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

Diabetes mellitus (DM) causes male infertility through the suppression of spermatogenesis and testosterone biosynthesis. The impact of DM on male reproduction has mainly been investigated in adulthood, therefore we aimed to study the developmental effects of DM, induced in early life, on testicular cell population and fertility. Neonatal (NDM) and prepubertal 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 the measurement of serum testosterone levels and the protein expression of androgen receptor. Glucose levels were higher in PDM than in NDM. Incomplete spermatogenesis and reduced GC number were found in PDM but not in NDM. LC number, testosterone, and luteinizing hormone (LH) levels were differently altered by both types of DM with a pronounced negative impact of PDM. Protein expression of androgen receptor in SCs was altered only in PDM. Reduced sperm concentration and motility was found in both groups. Thus, our results provide new insights into different mechanisms of action of PDM and NDM on developing germ cells that involved disturbances in androgen production by Leydig cells and androgen action in Sertoli cells.