Expression of insulin-like peptide 3 in the postnatal rat Leydig cell lineage: timing and effects of triiodothyronine-treatment

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Abstract
Fetal (FLC) and adult Leydig cells (ALC) secrete insulin-like peptide 3 (INSL3), which is linked to cryptorchidism in the newborn rat. Its gene regulation appears to be independent of that for most steroidogenic enzymes, and may thus be a marker for other aspects of ALC differentiation. Our study examined the following on INSL3 peptide expression in ALC lineage (i) timing, (ii) which cell stage, and (iii) effects of triiodothyronine (T3). Male Sprague–Dawley (SD) rats of postnatal days (pd) 1, 5, 7–21, 28, 40, 60, and 90 were used for the objectives (i) and (ii). For the objective (iii), control and T3-treated (daily T3 SC, 50 μg/kg bw) SD rats of pd7–16 and 21 were used. INSL3 was immunolocalized in Bouin’s-fixed testes. FLC were positive and mesenchymal and Leydig progenitor cells were negative for INSL3 at tested ages. INSL3 in ALC lineage was first detected in newly formed ALC on pd16, although they were present from pd10. The intensity of INSL3 label was greater in ALC of pd40–90. ALC were present in T3-treated testes at pd9, but INSL3 first detected in them was on pd12. While INSL3 in FLC regulates testicular descent, INSL3 in ALC still has no well-defined function. However, its pattern of expression correlates temporally with the development of steroidogenic function and spermatogenesis. Thus, the delay between ALC differentiation and INSL3 expression in them implies that INSL3 in ALC is associated with maturation. The advancement of INSL3 expression in the ALC of T3-treated rats implies that this function is established earlier with T3-treatment.