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Focus on Endocrine and Metabolic Research Priorities in PCOS/PMOS
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Focus on Endocrine and Metabolic Research Priorities in PCOS/PMOS

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 30 November 2026 | Viewed by 10235

Editor

Dr. Jim Parker

E-Mail Website
Guest Editor
School of Medicine, University of Wollongong, Wollongong, NSW 2522, Australia
Interests: polycystic ovary syndrome; evolutionary origins; developmental origins; pathogenesis; microbiome; pathophysiology; epigenetics; nutritional biochemistry; pregnancy complications; lifestyle management
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Polycystic Ovary Syndrome (PCOS) has recently been renamed to Polyendocrine Metabolic Ovarian Syndrome (PMOS). During the transition phase to the new name, we will refer to PCOS as PCOS/PMOS. This Special Issue is focused on the endocrine and metabolic research priorities in relation to PCOS/PMOS.

PCOS/PMOS contributes to the chronic disease epidemic and presents a significant global health challenge. PCOS/PMOS affects 8–13% of women, and it usually presents in adolescence with a complex mixture of symptoms that result from underlying metabolic and endocrine disturbance. The programming of inherited gene variants predisposes women with PCOS to reduced insulin sensitivity, a proinflammatory immune response, dysregulated hypothalamic–pituitary–ovarian–adrenal function, and altered ovarian steroidogenesis that results in reduced estradiol production, hyperandrogenism, and anovulation.

A recent collaboration of the PCOS/PMOS International Guideline Network generated a consensus roadmap for 150 clinical research priorities in PCOS/PMOS. Surveys of women, stakeholder groups and healthcare providers called for a greater understanding of the long-term metabolic implications of PCOS/PMOS and an enhanced focus on the metabolic aspects of the condition.

Insulin resistance is a key driver of metabolic dysfunction and there is a pressing need for research into accurate diagnostic tests, standardized reference values, predictive surrogate markers, and lifestyle and therapeutic treatment options that are tailored to a more personalized approach. A focus on precision medicine offers promising avenues for alleviating the burden of illness by tailoring prevention, diagnosis and treatment strategies for insulin resistance in PCOS/PMOS.

This Special Issue would like to invite research directed to investigating the endocrine and metabolic aspects of PCOS/PMOS, particularly those that address evidence–practice gaps. We encourage the submission of a wide range of related research topics. This could include discovery research to help understand the pathophysiological causes and mechanisms of PCOS/PMOS, clinical research to improve diagnosis and management, clinical trials focused on integrated multiomics, the assessment of wearable, digital, personalized monitoring technology, or research investigating the bidirectional relationships between insulin resistance, chronic inflammation, and hyperandrogenism. We welcome original papers and reviews.

Dr. Jim Parker
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • polycystic ovary syndrome
  • metabolism
  • insulin resistance
  • inflammation
  • hyperandrogenism

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Published Papers (3 papers)

