ArticleThe Journal of clinical endocrinology and metabolism2014
Parent-of-origin effects on glucose homeostasis in polycystic ovary syndrome.
Article in The Journal of clinical endocrinology and metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- The stromal microenvironment of ovary: a novel area in polycystic ovary syndrome.Journal of ovarian research · 2026Review
- On the Intimate Relationship of Adiposity to Polycystic Ovary Syndrome.The Journal of clinical endocrinology and metabolism · 2025Review
- Autoantibodies Targeting the Hypothalamic-Pituitary-Ovarian Axis in Polycystic Ovary Syndrome: Emerging Key Players in Pathogenesis?International journal of molecular sciences · 2025Review
- Deconstructing a Syndrome: Genomic Insights Into PCOS Causal Mechanisms and Classification.Endocrine reviews · 2022Article
- Impact of Endocrine Disruptors upon Non-Genetic Inheritance.International journal of molecular sciences · 2022Review
- Profile of Daughters and Sisters of Women With Polycystic Ovary Syndrome: The Role of Proband's Glucose Tolerance.The Journal of clinical endocrinology and metabolism · 2022Observational
- Epigenetic transgenerational inheritance of parent-of-origin allelic transmission of outcross pathology and sperm epimutations.Developmental biology · 2020Article
- The tempo of human childhood: a maternal foot on the accelerator, a paternal foot on the brake.Evolutionary anthropology · 2018Review
- Genetic Variants Associated with Hyperandrogenemia in PCOS Pathophysiology.Genetics research international · 2018Review
- The Pathogenesis of Polycystic Ovary Syndrome (PCOS): The Hypothesis of PCOS as Functional Ovarian Hyperandrogenism Revisited.Endocrine reviews · 2016 · on this mapReview
- Sex and Gender Differences in Risk, Pathophysiology and Complications of Type 2 Diabetes Mellitus.Endocrine reviews · 2016Review
- Perspectives in Polycystic Ovary Syndrome: From Hair to Eternity.The Journal of clinical endocrinology and metabolism · 2016Article
- Review
- Polycystic ovary syndrome as a paradigm for prehypertension, prediabetes, and preobesity.Current hypertension reports · 2014Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
contextPolycystic ovary syndrome (PCOS) is a highly heritable complex trait. Parents of affected women have reproductive and metabolic phenotypes.
objectiveWe tested the hypothesis that there are parental effects on the heritability of fasting dysglycemia in women with PCOS. DESIGN AND
settingThis was a cross-sectional study at an academic medical center.
participantsPARTICIPANTS included 367 women with PCOS and their parents (1101 total subjects).
main outcome measuresWe compared maternal and paternal contributions to heritability of fasting dysglycemia and to transmission of the PCOS susceptibility allele of D19S884 within the fibrillin-3 gene (D19S884-A8) on fasting dysglycemia.
resultsFathers had higher fasting glucose levels, prevalence of fasting dysglycemia and proinsulin to insulin molar ratios (P < .0001), a marker of defective insulin processing, compared with mothers. Heritability of fasting dysglycemia was significant in PCOS families (h(2) = 37%, SE = 10%, P = .001). Maternal heritability (h(2) = 51%, SE = 15%, P = .0009) was higher than paternal heritability (h(2) = 23 %, SE = 23%, P = .186) of fasting dysglycemia after adjustment for age and body mass index. Within dysglycemic probands, there was increased maternal compared with paternal transmission of D19S884-A8 (maternal 84% vs paternal 45%, χ(2) = 6.51, P = .011).
conclusionsThere was a sex difference in the parental metabolic phenotype with fathers having an increased risk of fasting dysglycemia and evidence for pancreatic β-cell dysfunction compared with mothers. However, only maternal heritability had significant effects on the prevalence of fasting dysglycemia in women with PCOS. Furthermore, there were maternal parent-of-origin effects on transmission of D19S884-A8 probands with fasting dysglycemia. These findings suggest that maternal factors, genetic and perhaps epigenetic, contribute to the metabolic phenotype in affected women.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.