ArticleEndocrine connections2021
Androgens impair β-cell function in a mouse model of polycystic ovary syndrome by activating endoplasmic reticulum stress.
Article in Endocrine connections, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Molecular mechanisms of insulin resistance and altered carbohydrate metabolism in PCOS: a scoping review.Frontiers in endocrinology · 2026Article
- Pathogenesis and treatment of obesity-related polycystic ovary syndrome.Journal of ovarian research · 2025Review
- The Role of Endoplasmic Reticulum Stress in Polycystic Ovary Syndrome and Exploration of Potential Therapeutic Targets.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Opportunities and challenges: interleukin-22 comprehensively regulates polycystic ovary syndrome from metabolic and immune aspects.Journal of ovarian research · 2023Review
- Roles of endoplasmic reticulum stress in the pathophysiology of polycystic ovary syndrome.Frontiers in endocrinology · 2023Review
- The Roles of Androgens in Humans: Biology, Metabolic Regulation and Health.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAndrogens excess results in endoplasmic reticulum (ER) stress, which is an important cause of β cells dysfunction. Here, we investigated the molecular regulation of androgens excess, ER stress, and β-cell function in polycystic ovary syndrome (PCOS).
methodsPCOS mouse model was established by injection of DHEA. Primary cultured mouse islets were used to detect testosterone (TE)-induced ER stress. The response of ER stress, apoptosis, and hyperinsulinemia were analyzed in INS-1 cells with or without TE exposure. Androgen receptor (AR) antagonist and ER stress inhibitor treatment was performed to evaluate the role of TE in ER stress and proinsulin secretion of PCOS mice.
resultsPCOS mice had higher ER stress in islets. TE exposure induced ER stress and apoptosis significantly through sustaining insulin overexpression in β cells, which in turn impaired proinsulin maturation and secretion. Blocking this process could significantly relieve ER stress and apoptosis and improve insulin homeostasis.
conclusionER stress activated by androgens excess in PCOS contributes to β cell dysfunction and hyperinsulinemia.
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