Testicular germ cell apoptosis and sperm defects in mice upon long‐term high fat diet feeding

• Published in: Journal of cellular physiology Vol. 233; no. 10; pp. 6896 - 6909
• Main Authors: Ghosh, Songita, Mukherjee, Sutapa
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01.10.2018
• Subjects: Antioxidants; Apoptosis; Atrophy; Deregulation; Diet; Germ cells; High fat diet; Infertility; Insulin; Mice; Mitochondria; Morphology; Oxidative stress; Reactive oxygen species; Sperm; sperm defects; Spermatozoa; Testes; testicular germ cells; Time dependence; Tubules; apoptosis; sperm defects; high fat diet; oxidative stress; testicular germ cells
• DOI: 10.1002/jcp.26581
• ISSN: 0021-9541; 1097-4652

The growing prevalence of male infertility is a matter of serious concern. One of the putative causes being nutritional excess from continuous consumption of high fat diet (HFD) leading to insulin resistance albeit the specific relationship is not fully understood. Besides, there are many contradictions in the available literature on the subject. Therefore, we sought to characterize in detail the effects of HFD upon testicular function and sperm quality in mice with particular focus on isolated testicular germ cells and spermatozoa, respectively. In this study, we treated 8‐week old male Swiss albino mice with HFD for the duration of 5 months; control animals were reared on standard diet. We observed HFD induced progressive deterioration of testicular histoarchitecture leading to disruption of seminiferous tubules, increased vacuolization, and partial to complete tubular atrophy. Time dependent adverse effects on sperm count, motility, and morphology were noticed. Interestingly, numerous anomalies were detectable in sperm head and tail structures reflecting loss of reproductive capacity due to HFD. Maximal tissue and sperm damage was conspicuous at the endpoint, prompting us to examine oxidative stress markers. Enhanced intracellular reactive oxygen species (ROS) generation, augmentation of prooxidant activities, and compromised testicular antioxidant defences clearly implied conditions of oxidative stress in long‐term HFD treated mice. This was concomitant with the onset of abnormally enhanced testicular germ cell apoptosis involving the mitochondrial intrinsic pathway. Thus, our findings revealed that ROS mediated deregulation of testicular germ cell apoptosis is critical in male reproductive impairment due to diet induced obesity. The present study highlights the impact of long‐term continuous consumption of high dietary fat upon male fertility. It is evident that reactive oxygen species (ROS) mediated deregulation of testicular germ cell apoptosis and sperm dysfunction is critical in male reproductive impairment under conditions of obesity and insulin resistance.