The effect of paternal diet-induced obesity on sperm function and fertilization in a mouse model

• Published in: International journal of andrology 2011-10, Vol.34 (5pt1), p.402-410
• Main Authors: Bakos, H. W., Mitchell, M., Setchell, B. P., Lane, M.
• Format: Article
• Language: English
• Subjects: Acrosome Reaction; Animals; Biological and medical sciences; Body Weight; Diet; DNA Damage; Fertilization; Fundamental and applied biological sciences. Psychology; Gynecology. Andrology. Obstetrics; Male; male fertility; Male genital diseases; Mammalian male genital system; Medical sciences; Metabolic diseases; Mice; Mice, Inbred C57BL; Models, Animal; Obesity; Obesity - etiology; Obesity - metabolism; Paternal Exposure; Reactive Oxygen Species - metabolism; sperm; Sperm Capacitation; sperm function; Spermatozoa - metabolism; Spermatozoa - physiology; Testosterone - blood; Vertebrates: reproduction
• ISSN: 0105-6263; 1365-2605
• DOI: 10.1111/j.1365-2605.2010.01092.x

Summary Although obvious effects of obesity on female reproduction and oocytes are emerging, the effects on male fertility and sperm quality are less clear with studies reporting conflicting results. We hypothesize that male obesity affects sperm function and physiology probably as a result of elevated oxidative stress in spermatozoa and therefore elevated levels of sperm DNA damage and loss of function. Six‐week‐old C57/Bl6 male mice (n = 36) were randomly allocated to two groups: group 1 (n = 18) received a control diet, whereas group 2 (n = 18) received a high‐fat diet (HFD). At the completion of a 9‐week period, mice were sacrificed and spermatozoa were obtained. Sperm motility, concentration, intracellular reactive oxygen species (ROS) production and sperm DNA damage were measured. The ability of the sperm to undergo capacitation, acrosome reaction, sperm binding and ability to fertilize an oocyte were also assessed. The percentage of motile spermatozoa was decreased in the HFD group compared with controls (36 ± 2% vs. 44 ± 4%; p