## 3 Discussion
It is important to note that the stimulatory effect of TP4/2 on the expression of genes encoding StAR and cytochrome CYP17A1 was not so pronounced in comparison with hCG treatment, which indicates a more moderate effect of LMW allosteric agonist on the testicular steroidogenesis (Figure 4A). Thus, five-day administration of TP4/2 provides a stable increase in T levels, but does not cause hyperactivation of the steroidogenesis system and does not suppress the LHCGR gene expression. In women, the main area of possible use of LMW agonists of LHCGR is the assisted reproductive technologies, primarily in vitro fertilization [19; 20]. In men, the prospects for their use are associated with the treatment of hypogonadotrophic hypogonadism, androgen deficiency and infertility. Production of androgens and the sperm count and quality in men are decreased in a number of metabolic and endocrine diseases, including T1 DM [28; 29; 31], as well as in aging [32; 33; 34; 62]. Despite the differences in etiology and pathogenesis of reproductive dysfunctions in T1 DM and aging, the main causes of androgen deficiency and impaired spermatogenesis are the reduced T production by Leydigcells due to an increase in oxidative stress, inflammation and apoptosis in the testes, as well as the hormonal dysregulation due to an imbalance between signaling cascades regulated by gonadotropins, insulin, insulin-like growth factor-1 and adipokines in testicular cells [28; 38; 63]. We demonstrated a decrease in hCG-induced AC stimulation in the testicular membranes of diabetic and aging rats (Figure 1), as well as a weakening of the stimulating effect of hCG on the blood and intratesticular T levels and on the testicular expression of genes encoding StAR and cytochrome CYP17A1 (Figures 2-4; Table 2). Since cAMP-dependent cascades are directly involved in the regulation of steroidogenesis in Leyd cells, controlling the gene expression and activity of StAR and steroidogenic enzymes [6; 7; 9; 10; 11; 12], the weakening of the AC response to hCG shown by us indicates an important contribution of disturbances in the gonadotropin-regulated AC signaling system into a decrease in hCG-stimulated steroidogenesis in T1 DM and aging. In diabetic and aging rats treated with hCG, we found different changes in the testicular expression of steroidogenic genes, which we believe may be compensatory. In hCG-treated diabetic rats, expression of the _Cyp11a_ gene encoding cytochrome P450\({}_{\text{scc}}\), responsible for synthesis of pregnenolone, was decreased, while the expression of the _Hsd3b_ gene encoding dehydrogenase HSD3\(\beta\), which catalyzes the next stage of steroidogenesis, the conversion of pregnenolone into progesterone, was increased (Figure 4). At the same time, in aging rats, the stimulating effect of hCG on the _Cyp11a1_ expression remained the same as in the control, and we did not detect an increase in the _Hsd3b_ gene expression, as in T1 DM (Figure 4). The changes in the expression of steroidogenic genes in T1 DM and aging were shown by other authors [64; 65; 66]. Chinese scientists reported that in Leyd cells under the conditions of severe hyperglycemia and increased levels of advanced glycation end products, expression of the _Star_, _Cyp11a1_ and _Hsd3b_ genes was reduced [66]. In our case, the baseline expression of these genes was changed insignificantly, which may be due to a moderate form of T1 DM. In aging brown Norwegian rats, along with T deficiency, a decrease in the expression of the _Star_ and _Cyp11a1_ genes and a decrease in the amount of StAR and cytochrome P450\({}_{\text{scc}}\) proteins encoded by them were detected [64], and in two-year-old Wistar rats, the expression of the steroidogenic genes was decreased to varying degrees [65]. In our study of aging rats, there were no significant changes in the baseline expression of the steroidogenic genes, but a decrease in the hCG stimulating effect on the _Star_ expression was shown (Figure 4).