Thecal Cell Sensitivity to Luteinizing Hormone and Insulin in Polycystic Ovarian Syndrome
Open accessAbstract
This study examined whether a defect of steroid synthesis in ovarian theca cells may lead to the development of PCOS, through contributions to excess androgen secretion. Polycystic ovarian syndrome (PCOS) is one of the leading causes of infertility worldwide affecting around 1 in 10 of women of a reproductive age. One of the fundamental abnormalities in this syndrome is the presence of hormonal irregularities, including hyperandrogenemia, hyperinsulinemia and hypersecretion of luteinizing hormone (LH). Studies suggest that insulin treatment increases progesterone and androstenedione secretion in PCOS theca cells when compared to insulin treated normal theca cells. Furthermore the augmented effects of LH and insulin have been seen to increase ovarian androgen synthesis in non-PCOS theca cultures whilst also increasing the expression of steroidogenic enzymes specific to the PI3-K pathway. Our examination of primary thecal cultures showed an increase in both the expression of the steroidogenic enzyme CYP17 and androgen secretion in PCOS theca cells under basal conditions, when compared to non-PCOS cells. This was increased significantly under treatments of LH and insulin combined. Our results support the previous reported hypothesis that a dysfunction may exist within the PI3-K pathway. Specifically, that sensitivity exists to physiological symptoms including hyperinsulinemia and hyper secretion of LH found in PCOS through co-stimulation. The impact of these findings may allow the development of a therapeutic target in PCOS.
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Insulin acts on ovarian theca cells by further increasing LH stimulatory effect.
“Insulin acts on ovarian theca cells by further increasing LH stimulatory effect [63].”
From The Role of Glp-1 Receptor Agonists in Insulin Resistance with Concomitant Obesity Treatment in Polycystic Ovary Syndrome (2022) · cites this paper as [63]
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- Authors
- Cadagan, D., Khan, R., & Amer, S.
- Affiliations
- University of Nottingham (GB)
- Corresponding author
- Cadagan, David
- Venue
- Reproductive Biology
- Publisher
- Elsevier BV
- Published
- 2016-03
- Volume
- 16
- Issue
- 1
- Pages
- 53-60
- ISSN
- 1642-431X (ISSN-L)
- OpenAlex
- W2292109795
- Cited by
- 92
- References
- 33
- Citations by year
- 2026: 13 · 2025: 9 · 2024: 10 · 2023: 9 · 2022: 11 · 2021: 15 · 2020: 7 · 2019: 6 · 2018: 6 · 2017: 5 · 2016: 1
- FWCI
- 7.97
- Type
- journal article
- Language
- en
- Open access
- Licence
- Locations
- Reproductive Biology (publishedVersion)
- PubMed (publishedVersion)
- Nottingham ePrints (University of Nottingham) (submittedVersion, cc-by)
- Repository@Nottingham (University of Nottingham) (submittedVersion, cc-by)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Ovarian function and disorders
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Reproductive Biology and Fertility
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Keywords
- polycystic ovary syndrome, theca cells, luteinizing hormone, insulin, androgen production, CYP17, PI3K signaling, steroidogenesis, hyperandrogenemia, hyperinsulinemia, insulin resistance, androstenedione, progesterone
- MeSH terms
- Adult, Androstenedione, Cells, Cultured, Female, Humans, Insulin, Luteinizing Hormone, Middle Aged, Polycystic Ovary Syndrome, Steroid 17-alpha-Hydroxylase, Theca Cells, Gene Expression Regulation, Enzymologic, Young Adult
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