Role of Cathepsin S and Insulin Resistance in Iraqi Women with Polycystic Ovary Syndrome

Background & Objective: Polycystic ovary syndrome is the prevailing endocrine disorder in females and one of the main causes of anovulatory sterility.  It is associated with symptoms, disturbs females of reproductive age and affects their quality of life. Cathepsins are proteases that perform a variety of physiological tasks, including activating the complement system, regulating the immune system, and regulating, tissue homeostasis, and ion channel functioning. There are various subtypes, including aspartic, cysteine, and serine cathepsins. Cat S belongs to the family of cysteine cathepsin proteases. A lysosomal protease can encourage the endo-lysosomal pathway's destruction of undesirable or damaged proteins. The present study was conducted with aim to investigate the relationship between cathepsin S and Insulin Resistance in Iraqi women with PCOS.Materials & Methods: An Observational Case-Control Study was performed. The levels of cathepsin S, Insulin, glucose, and insulin resistance were evaluated for ۱۳۵ blood samples (۹۰ patients and ۴۵ controls). Cathepsin S and Fasting Insulin were estimated by sandwich ELISA method, while glucose was performed using the COBAS INTEGRA ۴۰۰ plus analyzer. Insulin resistance was calculated by the HOMA-IR formula. All the test procedures were performed at the College of Medicine’s Research Unit /Al-Nahrain University/ Baghdad-Iraq.  The study was conducted from December to the end of March of ۲۰۲۳.Results: The levels of cathepsin S, Insulin, HOMA-IR, and glucose were elevated among PCOS patients with a high significant difference (HS) (P<۰.۰۰۰۱) between the patient and the control groups.Conclusion: According to the results of this study, Cat S has the potential to be a novel vital component among PCOS parameters. Insulin Resistance continues to rise among PCOS women leading to a necessity for studying its specific mechanism and its genetic origins.

کلیدواژه ها:

PCOS ، IR ، HOMA-IR ، CatS