ArticleReproductive biology and endocrinology : RB&E2020
Decreased brain and muscle ARNT-like protein 1 expression mediated the contribution of hyperandrogenism to insulin resistance in polycystic ovary syndrome.
Article in Reproductive biology and endocrinology : RB&E, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Accurate Measurement of Serum Free Testosterone Levels via Liquid Chromatography‒Tandem Mass Spectrometry (LC‒MS/MS) has Predictive Value in the Diagnosis of Polycystic Ovary Syndrome and Associated Metabolic Disorders.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- The crosslink between autophagy and ferroptosis in polycystic ovary syndrome: from synergistic pathogenesis to targeted therapy.Journal of ovarian research · 2026Review
- Developmental programming: gestational exposure to excess testosterone disrupts maternal steroid homeostasis and perturbs the steroid-lipid relationship in sheep.Molecular and cellular endocrinology · 2026Article
- Molecular mechanisms of insulin resistance and altered carbohydrate metabolism in PCOS: a scoping review.Frontiers in endocrinology · 2026Article
- Ameliorative effects ofJournal of traditional and complementary medicine · 2025Article
- Research progress on the pathogenesis, clinical impact, and traditional Chinese medicine treatment of polycystic ovary syndrome complicated by insulin resistance.Frontiers in pharmacology · 2025Review
- Exploration of the molecular mechanism of melatonin against polycystic ovary syndrome based on a network pharmacology approach and experimental validation.Frontiers in endocrinology · 2025Article
- Lower Serum ATG7 Levels Linked to Insulin Resistance in Women with Polycystic Ovary Syndrome.Medical science monitor : international medical journal of experimental and clinical research · 2024Article
- Period circadian regulator 2-mediated steroid hormone synthesis by regulating transcription of steroidogenic acute regulatory protein in porcine granulosa cells.Journal of animal science · 2024Article
- Circular RNA as a Novel Regulator and Promising Biomarker in Polycystic Ovary Syndrome.Biomolecules · 2023Review
- Antioxidative Effects of StandardizedAntioxidants (Basel, Switzerland) · 2022Article
- Therapeutic potential of exosomes/miRNAs in polycystic ovary syndrome induced by the alteration of circadian rhythms.Frontiers in endocrinology · 2022Review
- Melatonin, Clock Genes, and Mammalian Reproduction: What Is the Link?International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe interface between environmental risk factors and genetic factors could contribute to the pathogenesis of hyperandrogenism and insulin resistance in polycystic ovary syndrome (PCOS); however, the underlying complex mechanism remains to be elucidated.
methodsWe used dehydroepiandrosterone (DHEA)-induced PCOS-like rat model to measure circadian clock genes and insulin resistance-related genes. Additionally, we performed in vitro experiments in mature adipocytes to verify the molecular mechanisms.
resultsDHEA-induced PCOS-like rats exhibited insulin resistance and arrhythmic expression of circadian clock genes in the liver and adipose tissues, particularly showing decreased brain and muscle ARNT-like protein 1 (BMAL1) expression. In addition, hyperandrogenism gave rise to negative regulation of BMAL1 expression to nicotinamide phosphoribosyltransferase and sirtuin 1, which further inhibited downstream glucose transporter type 4, leading to insulin resistance in mature adipocytes, which was consistent with our previous results in HepG2 cells.
conclusionsDecreased BMAL1 expression in the liver and adipose played a potentially novel role in the contribution of hyperandrogenism to insulin resistance, which might be a possible mechanism accounting for the pathogenesis of PCOS.
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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.