Abstract

This work studies the role of serum apelin-36 and Glutathione S-transferases (GST) activity in association with the hormonal, metabolic profiles and their link to the risk of cardiovascular disease (CVD) in healthy and patients' ladies with polycystic ovary syndrome (PCOS). A total of fifty-four (PCOS) patients and thirty-one healthy woman as a control have been studied. The PCOS patients were subdivided on the basis of body-mass-index (BMI), into 2-subgroups (the first group was obese-PCOS with BMI ≥ 30 and the second group was non-obese PCOS MBI<30). Fasting-insulin-levels and Lipid-profile, Homeostatic-model assessment-of-insulin-resistance (HOMA-IR), follicle-stimulating-hormone (FSH), luteinizing-hormone (LH), testosterone and serum Apelin-36 (AP-36) levels, GST-Activity were done for all groups. PCO patients showed higher concentricity of apelin-36 than healthy (160.43 ±20.81 (pg/ml) versus 85.49 ± 17.85 (pg/ml), P=0.008),while GST-activity decreased in PCOS patients and was higher in the control (7.99 ± 1.19(IU/L)versus 12.96 ±1.90(IU/L)respectively,with a P-value=0.022). Apelin-36 levels are directly interrelated with BMI and Very-low-density-lipoprotein (VLDL) in PCOS patients, but GST-activity levels correlated significantly negatively with (BMI) in PCOS patients. Moreover, obese-PCOS patients show increased AP-36 levels more than non-obese PCOS (185.76± 92.0(pg/ml) versus 123.59±27.65 (pg/ml), P=0.127) respectively, whilst the GST-activity was exhibited to be lower in obese-PCO patients more than in non-obese PCOS (6.99 ± 1.4(IU/L) versus 9.44 ± 2.0(IU/L), P=0.102). The data showed that AP-36 level is negatively associated with GST-activity in PCOS patients. AP-36 isn't legitimately ensured in the pathogenesis of PCO disorder, yet it may be included as an adipokine that is influenced by BMI. The oxidants increased because of the highly levels of VLDL and the lower in the activities of antioxidant, that may be a response to higher levels of oxidative stress. A decrease in the antioxidant capacity and an increase in AP-36 levels leads to an increased the risk of cardiovascular disease in PCOS patients.

Highlights

  • Polycystic ovary syndrome (PCOS), as a popular endocrine issue in procreative age, is a heterogeneous condition described by clinical symptoms, including reproductive, cardiac and psychological disorders [1, 2]

  • The proportion of luteinizing hormone (LH)/FSH, LH levels, fasting insulin, Homeostatic-model assessment-of-insulin-resistance (HOMA-insulin resistance (IR)), and T were essentially higher, though the FSH level was decreased in the PCOS groups compared with healthy, true to form (p < 0.05)

  • It has been found that Glutathione S-transferases (GST) activity was lower in PCOS patients when compared with the healthy group

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Summary

Introduction

Polycystic ovary syndrome (PCOS), as a popular endocrine issue in procreative age, is a heterogeneous condition described by clinical symptoms, including reproductive, cardiac and psychological disorders [1, 2]. Other potential systems of weight related hyperandrogenemia incorporate upgraded androgen generation in extending the lipid lump and possible impact of unusual levels in each of cytokine and adipokine [10].Insulin resistance is the main cause of pathogenic factor in the background of increased metabolic disorders in women with PCOS, which is irregular menstruation and other metabolic manifestations associated with PCOS, but insulin resistance is not a standard diagnosis of the syndrome, yet one of its symptoms. Greasy tissue works about as a member of the endocrine glands that produce an assortment of molecules signaling that direct conduct of nourishment, vitality use, digestion, generation, endocrine and immunological capacity [12] In this way, corpulence in ladies with PCOS is predominantly described by an expansion in the volume of fat cells (intemperate heftiness obesity) as opposed to expanding the quantity of fat cells (hyperplastic weight) [13]. The purpose of this work: is to investigate the association between CVD risk factors with PCOS through measuring the apelin-36 concentration and the activity of the enzyme glutathione S transferase

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