Differentiation of adult Leydig cells

Key factors in the regulation of fetal and postnatal leydig cell development

“…Mesenchymal Leydig cell precursors proliferate in the prepubertal testis and are recognizable as PLCs at postnatal Day 14-18 in the rat when they first express steroidogenic enzymes (Benton et al, 1995;Ge et al, 1996;Ariyaratne and Chamindrani MendisHandagama, 2000). These cells differentiate into a transitional state, the ILCs which are abundant during puberty.…”

“…In the sexually mature adult, androgens are essential for spermatogenesis, reproductive competence, and maintenance of masculine characteristics. Although all Leydig cells have the capacity to synthesize androgens and share common origins, the fetal and postnatal populations of Leydig cells differ morphologically and have distinct profiles of gene expression (Benton et al, 1995). Soon after testicular determination, fetal Leydig cells differentiate from their interstitial mesenchymal precursors and acquire androgen biosynthetic capacity (Byskov, 1986;Kerr and Knell, 1988).…”

“…These cells do not originate from fetal Leydig cells, but are newly differentiated Leydig cells that arise from pluripotent mesenchymal precursors (Mendis-Handagama et al, 1987). As postnatal Leydig cells differentiate, they transition through three discrete maturational stages termed PLCs, immature (ILCs), and adult Leydig cells (ALCs) (Benton et al, 1995;Ge et al, 1996). These progressively more differentiated states are characterized by decreasing proliferative rate and increasing testosterone biosynthetic capacity (Ge et al, 1996;Mendis-Handagama and Ariyaratne, 2001).…”

Insulin growth factor I and hypogonadism in cirrhosis

“…The need for LH is most likely because of an LH-induced increase in IGF-I receptor number. 13 Leydig cells of mice with a targeted deletion of IGF-I remain histologically immature and produce lower levels of testosterone. 13 On the other hand, administration of IGF-I to patients with IGF-I deficiency caused by absence of GH receptors (Laron syndrome) results in increased testicular size and serum testosterone levels.…”

“…13 Leydig cells of mice with a targeted deletion of IGF-I remain histologically immature and produce lower levels of testosterone. 13 On the other hand, administration of IGF-I to patients with IGF-I deficiency caused by absence of GH receptors (Laron syndrome) results in increased testicular size and serum testosterone levels. 14 The main source of IGF-I for maintaining testicular function is circulating IGF-I.…”