Specific binding sites for insulin-like growth factor I in the ovarian stroma of women with polycystic ovarian disease and stromal hyperthecosis
Article Abstract:
Women with hyperandrogenism (high levels of androgens, male sex hormones) due to ovarian hyperthecosis (overgrowth of cells) often also have hyperinsulinemia (high blood insulin levels) and increased tissue resistance to insulin actions. Insulin acts by binding receptors, proteins on the cell surface which are selective for insulin, and the actions the bound receptors stimulate are responsible for tissue sensitivity or resistance to insulin. Insulin can stimulate ovarian androgen production in laboratory studies, but is not likely to do so in these women due to the widespread insulin receptor-linked insulin resistance. However, insulin can also act through a second group of receptors which are regulated by insulin-like growth factors. To determine the relevance of these types of receptors to hyperandrogenism, the levels of receptors for insulin and insulin-like growth factor I were measured in seven healthy women and five women with ovarian hyperthecosis. Women with hyperthecosis had fewer apparent ovarian insulin receptors. Receptors for insulin-like growth factor I were similar in both groups of women. Insulin bound poorly to receptors for the growth factor, and further research is needed to determine whether insulin can stimulate ovarian androgen production by acting through insulin-like growth factor I receptors. The authors claim that the findings suggest that in women with both hyperthecosis and hyperinsulinemia, insulin-like growth factor may stimulate synthesis of ovarian androgen. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Obstetrics and Gynecology
Subject: Health
ISSN: 0002-9378
Year: 1990
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Steroid biosynthesis in the Sertoli-Leydig cell tumor: effects of insulin and luteinizing hormone
Article Abstract:
Sertoli-Leydig cell tumor (arrhenoblastoma) is a rare tumor of the ovary in which cells, similar to those found in the testicles, secrete the male steroid hormone testosterone. Women having this tumor stop menstruating, and develop male characteristics, such as excess hair and a deep voice. It is thought that male cells remaining during ovarian development cause the growth of this tumor. Sertoli-Leydig cell tumors have been reported in some women with polycystic ovarian syndrome, a condition characterized by excess hair and infertility due to the absence of ovulation and menstruation. In addition to having higher levels of testosterone, women with polycystic ovarian syndrome commonly have high levels of the female luteinizing hormone (LH) and insulin. The cells removed from a 44-year-old patient with Sertoli-Leydig cell tumor were grown in the laboratory to study the pattern of steroid production and the effects of LH and insulin on cell activity. It was found that testosterone increased because the precursors needed to make testosterone were elevated. When the cultured cells were exposed to LH, male hormone production increased. Receptors on the surface of the tumor cells had a particular affinity for insulin. The results suggest that high insulin and LH levels may play a role in the development of Sertoli-Leydig cell tumors in patients with polycystic ovarian syndrome. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Obstetrics and Gynecology
Subject: Health
ISSN: 0002-9378
Year: 1989
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Specific binding and growth-promoting activity of insulin in endometrial cancer cells in culture
Article Abstract:
Insulin seems capable of stimulating endometrial cancer cells. Researchers used radioactively labelled insulin to test the effect of insulin on five different types of endometrial cancer cells in culture. The insulin bound to the cells, indicating that the cells have a receptor for insulin. Insulin-like growth factors I and II also bound to the cells, although not as strongly as insulin. Insulin also caused the cells to proliferate. This indicates that excess levels of insulin, a condition called hyperinsulinemia, could stimulate endometrial cancer.
Publication Name: American Journal of Obstetrics and Gynecology
Subject: Health
ISSN: 0002-9378
Year: 1998
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