Effect of a high-fat diet on male fertility and sperm physiology in high fertility performance mice

GIACCAGLI MM; CUASNICU PS; RAINERO CACERES T; DE SIERVI A; DA ROS V; GOMEZ ELIAS M; DALTON N; COHEN DJ

Congreso; ESHRE Annual Meeting; 2019

The prevalence of metabolic syndrome (MetS)has increased in alarming proportions, affectingaround 20?25% of the global population.1 MetShas been defined as an increase in at least threeof the following factors: abdominal obesity, bloodpressure, triglycerides, cholesterol, and fastingglucose.2 Although MetS had been originallyassociated with advanced age, changes inlifestyle have accelerated the appearance of thesymptoms, coinciding with reproductive agebecoming a risk factor for fertility disorders.Therefore, the study of the effect of MetS onfertility emerges as a novel area of research.However, a direct correlation of MetS with maleinfertility still remains unclear. In the case of themouse model, most of the studies publishedso far have been performed in the C57BL/6strain.3 Considering both that C57BL/6 miceare poor reproducers and that the multifactorialsyndrome could be attributable to susceptibilitygenes modulated by the genetic background,the authors wondered whether the acquisition ofa metabolic disorder could affect the fertility ofmales from a different mouse strain without preexistingreproductive deficiencies. In view of this,the present study evaluates whether MetS hasa negative impact on fertility and sperm functionof hybrid male mice with high reproductiveperformance.To induce a MetS-like condition, C57BL/6xBALB/cF1 (B6CF1) male mice were fed a high-fat diet(HFD, 30% fat) for 19 weeks, while controlsreceived a normal-fat diet (NFD, 6% fat). HFDfedmice ingested a higher amount of fat (p<0.01)but less total food (p<0.01) and only 12% morecalories than NFD-fed animals (p<0.05), indicatingthat HFD-fed animals received a poor-qualitydiet. Since Week 13 of treatment, HFD-fed micegained more weight compared to NFD-fed mice(p<0.001). At the end of the treatment, serumtriglyceride levels were similar in both groups,but there was a significant increase in cholesterol(p<0.001), fasting glucose levels (p<0.05), andglucose intolerance (p<0.05) in HFD-fed mice,compatible with MetS acquisition. When fertilitywas evaluated, there was no significant differencebetween groups in the in vivo fertilisation rate orin the percentage of embryos that developedin vitro to blastocysts. While testicular weightand morphology were similar in both groups,HFD-fed mice presented lighter epididymis? andhigher amounts of gonadal fat compared tocontrols (p<0.01). In vitro studies were performedas a more restricted condition to unveil spermdefects. Whereas there was no difference insperm viability, motility, or acrosome reactionbetween groups, sperm count was lower in HFDdietmice compared to control (p<0.05). Finally, invitro fertilisation assays showed no differences ineither fertilisation or embryo development ratesbetween groups.In summary, HFD-fed B6CF1 animals developeda physiological condition compatible withMetS. However, this metabolic condition did notimpact on the reproductive performanceof hybrid B6CF1 animals, albeit a significantdecrease in sperm count. These findings supportthe possibility that fertility impairment in humanscould be the result of a combination of differentenvironmental and genetic factors that may actin a cumulative manner with other predisposingfactors from either of the additional twoMetS manifestations.