In type 1 diabetes mellitus (DM1), testicular synthesis of testosterone is impaired, leading to androgen insufficiency and disorders of spermatogenesis. Long-term use of high gonadotropin doses for the correction of these abnormalities leads to a decrease in the sensitivity of luteinizing hormone/human chorionic gonadotropin (LH/hCG) receptors in Leydig cells. The aim of this work was to study the effect of 3-day treatment of DM1 (streptozotocin-induced, 45 mg/kg) male Wistar rats with the allosteric LH/hCG receptor agonist 5-amino-N-tert-butyl-2-(methylsulfanyl)-4-(3-(nicotinamido)phenyl)thieno[2,3-d]pyrimidine-6-carboxamide (TP03, 15 mg/kg per day) on the effects of a relatively low hCG dose (10 IU/rat, single dose, s.c.) on blood testosterone levels, expression of steroidogenesis genes, and morphometric parameters of the seminiferous tubules. Pretreatment of rats with TP03 enhanced the stimulating effect of hCG on blood testosterone levels. This effect was produced, on the one hand, by enhanced steroidogenesis due to an increase in the expression of the Cyp11a1 gene, which encodes the mitochondrial cytochrome P450 side-chain cleavage enzyme (P450scc) responsible for the first stage of testosterone synthesis, and, on the other hand, by improved testicular sensitivity to gonadotropins due to an increase in the testicular LH/hCG receptor content in DM1 rats. In addition, pretreatment of DM1 rats with TP03 followed by hCG stimulation resulted in a more pronounced improvement in the morphometric parameters of the seminiferous tubules as compared to the groups that received TP03 or hCG alone. Thus, TP03 enables to increase the effectiveness of the hCG steroidogenic effect and reduce the dose of gonadotropin, which compensates for an androgen deficiency in diabetes.