Evaluation of Rat Testicular Cell Populations in Experimental Condition of Diabetes Induced in Early Postnatal Life

Diabetes mellitus (DM) causes male infertility by suppression of spermatogenesis and testosterone biosynthesis. The impact of DM on male reproduction was investigated mainly in adulthood, therefore we aimed to study developmental effects of DM, induced in early life, on testicular cell population and fertility. Neonatal (NDM) and pre-pubertal DM (PDM) were induced in immature rats by streptozotocin administration on day 1 or day 10, respectively. Germ (GCs) and somatic cells (Sertoli – SCs and Leydig cells – LCs) were counted in pubertal (25 day) and post-pubertal (45 day) rats in tandem with evaluation of serum testosterone levels and protein expression of androgen receptor. Glucose levels were higher in PDM than in NDM. SCs number was not significantly changed while GCs were reduced only in PDM as a result of incomplete spermatogenesis. Decreased number of LCs at puberty did not affect testosterone production due to higher ratio nuclear/cytoplasm volume. Later, testosterone synthesis diminished more pronounced in PDM. Protein expression of androgen receptor in SCs was altered only in PDM. Reduced sperm concentration and motility was found in both groups. Differential response of testicular cell populations in developing rats to PDM and NDM was suggested associated with altered androgen production and action.