General

Luteinizing hormone (LH) and follicle stimulating hormone (FSH) are required for the development and maintenance of testicular functions. LH is the most important hormone for control of Leydig cell functions, but other hormones and locally produced factors also play a role. Hormones regulate steroid production by controlling the metabolic activities in existing cells, but they also control the size of the Leydig cell population via control of proliferation and differentiation (Chemes 1996). In the foetal period around 14 weeks of gestation there is a sharp increase in the number and activity of Leydig cells. In this developmental period maternal hCG plays an important role for the regulation of Leydig cell activities. It is less clear what controls Leydig cell development before this period, but there is good evidence that early Leydig cell development and onset of steroid production take place without gonadotropin stimulation. During postnatal development of the human testis major changes occur in the Leydig cell population. In the early neonatal period gonadotropins stimulate the development and activity of foetal Leydig cells to such an extent that during the first three months of life peripheral and testicular levels of testosterone are similar, as during puberty. In the next period of the first year these foetal Leydig cells regress via ill-defined mechanisms and a dormant phase remains until puberty. During puberty a second wave of proliferation and differentiation occurs under the influence of rising plasma LH levels. This ultimately leads to the adult population of Leydig cells (Chemes 1996; Saez 1994)

Many studies on the short-term effects of LH on steroid production have been carried out with isolated cells from rats or mice. These in vitro systems are less suitable for investigations on long-term or trophic effects of hormones, since isolated cells change their phenotypic properties after prolonged culture periods owing to the absence or abnormal composition of local growth factors. Tumour cell lines, such as the MA-10 mouse tumour cell line, are much more constant in their functional properties and are thus a better choice for these investigations of trophic effects. However, the regulatory systems in tumour cells and normal cells are not always the same.

Basically, regulation of Leydig cell function is the same as for other somatic cells. Via their receptors protein hormones and growth factors control phosphorylation of important cellular proteins, either via direct activation of kinases or indirectly via elevations in the level of intracellular second messengers. The covalently modified or newly synthesized proteins can then affect a variety of activities in discrete subcellular structures (plasma membrane, mitochondria, cytoskeleton, nuclei, etc.). As a result of a complex interplay between these intracellular activities, different physiological responses are generated (steroid production, energy production, cell growth, protein secretion, etc.). Since one hormone often stimulates multiple transducing systems (pleiotypic response) that may show different response kinetics, it is not easy to link specific transducing pathways to particular responses (see Figure 1.4).

Hair Loss Prevention

Hair Loss Prevention

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