POLYCYSTIC OVARY SYNDROME: ORIGINS AND IMPLICATIONS: Polycystic ovary syndrome: an evolutionary metabolic adaptation.
Dumesic DA., Padmanabhan V., Abbott DH.
Narrative Review on Type 2 Diabetes, Scar, published in Reproduction (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Narrative Review
- Journal
- Reproduction (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40080428
- PMCID
- PMC12004336
- DOI
- 10.1530/REP-25-0021
- Citations
- 8
Abstract (original English)
In brief Polycystic ovary syndrome has ancient genetic origins that favored preferential abdominal fat accumulation, ovarian hyperandrogenism and insulin resistance. This review examines how endocrine-metabolic changes in normal-weight hyperandrogenic PCOS women originated as an evolutionary metabolic adaptation to balance enhanced fat storage with increased glucose and fatty acid availability for optimal energy use for survival and reproduction. Abstract Polycystic ovary syndrome (PCOS) is a common endocrinopathy of reproductive-aged women, characterized by hyperandrogenism, oligo-anovulation and insulin resistance in combination with preferential abdominal fat accumulation. As an ancestral primate trait, PCOS in humans likely underwent relatively recent preferential selection when scarcity of food in hunter-gatherers of the Pleistocene selected for enhanced fat storage and insulin resistance as a survival advantage to maintain glucose homeostasis for brain and reproductive function. As an evolutional model for PCOS, healthy normal-weight women with hyperandrogenic PCOS have subcutaneous (SC) abdominal adipose stem cells that favor exaggerated lipid accumulation during adipocyte development in vitro accompanied by reduced systemic insulin sensitivity and preferential accumulation of highly lipolytic intra-abdominal fat. Programmed by genetic inheritance and epigenetic events d
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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