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Erschienen in:
01.11.2003 | Original Article
Effects of insulin on luteinizing hormone and prolactin secretion and calcium signaling in female rat pituitary cells
Erschienen in: Archives of Gynecology and Obstetrics | Ausgabe 1/2003
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Introduction
Polycystic ovary syndrome (PCOS) is associated with insulin resistance and hyperinsulinemia, which might contribute to the hypersecretion of luteinizing hormone (LH). Hyperprolactinemia is another finding in a subgroup of patients with PCOS, whereas its relation to hyperinsulinemia is not fully understood yet.
Methods
In the present study we tested the hypothesis that insulin might affect LH or prolactin secretion of cultured female rat pituitary cells. To address the mechanisms by which insulin could act at the intracellular level we examined the GnRH- and TRH-induced Ca2+ signals in single gonadotrophs and lactotrophs, because Ca2+ is an important component of GnRH signal transduction that is closely related to exocytosis.
Results
Cells treated for 24 h with insulin (10−9 M) showed an enhancement of basal and agonist-induced LH and prolactin secretion. Insulin did not affect GnRH- and TRH-induced Ca2+ signals compared to controls. There were no differences neither in the frequency nor in the amplitude of the Ca signal.
Conclusion
Our findings suggest that insulin might contribute to LH hypersecretion. Insulin might be partially responsible for hyperprolactinemia. Since insulin did not affect Ca signaling, other components of the GnRH signal transduction pathway might be involved in LH hypersecretion.