Thecal cell sensitivity to luteinizing hormone and insulin in polycystic ovarian syndrome
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...
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| Format: | Article |
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Elsevier
2016
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| Online Access: | https://eprints.nottingham.ac.uk/44223/ |
| _version_ | 1848796865830584320 |
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| author | Cadagan, David Khan, Raheela Amer, Saad A. |
| author_facet | Cadagan, David Khan, Raheela Amer, Saad A. |
| author_sort | Cadagan, David |
| building | Nottingham Research Data Repository |
| collection | Online Access |
| description | 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. |
| first_indexed | 2025-11-14T19:54:47Z |
| format | Article |
| id | nottingham-44223 |
| institution | University of Nottingham Malaysia Campus |
| institution_category | Local University |
| last_indexed | 2025-11-14T19:54:47Z |
| publishDate | 2016 |
| publisher | Elsevier |
| recordtype | eprints |
| repository_type | Digital Repository |
| spelling | nottingham-442232020-05-04T17:39:20Z https://eprints.nottingham.ac.uk/44223/ Thecal cell sensitivity to luteinizing hormone and insulin in polycystic ovarian syndrome Cadagan, David Khan, Raheela Amer, Saad A. 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. Elsevier 2016-03-31 Article PeerReviewed Cadagan, David, Khan, Raheela and Amer, Saad A. (2016) Thecal cell sensitivity to luteinizing hormone and insulin in polycystic ovarian syndrome. Reproductive Biology, 16 (1). pp. 53-60. ISSN 2300-732X 17α-Hydroxylase Androgen Insulin Luteinizing hormone Theca https://doi.org/10.1016/j.repbio.2015.12.006 doi:10.1016/j.repbio.2015.12.006 doi:10.1016/j.repbio.2015.12.006 |
| spellingShingle | 17α-Hydroxylase Androgen Insulin Luteinizing hormone Theca Cadagan, David Khan, Raheela Amer, Saad A. Thecal cell sensitivity to luteinizing hormone and insulin in polycystic ovarian syndrome |
| title | Thecal cell sensitivity to luteinizing hormone and insulin in polycystic ovarian syndrome |
| title_full | Thecal cell sensitivity to luteinizing hormone and insulin in polycystic ovarian syndrome |
| title_fullStr | Thecal cell sensitivity to luteinizing hormone and insulin in polycystic ovarian syndrome |
| title_full_unstemmed | Thecal cell sensitivity to luteinizing hormone and insulin in polycystic ovarian syndrome |
| title_short | Thecal cell sensitivity to luteinizing hormone and insulin in polycystic ovarian syndrome |
| title_sort | thecal cell sensitivity to luteinizing hormone and insulin in polycystic ovarian syndrome |
| topic | 17α-Hydroxylase Androgen Insulin Luteinizing hormone Theca |
| url | https://eprints.nottingham.ac.uk/44223/ https://eprints.nottingham.ac.uk/44223/ https://eprints.nottingham.ac.uk/44223/ |