Background: kisspeptin (kiss1) is a hypothalamic neuropeptide, expressed also peripherally in the placental trophoblast, pancreatic cells, liver and adipose tissue suggesting its role in regulating metabolic homeostasis as well as normal fetal implantation and placentation. There are contradictory reports about the circulating and placental levels of kiss1 during preeclampsia in either lean or obese pregnant women. Aim: This study was designed to evaluate serum and placental kiss1 levels in normotensive non-pregnant, pregnant and preeclamptic females and to detect any potential association of those levels with some homeostatic parameters occurring in these conditions with and without obesity. Design: This study was conducted on 54 female subjects at the reproductive period. They were divided according to WHO classification of BMI into two equal groups: Group I (lean group with normal BMI 18.50-24.99kg/m 2 ), and Group II (obese group with BMI 30 -34.99 kg/m) 2 , each group was subdivided into: normotensive non-pregnant group, normotensive pregnant group and preeclamptic group. Moderate degree of preeclampsia was confirmed by presence of proteinuria (> 300mg/24h) and hypertension (≥150/100). Placental kiss1 and serum kiss1, insulin, glucose, lipid profile, TNF-α, urea, creatinine and sex hormones levels were measured. BMI and HOMA-IR were calculated in all groups. Results: Serum and placental kiss1 levels were significantly higher in normotensive pregnant while these levels were significantly lower in preeclamptic than normotensive pregnant groups and this decrease was more pronounced in obese than lean subjects. Kiss1 negatively correlated with blood pressure, BMI, glucose, insulin, HOMA-IR, TC, TG, LDL, TNF-α and positively correlated with HDL-C, sex hormones. Conclusion:The decrease in kiss1 levels may play a role in pathogenesis of PE, and may represent a novel link between metabolic disturbance and PE in obese pregnant females since this peptide was correlated with BMI, HOMA-IR, dyslipidemia and TNF-α.

Background: Poly cystic ovary syndrome (PCOS) is the principal cause of anovulatory infertility.Adropin is a nutrient-regulated metabolic hormone shown to encourage glucose oxidation over fatty acid oxidation.Vaspin expression in visceral adipose tissue is associated with metabolic derangement in rat model of obesity and T2DM.Some studies addressed adropin and vaspin levels in PCOS, however, the results are controversial. Aim of the study: This study was designed to evaluate both serum adropin and vaspin levels in obese rats with PCOS and to detect any possible association of these levels with metabolic and hormonal changes in this condition with and without metformin treatment. Material and Methods: Twenty four female albino rats were divided into three equal groups. Group I:Control,Group II:obese rats with PCOS fed HFD for 9 weeks and given letrozole(1mg/kg BW)by gavage daily for the last 21 consecutive days.Group III:Metformin pretreated obese PCOS rats,at a dose of 200 mg/kgBWdaily along with letrozole for the last 21days.At the end of the experiment,Serum adropin,vaspin,sex hormones,insulin,glucose,lipid profile,TNF,plasma D-dimer and ovarian MDA levels were estimated.BMI, HOMA-IR were calculated.Ovarian histopathology was done. Results: Obese PCOS group showed significantly lower serum adropin and higher vaspin levels when compared to control group.Metformin pretreated group showed significantly higher serum adropin and lower vaspin levels when compared to obese PCOS group.Adropin was negatively correlated with all parameters except sex hormones.Vaspin was positively correlated with all parameters except sex hormones in all groups. Conclusion: Adropin and vaspin may represent a novel link between obesity and metabolic disturbance in obese PCOS rats.