Does obesity affect serum anti-müllerian hormone or inhibin B levels in polycystic ovary syndrome? Results of a systematic review and meta-analysis

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BACKGROUND: Anti-Müllerian hormone (AMH) and inhibin B (INHB) are validated ovarian reserve biomarkers with key roles in polycystic ovary syndrome (PCOS) pathogenesis. Serum AMH has specific diagnostic value for PCOS, yet their differential expression and clinical significance in obese versus non-obese PCOS phenotypes remain unclear. To fill this gap, we performed the first systematic review and meta-analysis comparing serum AMH and INHB levels between obese and non-obese women with PCOS, and explored heterogeneity sources. METHODS: Thirty-eight observational studies (n = 15,003) were systematically retrieved and quality-assessed via the Newcastle-Ottawa Scale (NOS), with all scoring ≥ 7. Meta-analyses calculated pooled standardized mean differences (SMDs) for AMH and INHB levels, with subgroup analyses stratified by geographic region, BMI category, and age. Meta-regression analyzed the effects of these factors on AMH levels; sensitivity analyses and publication bias assessments verified result robustness. RESULTS: Obese PCOS women had significantly lower serum AMH (SMD: -0.16; 95% CI: -0.29 to -0.02; P=0.02; I²=86%) and INHB (SMD: -0.98; 95% CI: -1.60 to -0.36; P=0.002; I²=90%) than non-obese counterparts. Meta-regression found no significant associations between AMH levels and geography (P=0.6516), BMI (P=0.2598), or age (P=0.5353). Subgroup analyses showed the most pronounced AMH differences in BMI ≤28 kg/m² (P=0.01) and ≥18-year-old (P=0.02) subgroups, with reduced heterogeneity here. AMH results were stable in sensitivity analysis, while INHB findings relied on a single study; funnel plot asymmetry suggested potential publication bias for AMH studies. CONCLUSION: Obesity correlates with markedly reduced AMH and INHB in PCOS, indicating metabolic impacts on ovarian reserve biomarkers. These findings highlight the need for weight-stratified interpretation of such markers and further investigation into obesity-related mechanisms in PCOS.