Abstract
Luteinizing hormone (LH) is absolutely required for the maintenance of Leydig cell-specific functions, and this hormone is the main factor that under physiological conditions controls Leydig cell testosterone (T) secretion. It is clear that the ability of LH or human chorionic gonadotropin (hCG), which shares structural, biological, and receptor binding properties with LH (1), to stimulate Leydig cells depends not only on the levels of these hormones, but also on the number and functional activity of the LHIhCG receptor (LH/hCG-R). The interaction of LH/hCG with its receptors initiates a sequence of events at the membrane level, followed by the induction of a number of intracellular events, including activation of adenylate cyclase and cAMP-dependent protein kinase, which is believed to be responsible for most of the effects of the hormone. After the initial stimulation of target cell function, many in vivo and in vitro studies have shown that treatment with LH/hCG also decreases the number of its binding sites and causes desensitization (reviewed in 2, 3). However, the molecular bases of this regulation are poorly understood.
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© 1994 Springer-Verlag New York, Inc.
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Chuzel, F., Schteingart, H., Avallet, O., Vigier, M., Saez, J.M. (1994). Induction by LH/hCG of an Increase in the Rate of Pig Leydig Cell Receptor mRNA Degradation. In: Bartke, A. (eds) Function of Somatic Cells in the Testis. Serono Symposia, USA. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-2638-3_19
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DOI: https://doi.org/10.1007/978-1-4612-2638-3_19
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