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Research

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20 pages, 3218 KB  
Article
Lipid Challenge Reveals Amplified Apolipoprotein Responses with Preserved Temporal Pattern in Polyendocrine Metabolic Ovarian Syndrome: An Exploratory Study
by Ebrahim Rajab, Abu Saleh Md Moin, Manjula Nandakumar, Thozhukat Sathyapalan, Alexandra E. Butler and Stephen L. Atkin
Int. J. Mol. Sci. 2026, 27(15), 6656; https://doi.org/10.3390/ijms27156656 - 25 Jul 2026
Viewed by 280
Abstract
Acute elevation in circulating lipids induces reversible insulin resistance and alters triglyceride-rich lipoprotein flux. Whether insulin-regulated remodelling of high-density lipoprotein (HDL)-associated apolipoproteins is altered during defined lipid stress in women with polyendocrine metabolic ovarian syndrome (PMOS) remains unclear. In this exploratory, randomized, cross-over [...] Read more.
Acute elevation in circulating lipids induces reversible insulin resistance and alters triglyceride-rich lipoprotein flux. Whether insulin-regulated remodelling of high-density lipoprotein (HDL)-associated apolipoproteins is altered during defined lipid stress in women with polyendocrine metabolic ovarian syndrome (PMOS) remains unclear. In this exploratory, randomized, cross-over study, 10 healthy women and 12 women with PMOS underwent 5-h saline or lipid infusion, with a hyperinsulinemic–euglycemic clamp commencing at 180 min. Plasma proteomics were performed at baseline, 180 min and 300 min using linear modelling (limma). Lipid infusion induced the coordinated suppression of ApoA1 and ApoE isoforms at 180 min in both groups (FDR-adjusted p < 0.01), followed by partial recovery during hyperinsulinemia. Women with PMOS exhibited greater early suppression of ApoA1 (log2 fold-change −2.20, p = 0.001) and more persistent suppression of ApoE isoforms at 300 min (ApoE3 log2 −1.64, p = 0.001). ApoA1 suppression correlated inversely with NEFA exposure during lipid infusion (Spearman ρ = −0.54, p = 0.021). Controlled lipid challenge reveals amplified but reversible dysregulation of HDL-associated apolipoproteins in PMOS, with the preservation of the overall response pattern, but impaired recovery under hyperinsulinemic conditions. These findings suggest impaired adaptation to acute lipid stress in PMOS, with ApoA1 changes appearing to relate more closely to acute NEFA exposure than to clamp-derived insulin sensitivity. Full article
(This article belongs to the Special Issue Focus on Endocrine and Metabolic Research Priorities in PCOS/PMOS)
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20 pages, 641 KB  
Article
Associations of Serum GIP, GLP-1, and DPP-4 with Metabolic and Hormonal Profiles and Tobacco Exposure in Women with Polycystic Ovary Syndrome
by Anna Bizoń, Julia Borkowska, Grzegorz Franik and Agnieszka Piwowar
Int. J. Mol. Sci. 2025, 26(15), 7097; https://doi.org/10.3390/ijms26157097 - 23 Jul 2025
Cited by 1 | Viewed by 3006
Abstract
Disorders in glucose metabolism are well-established features of polycystic ovary syndrome (PCOS) and are linked to its clinical severity and phenotypic variability. This study aimed to assess serum concentrations of glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and dipeptidyl peptidase-4 (DPP-4) and to [...] Read more.
Disorders in glucose metabolism are well-established features of polycystic ovary syndrome (PCOS) and are linked to its clinical severity and phenotypic variability. This study aimed to assess serum concentrations of glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and dipeptidyl peptidase-4 (DPP-4) and to examine their relationships with glucose and insulin levels, selected sex hormone concentrations, body weight, and exposure to tobacco smoke. Women with PCOS exhibited significantly elevated levels of fasting glucose, insulin, GIP, and GLP-1 compared to controls. Tobacco smoke exposure in women with PCOS was associated with reduced DPP-4 levels, which were approximately two-fold lower in smokers than in non-smokers. A significant negative correlation between DPP-4 and cotinine levels further supported this relationship. Comorbidities such as overweight/obesity or insulin resistance (IR) were also linked to elevated incretin hormone levels. However, no significant age-related trends in incretin levels were identified, despite the known association between age and glucose dysregulation. The notable alterations in incretin hormone profiles in PCOS, along with the consistent patterns of GIP or GLP-1 with metabolic and hormonal parameters, suggest that these hormones may play coordinated regulatory roles in the pathophysiology of PCOS. Full article
(This article belongs to the Special Issue Focus on Endocrine and Metabolic Research Priorities in PCOS/PMOS)
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Review

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36 pages, 2235 KB  
Review
Molecular Impact of Metabolic and Endocrine Disturbance on Endometrial Function in Polycystic Ovary Syndrome
by Jim Parker, Claire O’Brien, Talat Uppal and Kelton Tremellen
Int. J. Mol. Sci. 2025, 26(20), 9926; https://doi.org/10.3390/ijms26209926 - 12 Oct 2025
Cited by 17 | Viewed by 5623
Abstract
Polycystic ovary syndrome (PCOS) is a systemic metabolic and endocrine disorder that significantly disrupts reproductive physiology and endometrial function. In this narrative review, we examine the molecular impact of metabolic and hormonal imbalances on the endometrium of women with PCOS. We investigate the [...] Read more.
Polycystic ovary syndrome (PCOS) is a systemic metabolic and endocrine disorder that significantly disrupts reproductive physiology and endometrial function. In this narrative review, we examine the molecular impact of metabolic and hormonal imbalances on the endometrium of women with PCOS. We investigate the specific mechanisms that delineate how hyperinsulinemia and insulin resistance, chronic low-grade inflammation, and estrogen/progesterone/androgen imbalance contribute to altered epigenetic, transcriptomic, metabolomic, and signaling profiles in a wide array of different cell types within endometrial tissues. The synergistic interplay between upregulated inflammatory cytokines (e.g., IL-1,2,6,8,17,18, and TNF-α), along with key changes in critical molecular pathways associated with hyperinsulinemia and insulin resistance (e.g., PI3K/AKT/MAPK, and Wnt/β-catenin), in addition to aberrant sex steroid hormone signaling (e.g., CYP19A1, COX-2, PGE2, HOXA10, 11βHSD2), promotes deleterious changes within the endometrial microenvironment. These anomalies underpin a spectrum of clinical manifestations observed in women with PCOS at each stage of the life course, including abnormal uterine bleeding in reproductive-age women, impaired decidualization in pregnancy, and altered postmenopausal endometrial physiology. Clinically, these alterations are associated with abnormal uterine bleeding, subfertility, implantation failure, miscarriage, pregnancy complications, and postmenopausal endometrial hyperplasia and cancer. Overall, our review provides novel insights into the molecular mechanisms linking systemic metabolic and endocrine dysfunction with endometrial pathology in PCOS and has broader implications that apply to all women. Full article
(This article belongs to the Special Issue Focus on Endocrine and Metabolic Research Priorities in PCOS/PMOS)
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