ArticleEndocrine2016
Metabolic actions of insulin in ovarian granulosa cells were unaffected by hyperandrogenism.
Article in Endocrine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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
10 citing papers in PubMed, 22 citations in OpenAlex.
- Glycolysis in polycystic ovary syndrome: pathogenesis and treatment.Journal of ovarian research · 2025Review
- Androgen-Induced Lactic Acid Accumulation Contributes to the Apoptosis of Ovarian Granulosa Cells in Polycystic Ovary Syndrome Mice.Antioxidants (Basel, Switzerland) · 2025Article
- An Update on Physiopathological Roles of Akt in the ReprodAKTive Mammalian Ovary.Life (Basel, Switzerland) · 2024Review
- Essential Role of Granulosa Cell Glucose and Lipid Metabolism on Oocytes and the Potential Metabolic Imbalance in Polycystic Ovary Syndrome.International journal of molecular sciences · 2023Review
- Resveratrol regulates insulin resistance to improve the glycolytic pathway by activating SIRT2 in PCOS granulosa cells.Frontiers in nutrition · 2022Article
- Aberrant elevation of GDF8 impairs granulosa cell glucose metabolism via upregulating SERPINE1 expression in patients with PCOS.Molecular therapy. Nucleic acids · 2021Article
- Article
- Combined use of Diane-35 and metformin improves the ovulation in the PCOS rat model possibly via regulating glycolysis pathway.Reproductive biology and endocrinology : RB&E · 2020Article
- microRNA-126 Is a Tumor Suppressor of Granulosa Cell Tumor Mediated by Its Host Gene EGFL7.Frontiers in oncology · 2019Article
- Follicular hyperandrogenism and insulin resistance in polycystic ovary syndrome patients with normal circulating testosterone levels.Journal of biomedical research · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycystic ovary syndrome (PCOS) patients have intra-ovarian hyperandrogenism and granulosa cells (GCs) from PCOS patients have impaired insulin-dependent glucose metabolism and insulin resistance. The purpose of this study is to determine whether excess androgen affects glucose metabolism and induces insulin resistance of GCs. We firstly explored the insulin metabolic signaling pathway and glucose metabolism in cultured GCs. The Akt phosphorylation and lactate production were increased after insulin treatment. Pre-treatment with PI3-K inhibitor attenuated insulin-induced phosphorylation of Akt and lactate accumulation. However, after treating GCs with different concentrations of testosterone for 5 days, insulin-induced phosphorylation of Akt and lactate production showed no significant change comparing with those of control cells. Finally, mRNA expression of insulin signaling mediators including INSR, IRS-1, IRS-2, and GLUT-4 in GCs was also not significantly altered after testosterone treatment. In conclusion, insulin activates PI3-K/Akt signaling pathway and promotes lactate production in ovarian GCs, but high androgen exerted no obvious influence on insulin signaling pathway and metabolic effect in GCs, suggesting that metabolic actions of insulin in ovarian GCs were unaffected by hyperandrogenism directly.
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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 Socratic graph.