High-Fat Diet Promotes a Pro-Inflammatory Environment in Testis and Inhibits Antioxidant Defenses in the Progeny

Abstract

The adoption of high-fat diets (HFDs) is a major contributor to the increasing prevalence of obesity worldwide. Herein, we study the impact of an HFD from early age in testicular physiology and sperm parameters in two generations of mice, with a focus on testicular oxidative status. Mice of the diet-challenged generation (F0; n = 36) were randomly fed after weaning with standard chow (CTRL), a high-fat diet (HFD) for 200 days, or a transient high-fat diet (HFDt) (60 days of HFD + 140 days of standard chow). The offspring generation (F1; n = 36) was obtained by mating normoponderal females with those fed a chow diet 120 days post-weaning. Mice fed an HFD for a lifetime presented impaired insulin tolerance, a trait inherited by their sons. The sons of mice fed HFD inherited decreased catalase activity and displayed lower activities of mitochondrial complexes I and IV. Similar to their progenitors, the sons of HFD mice had a higher prevalence of pinhead and bent neck defects than that of the sons of the CTRL mice. The adoption of HFD impaired testicular antioxidant defenses and mitochondrial function in the progeny, which is detrimental to sperm morphology.