ArticleDisease models & mechanisms2012
Loss of PKBβ/Akt2 predisposes mice to ovarian cyst formation and increases the severity of polycystic ovary formation in vivo.
Article in Disease models & mechanisms, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Prenatal Exposure to PFOA Induces Ovarian Function Impairment via the Disruption of the PPARγ/ANGPTL4 Pathway.Environment & health (Washington, D.C.) · 2026Article
- Deconvolution at the single-cell level reveals ovarian cell-type-specific transcriptomic changes in PCOS.Reproductive biology and endocrinology : RB&E · 2024Article
- Metabolic hormones are integral regulators of female reproductive health and function.Bioscience reports · 2024Review
- Chamomile and Urtica dioica extracts improve immunological and histological alterations associated with polycystic ovarian syndrome in DHEA -induced mice.BMC complementary medicine and therapies · 2023Article
- SHORT Syndrome: an Update on Pathogenesis and Clinical Spectrum.Current diabetes reports · 2022Review
- Fractalkine and apoptotic/anti-apoptotic markers in granulosa cells of women with polycystic ovarian syndrome.Molecular biology reports · 2020Article
- Metformin Prevents Follicular Atresia in Aging Laying Chickens through Activation of PI3K/AKT and Calcium Signaling Pathways.Oxidative medicine and cellular longevity · 2020Article
- Animal Models for Human Polycystic Ovary Syndrome (PCOS) Focused on the Use of Indirect Hormonal Perturbations: A Review of the Literature.International journal of molecular sciences · 2019Review
- Article
- Molecular characterization of insulin resistance and glycolytic metabolism in the rat uterus.Scientific reports · 2016Article
- Fractalkine restores the decreased expression of StAR and progesterone in granulosa cells from patients with polycystic ovary syndrome.Scientific reports · 2016Article
- Insulin signalling and glucose transport in the ovary and ovarian function during the ovarian cycle.The Biochemical journal · 2016Review
- Genetic Rodent Models of Obesity-Associated Ovarian Dysfunction and Subfertility: Insights into Polycystic Ovary Syndrome.Frontiers in endocrinology · 2016Review
- Hepatic proteomic analysis revealed altered metabolic pathways in insulin resistant Akt1(+/-)/Akt2(-/-) mice.Metabolism: clinical and experimental · 2015Article
- PIK3R1 mutations cause syndromic insulin resistance with lipoatrophy.American journal of human genetics · 2013Article
- Molecular crosstalk between insulin-like growth factors and follicle-stimulating hormone in the regulation of granulosa cell function.Reproductive medicine and biologyReview
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ovarian cysts affect women of all ages and decrease fertility. In particular, polycystic ovarian syndrome (PCOS), in which multiple follicular cysts develop, affects 5-10% of women of reproductive age and can result in infertility. Current non-invasive treatments for PCOS can resolve cysts and restore fertility, but unresponsive patients must undergo severe ovarian wedge resection and resort to in vitro fertilization. PCOS is related to the deregulation of leutinizing hormone (LH) signaling at various levels of the hypothalamic-pituitary-ovarian axis and resultant hyperproduction of androgens. Because insulin resistance and compensatory hyperinsulinemia are observed in 50-70% of individuals with PCOS, deregulated insulin signaling in the ovary is considered an important factor in the disease. Here we report that aged mice specifically lacking the PKBβ (also known as Akt2) isoform that is crucial for insulin signaling develop increased testosterone levels and ovarian cysts, both of which are also observed in insulin-resistant PCOS patients. Young PKBβ knockout mice were used to model PCOS by treatment with LH and exhibited a cyst area that was threefold greater than in controls, but without hyperinsulinemia. Thus, loss of PKBβ might predispose mice to ovarian cysts independently of hyperactive insulin signaling. Targeted therapeutic augmentation of specific PKBβ signaling could therefore provide a new avenue for the treatment and management of ovarian cysts.
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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.