Abstract

Background: Adiponectin is a recently identified adipocyte-derived collagen-like protein. In humans, adiponectin levels were found to be decreased in obese, compared to normal individuals, whereas high adiponectin levels are independently associated with increased insulin sensitivity. The specific role of adiponectin in these metabolic conditions is not clear: it may have a causative role, or it could be regulated by insulin and serve as a marker for insulin resistance. Adiponectin levels hold great promise for use in clinical applications as a potent indicator of underlying metabolic complications. Aim of the work: The present study was aimed to evaluate the link between adiponectin and polycystic ovarian syndrome (PCOS) and the potential use of adiponectin as a biomarker for PCOS. Patients and methods: The study included 84 female patients presenting to the Reproductive and Infertility Clinics at Ain Shams University Maternity Hospital, starting from June 2016 till January 2017. They were divided into four groups based on the diagnosis of polycystic ovarian syndrome (PCOS); Cases were selected as: Group I non-obese PCOS group (n = 21), Group II obese PCOS group (n = 21). Controls were selected as: Group III non-obese control group (n = 21) and Group IV obese control group (n = 21). All the Control subjects had normal, regular menstruation, normal ovarian findings on ultrasound, and normal luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels. None displayed hirsutism. PCOS subjects were enrolled when they had satisfied two of the three following inclusion criteria: 1. Oligomenorrhea or amenorrhea. 2. Clinical or biochemical hyperandrogenism. 3. Ultrasonographic polycystic ovarian morphology. Serum adiponectin, metabolic and hormonal parameters were compared in PCOS patients with BMI matched controls. Measurement of plasma adiponectin levels done by Enzyme Immunoassay kit in Ain Shams University Maternity Hospital lab. Results: Serum adiponectin level was significantly lower among cases than controls (p value < 0.001). No significant difference was found between cases and controls regarding their hormonal profile except for testosterone and insulin levels which were significantly higher among cases (p value <0.001). As regard insulin resistance, there was a significant difference where cases were higher than control (p value <0.001). Conclusion: It could be concluded that PCOS was found to correlate with low adiponectin levels, independently of BMI. The relationships between adiponectin and insulin resistance and sensitivity, metabolic syndrome, and BMI in women with PCOS suggest that adiponectin potentially could serve as a marker for disease risk and provide opportunity for earlier intervention if knowledge is successfully translated from laboratory to clinical practice.

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