The synthesis of testosterone (T) in the male organism is carried out by Leydig cells located in the testes and controlled by luteinizing hormone (LH) produced by the anterior pituitary. The LH specifically binds to LH receptors located in the plasma membrane of Leydig cells and stimulates the activity of intracellular signaling pathways coupled with the receptor, which regulate the steroidogenesis. The main role in this regulation belongs to the adenylyl cyclase signaling system which, along with LH receptor, includes Gs-protein, the enzyme adenylyl cyclase catalyzing the cAMP synthesis, and cAMP-dependent effector proteins. In mammals, the process of steroidogenesis is carried out with the participation of StAR protein which transports cholesterol into the mitochondria, where the initial steps of T synthesis occur. The process also involves four steroidogenic enzymes, such as cytochrome P450scc, 3b-hydroxysteroid dehydrogenase (3b-HSD), cytochrome P450-17a possessing 17a-hydroxylase and C17,20-lyase activities, and 17b-hydroxysteroid dehydrogenase (17b-HSD). In different species of mammals and at the different stages of ontogenesis, the order of the reactions of T synthesis and their regulation are characterized by a number of differences. There are D4 and D5 ways of T synthesis, which differ in the stage of isomerization including the displacement of the double bond from the C5—C6 position to the C4—C5. The regulation of T synthesis can take place both by direct interaction of LH-dependent signaling pathways with StAR protein, and indirectly, through the regulation of transcription factors controlling the expression of genes encoding the steroidogenesis enzymes. In the present review the data on the molecular mechanisms of regulation and the ways of T synthesis in mammalian Leydig cells, the species specificity of these ways, as well as on the factors influencing the steroidogenesis are summarized and analyzed.