Mechanisms Linking Insulin Resistance to Ovarian Dysfunction in Lean versus Obese Phenotypes of Polycystic Ovary Syndrome
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Keywords
Polycystic ovary syndrome, Insulin resistance, Obesity, Ovarian dysfunction
Abstract
Background: Polycystic ovary syndrome (PCOS) is a common endocrine disorder in reproductive-aged women and insulin resistance is regarded as central to its reproductive and metabolic abnormalities. The extent to which insulin resistance drives ovarian dysfunction differs between lean and obese phenotypes and this relationship remains incompletely defined among South Asian women. This study aimed to compare metabolic, hormonal and ovarian morphological characteristics between lean and obese women with PCOS and to evaluate the association between insulin resistance and ovarian dysfunction.
Methods: This comparative cross-sectional study was conducted in the Department of Obstetrics and Gynaecology, Bangabandhu Sheikh Mujib Medical University, Dhaka, Bangladesh. Two hundred fifty women with PCOS were enrolled, comprising 125 lean and 125 obese participants diagnosed on established clinical, biochemical and ultrasonographic grounds. Anthropometric, biochemical, hormonal and ultrasonographic parameters were compared between groups and the homeostasis model assessment of insulin resistance (HOMA-IR) defined insulin resistance status.
Results: Obese participants had significantly higher body mass index, waist circumference, fasting insulin, HOMA-IR androgen levels and an unfavourable lipid profile than lean participants (p<0.001 for most variables). Insulin resistance, defined as HOMA-IR of 2.6 or more, was present in 73.6% of obese and 41.6% of lean participants. Ovarian volume, antral follicle count, oligo/anovulation and clinical hyperandrogenism were all significantly more frequent among participants with higher HOMA-IR, regardless of body weight category.
Conclusion: Insulin resistance was strongly and consistently associated with adverse metabolic, hormonal and ovarian features in both lean and obese phenotypes of PCOS, supporting its central pathogenic role independent of body weight.
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