Testicular degeneration and impaired epididymal spermatozoal quality in overweight and obese domestic cats.

Obesity is increasingly recognized as a major health problem in companion animals; however, its impact on male reproductive function in cats remains poorly understood. This study investigated the association between overweight/obese status and testicular morphology, oxidative stress, apoptosis-related cell death, and epididymal spermatozoal quality. Testicular tissues and epididymal spermatozoa obtained from normal-weight and overweight/obese cats were evaluated using histopathology, histomorphometry, immunohistochemistry, TUNEL assay, and functional sperm analyses. Overweight/obese cats exhibited significantly reduced testicular weight together with marked seminiferous tubular degeneration characterized by germinal epithelium thinning, germ cell desquamation, and degenerative changes. Semi-quantitative evaluation of PAS-stained sections confirmed significantly higher proportions of seminiferous tubules containing intraluminal desquamated germ cells, residual/degenerative germ cells in overweight/obese cats. Histomorphometric analysis demonstrated significantly reduced germinal epithelium thickness and cross-sectional surface area, whereas tubular diameter was unaffected. Immunohistochemical evaluation demonstrated significantly reduced PCNA immunoreactivity. A complementary stage-matched analysis further confirmed reduced spermatogonial proliferative activity in overweight/obese cats. In addition, Nrf2 immunoreactivity was significantly reduced, whereas Caspase-3 immunoreactivity and the TUNEL-derived apoptotic index were significantly increased. Epididymal spermatozoa from overweight/obese cats showed significantly reduced motility, concentration, and plasma membrane integrity, increased morphological abnormalities, and elevated mitochondrial reactive oxygen species. Correlation analysis demonstrated significant associations between germinal epithelium thickness and spermatozoal quality parameters. Collectively, these findings demonstrate that overweight/obese status is associated with structural, histomorphometric, molecular, and functional alterations of the feline testis and impaired epididymal spermatozoal quality. These associations suggest that oxidative imbalance and apoptosis-related cell death may contribute to obesity-associated male reproductive dysfunction in domestic cats.