbant assay technique and TG, Chol, HDL-C, FBS and GTT by enzymatic methods. The LDL-C level was calculated using the Friedewald formula. The results show that there were no significant variation in the amount of plasma FBS, GTT, Cho, TG, LDL and HDL between the two groups, whereas a significant increase was found in the amount of insulin (P = 0.02), Apo B100 (P = 0.001), OX-LDL (P = 0.001) and HOMA-IR (P = 0.03) in the case group as compared to the control group. We conclude that a family history of diabetic parents can lead to lipid parameters abnormalities and CVD risk factor via aggregation of inherited defected genes.