Adrenocorticotropic Hormone, a New Player in the Control of Testicular Steroidogenesis

Extract

Leydig cell’s principle function is to produce testosterone from cholesterol. In mammals, the ontogenesis of Leydig cell function involves at least two generations of cells. The first generation begins to develop during fetal life and is responsible for the masculinization of the male urogenital system in utero. Although most of the fetal Leydig cells regress in the first 3 months of life, some persist into adult life (1, 2). The second Leydig cell population appears during puberty and produces the testosterone required for the onset of spermatogenesis and maintenance of male reproductive function.

Morphological and functional maturation of the adult Leydig cells appears to be dependent on LH stimulation. Mice lacking either circulating LH or the LH receptor (3–6) fail to demonstrate the normal postnatal increase in Leydig cell numbers and have low or undetectable serum androgen levels (5–8). Furthermore, treatment of LH-deprived rats with LH or human chorionic gonadotropin (hCG) restores, at least partially, the structure and function of Leydig cells (9–12). Similarly, treatment of hypogonadal mouse with daily injections of LH produces a marked increase in most steroidogenic enzyme activity (13). Many in vitro studies using several Leydig cell types have confirmed and extended these observations in vivo (reviewed in Refs.14, 15).