title: The effect of paternal diet-induced obesity on sperm function and fertilization in a mouse model.
abstract: 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 < 0.05). Intracellular ROS was elevated (692 ± 83 vs. 409 ± 22 units; p < 0.01) in the HFD group compared with controls. Sperm DNA damage was also increased (1.64 ± 0.6% vs. 0.17 ± 0.06%; p < 0.05) in the HFD group compared with the control group. Furthermore, the percentage of non-capacitated sperm was significantly lower compared with controls (12.34% vs. 21.06%; p < 0.01). The number of sperm bound to each oocyte was significantly lower (41.14 ± 2.5 vs. 58.39 ± 2.4; p < 0.01) in the HFD group compared with that in controls and resulted in significantly lower fertilization rates (25.9% vs. 43.9%; p < 0.01). This report provides evidence that obesity may induce oxidative stress and sperm DNA damage as well as decreased fertilizing ability. This is important as DNA damage in the sperm as a result of oxidative stress has been linked to poor reproductive outcomes.
authors.affiliation: Discipline of Obstetrics & Gynaecology, School of Paediatrics & Reproductive Health, Research Centre for Reproductive Health, Robinson Institute, University of Adelaide, Adelaide, SA, Australia. hbakos@repromed.com.au
authors.forename: H W
authors.initials: HW
authors.lastname: Bakos
authors.forename: M
authors.initials: M
authors.lastname: Mitchell
authors.forename: B P
authors.initials: BP
authors.lastname: Setchell
authors.forename: M
authors.initials: M
authors.lastname: Lane
mesh_terms: D020101:Acrosome Reaction; D000818:Animals; D001835:Body Weight; D004249:DNA Damage; D004032:Diet; D005306:Fertilization; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D023421:Models, Animal; D009765:Obesity / Q000209:etiology* / Q000378:metabolism; D018812:Paternal Exposure; D017382:Reactive Oxygen Species / Q000378:metabolism; D013075:Sperm Capacitation; D013094:Spermatozoa / Q000378:metabolism / Q000502:physiology*; D013739:Testosterone / Q000097:blood
chemical_list: D017382:Reactive Oxygen Species; D013739:Testosterone