Is polyendocrine metabolic ovarian syndrome a legacy of excessive gestational weight gain? A review of developmental and transgenerational programming
- 1Department of the First School of Clinical Medicine, Zhejiang Chinese Medical University
- 2Department of Gynecology and Obstetrics, The First Affiliated Hospital of Zhejiang Chinese Medical University
Abstract
Polyendocrine Metabolic Ovarian Syndrome (PMOS), formerly known as Polycystic Ovary Syndrome (PCOS), is increasingly recognized as a systemic endocrine-metabolic disorder characterized by hyperandrogenism, ovulatory dysfunction, insulin resistance, adipose tissue dysfunction, and hypothalamic-pituitary-ovarian (HPO) axis alterations. Evidence suggests susceptibility may originate before reproductive maturity, potentially during fetal development. This review examines whether excessive gestational weight gain (EGWG) elevates offspring PMOS risk through developmental (intergenerational and, potentially, transgenerational) endocrine programming. EGWG, defined as weight gain above the recommended range for prepregnancy body mass index, may reflect heterogeneous changes in maternal and fetal tissues rather than excess maternal fat accumulation alone. In some pregnancies, EGWG co-occurs with insulin resistance, altered lipid metabolism, inflammation, or adipokine dysregulation. These changes could modify placental nutrient transfer and endocrine signaling, thereby influencing offspring metabolic and reproductive development. However, the pathways linking EGWG specifically to PMOS remain uncertain. Human studies associate maternal metabolic conditions and PMOS with selected offspring outcomes, but provide limited evidence that EGWG independently predicts PMOS in daughters. Experimental models show that prenatal androgen exposure and maternal dietary perturbations can produce PCOS-like reproductive and metabolic traits, supporting the biological plausibility of developmental programming. This review evaluates whether EGWG may act as a marker or modifier of intrauterine conditions relevant to later PMOS susceptibility, while considering prepregnancy adiposity, maternal PMOS, genetic predisposition, and postnatal exposures as alternative or interacting explanations. Prospective mother–daughter cohorts with repeated pregnancy measures, placental profiling, and follow-up through puberty and adulthood are needed to test this hypothesis.
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BibTeX
@article{ge2026polyendocrine,
title = {{Is polyendocrine metabolic ovarian syndrome a legacy of excessive gestational weight gain? A review of developmental and transgenerational programming}},
author = {Zhiwen Ge and Jie Wang and Chen Zhang},
journal = {Frontiers in Endocrinology},
year = {2026},
month = oct,
doi = {10.3389/fendo.2026.1978407},
url = {https://www.frontiersin.org/articles/10.3389/fendo.2026.1978407/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Is polyendocrine metabolic ovarian syndrome a legacy of excessive gestational weight gain? A review of developmental and transgenerational programming
AU - Zhiwen Ge
AU - Jie Wang
AU - Chen Zhang
PY - 2026
DA - 2026/10/30
JO - Frontiers in Endocrinology
DO - 10.3389/fendo.2026.1978407
UR - https://www.frontiersin.org/articles/10.3389/fendo.2026.1978407/full
AB - Polyendocrine Metabolic Ovarian Syndrome (PMOS), formerly known as Polycystic Ovary Syndrome (PCOS), is increasingly recognized as a systemic endocrine-metabolic disorder characterized by hyperandrogenism, ovulatory dysfunction, insulin resistance, adipose tissue dysfunction, and hypothalamic-pituitary-ovarian (HPO) axis alterations. Evidence suggests susceptibility may originate before reproductive maturity, potentially during fetal development. This review examines whether excessive gestational weight gain (EGWG) elevates offspring PMOS risk through developmental (intergenerational and, potentially, transgenerational) endocrine programming. EGWG, defined as weight gain above the recommended range for prepregnancy body mass index, may reflect heterogeneous changes in maternal and fetal tissues rather than excess maternal fat accumulation alone. In some pregnancies, EGWG co-occurs with insulin resistance, altered lipid metabolism, inflammation, or adipokine dysregulation. These changes could modify placental nutrient transfer and endocrine signaling, thereby influencing offspring metabolic and reproductive development. However, the pathways linking EGWG specifically to PMOS remain uncertain. Human studies associate maternal metabolic conditions and PMOS with selected offspring outcomes, but provide limited evidence that EGWG independently predicts PMOS in daughters. Experimental models show that prenatal androgen exposure and maternal dietary perturbations can produce PCOS-like reproductive and metabolic traits, supporting the biological plausibility of developmental programming. This review evaluates whether EGWG may act as a marker or modifier of intrauterine conditions relevant to later PMOS susceptibility, while considering prepregnancy adiposity, maternal PMOS, genetic predisposition, and postnatal exposures as alternative or interacting explanations. Prospective mother–daughter cohorts with repeated pregnancy measures, placental profiling, and follow-up through puberty and adulthood are needed to test this hypothesis.
SN - 1664-2392
ER -