Long-term diet-induced obesity disrupts testicular activity in Wistar rats: biochemical, hormonal, and structural evidence.

The increasing prevalence of obesity has been closely associated with male reproductive disorders. Studies on diet-induced obesity provided valuable insights into the factors involved in the decline of male reproductive potential in obese subjects. The aim of the present study was to investigate the consequences of long-term exposure to cafeteria diet, particularly on testicular activity, and pinpoint the most affected components by this condition. The study was conducted on male Wistar rats fed either a standard chow or a cafeteria diet during 16 weeks. A model of diet-induced obesity was assessed, and anthropometrical measures, hormonal, biochemical, and redox profiles were evaluated. Histological, transmission electron microscopic (TEM) and morphometric analysis of the testes as well as the immunolabelling of AR were carried out. DNA fragmentation index was also measured in both groups. The results showed an increase in body weight correlated with elevated BMI and Lee Index values. The elevated fat coefficient was also associated with unbalanced hormonal profile and biochemical parameters. Our histological findings showed altered cytoarchitecture, including sloughing of germ cells into the lumen, and degenerative organelles, along with morphometric measurement changes and decreased immunolabelling of androgen receptors. In addition, oxidative stress markers and DNA fragmentation index increased in the cafeteria diet fed group. Long-term exposure to cafeteria diet had significant impact on testicular function, particularly on structural integrity of seminiferous tubules. Chronic hyperglycemia, insulin resistance and oxidative stress appear to be key factors contributing to the impairment of the male reproductive potential.