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Ovarian Function and Disorders · Journal article
International Journal of Medical & Pharmaceutical Sciences · August 13, 2026
Reinforces what was already believed, rather than introducing something new.
This narrative review consolidates observational evidence that insulin resistance is a core physiological feature of PMOS, driving compensatory hyperinsulinemia and hyperandrogenism, and is detectable even in lean women and those with normal glucose tolerance. The work synthesizes findings on IR pathophysiology, biomarkers, and management from a Korean case-control study, a South Indian cross-sectional study, and broader literature, without reporting new intervention outcomes or clinical practice recommendations.
Narrative review synthesizing case-control and cross-sectional observational studies. Women with PMOS, including those with normal glucose tolerance and lean phenotype; broader PMOS epidemiology in India. Compared with: PMOS women versus controls (case-control); stratification by obesity and glucose tolerance status. Korea (case-control study), South India (cross-sectional study), global (narrative literature review).
Indian PMOS prevalence estimated between 2.2% and 26% Insulin resistance is only partly explained by obesity in PMOS IR is closely linked to hyperandrogenism in PMOS
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Clinicians should recognize insulin resistance as a core driver of PMOS pathophysiology independent of BMI, supporting assessment and management of IR even in lean patients with normal fasting glucose. This reinforces the rationale for metabolic screening and insulin-sensitizing approaches in PMOS management.
A narrative review synthesizing case-control and cross-sectional evidence that replicates established understanding of insulin resistance as central to PMOS pathophysiology, without new interventional trials or practice-level guidance.
As stated by the source record.
Quoted from the source exactly as published.
Clinicians should recognize insulin resistance as a core driver of PMOS pathophysiology independent of BMI, supporting assessment and management of IR even in lean patients with normal fasting glucose. This reinforces the rationale for metabolic screening and insulin-sensitizing approaches in PMOS management.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Polyendocrine metabolic ovarian syndrome (PMOS) is the most common endocrinopathy of reproductive-aged women, with an Indian prevalence estimated between 2.2% and 26%. Insulin resistance (IR) sits at the physiological core of the syndrome, driving compensatory hyperinsulinemia, ovarian and adrenal hyperandrogenism, and a long-term excess risk of type 2 diabetes mellitus (T2DM) and cardiovascular disease. This review consolidates findings from three complementary sources: a Korean case-control study evaluating oral glucose tolerance test (OGTT)-derived IR and β-cell indices in women with PMOS and normal glucose tolerance; a South Indian cross-sectional study correlating HOMA-IR with hirsutism, acanthosis nigricans, and BMI; and a broader narrative review of IR pathophysiology, biomarkers, and management. Across all three sources, IR emerges as a feature of PMOS that is only partly explained by obesity, is closely linked to hyperandrogenism, and is detectable even in lean women and those with normal glucose tolerance. We add context on assessment methods, novel adipokine biomarkers, psychological comorbidity, and current treatment strategies, and present the quantitative findings pictorially for ease of comparison.
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