DIABETES MELLITUS AND TESTICULAR DAMAGE: LITERATURE REVIEW

DIABETES MELLITUS AND TESTICULAR DAMAGE

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DOI:

https://doi.org/10.24862/cco.v21i2.2214

Abstract

Diabetes mellitus (DM) is a condition of chronic hyperglycemia and represents one of the greatest concerns for global health in modern times. It is considered a heterogeneous metabolic disorder resulting from a defect in insulin secretion, resistance to insulin action or both. Regardless of the type, DM is a recognized cause of male sexual dysfunction and affects male reproductive function, both in men and in animal models, at multiple levels, including endocrine control of spermatogenesis, spermatogenesis itself, dysfunction in penile erection and ejaculation. Testicular dysfunction is characteristically marked by a decrease in testicular weight, sperm count and motility, in addition to the morphology of the seminiferous epithelium. Changes in testosterone levels are also characteristic of diabetic animals. Previous studies demonstrate that DM increases apoptosis in testicular germ cells and can lead to an interruption in spermatogenesis, mainly influencing the Bcl-2 family of proteins and caspases. Furthermore, DM also causes increased oxidative stress in testicular cells. Excess production of reactive oxygen species (ROS), via the mitochondrial electron transport chain, has been demonstrated in DM. Understanding the various testicular disorders caused by DM can clarify several questions regarding sexual dysfunction caused by DM and even provide the development of strategies and/or medications that can contain the progression of these testicular damages, thus avoiding a compromise in testicular function in patients and animals with this disease.

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Published

2026-06-29

How to Cite

Caiaffo, V., Bezerra de Sa, F., Evêncio Neto, J., Duarte Ribeiro de Oliveira, B., & Amaro da Silva Júnior, V. (2026). DIABETES MELLITUS AND TESTICULAR DAMAGE: LITERATURE REVIEW: DIABETES MELLITUS AND TESTICULAR DAMAGE. Conexão Ciência Online, 21(2), 200–212. https://doi.org/10.24862/cco.v21i2.2214