In men with type 2 diabetes mellitus (T2DM), steroidogenesis and spermatogenesis are impaired. Metformin and the agonists of luteinizing hormone/human chorionic gonadotropin(hCG)‐receptor (LH/hCG‐R) (hCG, low‐molecular‐weight allosteric LH/hCG‐R‐agonists) can be used to restore them. The aim was to study effectiveness of separate and combined administration of metformin, hCG and 5‐amino‐N‐tert‐butyl‐2‐(methylsulfanyl)‐4‐(3‐(nicotinamido)phe-nyl)thieno[2,3‐d]pyrimidine‐6‐carboxamide (TP3) on steroidogenesis and spermatogenesis in male rats with T2DM. hCG (15 IU/rat/day) and TP3 (15 mg/kg/day) were injected in the last five days of five‐week metformin treatment (120 mg/kg/day). Metformin improved testicular steroidogenesis and spermatogenesis and restored LH/hCG‐R‐expression. Compared to control, in T2DM, hCG stimulated steroidogenesis and StAR‐gene expression less effectively and, after five‐day administration, reduced LH/hCG‐R‐expression, while TP3 effects changed weaker. In co‐administration of metformin and LH/hCG‐R‐agonists, on the first day, stimulating effects of LH/hCG‐R‐agonists on testosterone levels and hCG‐stimulated expression of StAR‐ and CYP17A1‐genes were increased, but on the 3–5th day, they disappeared. This was due to reduced LH/hCG‐R‐gene expression and increased aromatase‐catalyzed estradiol production. With co‐administration, LH/hCG‐R‐agonists did not contribute to improving spermatogenesis, induced by metformin. Thus, in T2DM, metformin and LH/hCG‐R‐agonists restore steroidogenesis and spermatogenesis, with metformin being more effective in restoring spermatogenesis, and their co‐administration improves LH/hCG‐R‐agonist‐stimulating testicular steroidogenesis in acute but not chronic administration.