Purpose: To consider the basic principles and methods of experimental modeling of hypogonadism in laboratory animals, to define the main benefits and drawbacks of each separate method in hypogonadism modeling. Materials and methods: We analyzed modern foreign and domestic literature using the following databases: PubMed / Medline, Embase, Google Scholar. Results: Presently, there are three main principles of modeling hypogonadism: surgical, genetic, and pharmacological. The principle of surgical modeling of hypogonadism is based on the removal of the gonads, or on the temporary imposition of a suture on the distal section of the spermatic cord, which leads to occlusion of the testicular artery that feeds the gonads. The principle of genetic modeling of hypogonadism is to induce mutations in the genes encoding the most important regulatory molecules, in particular kisspeptin, neurokinin B, and their receptors in laboratory animals. The principle of pharmacological modeling of hypogonadism is based on the administration of streptozocin to laboratory animals, which has a toxic effect on the gonads and pancreas. Conclusion: Hypogonadism represents a very common pathological condition that affects many organs and tissues. Therefore, the use of experimental models of hypogonadism to study fundamental pathophysiological and pathomorphological processes is a relevant research area. Each principle of hypogonadism modeling is unique in its own way, exhibits advantages and disadvantages, and allows the creation of specific conditions necessary for the development of hypogonadism in laboratory animals. Taking into account the numerous beneficial effects of testosterone on many cells and tissues of the human body, it becomes obvious that experimental models of hypogonadism can be in demand for many medical spheres.
Experimental models of inflammation in laboratory animals
