Metabolic–endocrine–reproductive remodelling after metabolic and bariatric surgery in women with obesity and PMOS/PCOS: an evidence-tiered framework for precision care

Obesity can aggravate insulin resistance, hyperandrogenism, ovulatory dysfunction, and pregnancy risk in polyendocrine metabolic ovarian syndrome (PMOS), formerly polycystic ovary syndrome (PCOS). Metabolic and bariatric surgery (MBS) produces substantial weight loss, but the reproductive evidence is uneven. Whether the observed changes form a coherent metabolic–endocrine–reproductive remodelling process, and how that process might inform more precise care, remain uncertain. We updated this narrative review using structured searches of PubMed/MEDLINE and ClinicalTrials.gov through 6 September 2026, supplemented by reference-list screening and targeted forward citation tracking. We prioritised PMOS/PCOS-specific randomised and comparative studies, used non-comparative cohorts for less frequently reported outcomes, and reviewed international PMOS/PCOS, MBS, and post-bariatric pregnancy guidance. Findings were organised by their proximity to human postoperative outcomes to construct an evidence-tiered conceptual framework rather than a formal GRADE assessment. MBS should be considered because a patient meets obesity and metabolic indications, not because PMOS/PCOS is present in isolation; lean PMOS/PCOS is therefore not an indication. In the BAMBINI randomised trial, sleeve gastrectomy increased the median number of biochemically confirmed ovulations from 2 to 6 over 52 weeks (incidence rate ratio 2.5, 95% confidence interval 1.5–4.2). Most other surgical evidence is observational. Menstrual regularity, androgen excess, insulin resistance, and spontaneous conception often improve, but there is no validated reproductive target BMI and no PMOS/PCOS-specific trial directly comparing a glucagon-like peptide-1 receptor agonist with MBS. Asian cohorts enter surgery at lower BMI thresholds, yet ethnicity is seldom reported. MBS also introduces procedure-specific nutritional, gastrointestinal, glycaemic, and pregnancy risks. Across these data, weight loss and improved insulin action form the strongest evidence tier; the insulin–SHBG–androgen pathway provides a plausible endocrine bridge, whereas hypothalamic, follicular, endometrial, and gut-mediated pathways remain early or indirect hypotheses. In appropriately selected women with PMOS/PCOS and clinically significant obesity, MBS can improve metabolic health and ovulation. We propose an evidence-tiered metabolic–endocrine–reproductive remodelling framework to integrate these findings. It is hypothesis-generating rather than a proven causal sequence or a validated procedure-matching algorithm. Precision care should therefore combine established bariatric indications with metabolic burden, reproductive goals, procedure-specific risk, and the time available before conception.