ArticleCell discovery2025
Transgenerational inheritance of diabetes susceptibility in male offspring with maternal androgen exposure.
Article in Cell discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Polyendocrine metabolic ovarian syndrome in pregnancy: pathophysiology and outcomes.Nature reviews. Endocrinology · 2026Review
- Liver sinusoidal endothelial cell fenestrations in metabolic liver disease: from molecular mechanisms to therapeutic perspectives.Cell communication and signaling : CCS · 2026Review
- The role of epigenetic signatures in type 2 diabetes: therapeutic advances and lifestyle interventions.Acta diabetologica · 2026Review
- Sex Differences in the Prevalence and Associated Factors of Metabolic Syndrome: A Cross-Sectional Study of University Employees in China.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Composite dietary antioxidant index is associated with the prevalence of metabolic syndrome in females: results from NHANES 2011-2016.Frontiers in nutrition · 2025Article
- Paternally multi-generational high-fat diet causes obesity and metabolic disorder through intergenerational DNA methylation.Frontiers in nutrition · 2025Article
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
Androgen exposure (AE) poses a profound health threat to women, yet its transgenerational impacts on male descendants remain unclear. Here, employing a large-scale mother-child cohort, we show that maternal hyperandrogenism predisposes sons to β-cell dysfunction. Male offspring mice with prenatal AE exhibited hyperglycemia and glucose intolerance across three generations, which were further exacerbated by aging and a high-fat diet. Mechanistically, compromised insulin secretion underlies this transgenerational susceptibility to diabetes. Integrated analyses of methylome and transcriptome revealed differential DNA methylation of β-cell functional genes in AE-F1 sperm, which was transmitted to AE-F2 islets and further retained in AE-F2 sperm, leading to reduced expression of genes related to insulin secretion, including Pdx1, Irs1, Ptprn2, and Cacna1c. The methylation signatures in AE-F1 sperm were corroborated in diabetic humans and the blood of sons with maternal hyperandrogenism. Moreover, caloric restriction and metformin treatments normalized hyperglycemia in AE-F1 males and blocked their inheritance to offspring by restoring the aberrant sperm DNA methylations. Our findings highlight the transgenerational inheritance of impaired glucose homeostasis in male offspring from maternal AE via DNA methylation changes, providing methylation biomarkers and therapeutic strategies to safeguard future generations' metabolic health.
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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.