High-Fat Diets Disturb Rat Epididymal Sperm Maturation

Abstract

Infertility is increasingly recognized as being closely linked to obesity in humans. The successful production of fertile spermatozoa requires adequate spermatogenesis within the testis and proper spermatozoa maturation through the epididymis. This study aimed to evaluate the impact of body adiposity on male fertility, focusing on sperm parameters, epididymal sperm maturation, and sperm capacitation in Wistar rats. Male rats were randomized into three dietary groups over four weeks: a control group receiving less than 4% lard, regular chow, a 10% lard group, and a 60% lard group. Following dietary interventions, fertility tests were conducted across the groups. The epididymis was dissected into caput, corpus, and cauda regions to assess sperm concentration, vitality capacitation, carbohydrate distribution, tyrosine phosphorylation, and phosphatidylserine levels. Additionally, serum testosterone levels were measured to evaluate hormonal influences on fertility. The rats subjected to high-fat diets leading to overweight and obesity exhibited significant alterations in fertility. These changes were characterized by impaired epididymal sperm maturation, as evidenced by lower testosterone levels, decreased sperm viability, and capacitation. Furthermore, increased adiposity was associated with a lack of asymmetry in the plasma membrane, alteration in carbohydrate distribution, and changes in tyrosine phosphorylation. This study underscores the adverse effects of high-fat diets on male fertility, particularly through mechanisms affecting sperm maturation in the epididymis. The evidence suggests that obesity-induced alterations in sperm parameters and hormonal profiles may contribute to reduced fertility in male rats, which could have implications for understanding similar human processes.

Keywords: epididymis; infertility; obesity; overweight; sperm parameters.

Figure 1

Distribution and weight of fat deposits in Wistar rats under varying dietary conditions. (I) Quantitative analysis of epididymal fat weight: balanced meal, high-fat diet (10%), and high-fat diet (60%) (n = 6). (II) Morphological assessment of fat distribution, highlighting total fat (F), mesenteric fat (MF; indicated by the slim black arrow), and peripheral epididymal fat (indicated by the gross black arrow) in Wistar rats across three dietary conditions: balanced meal (A), high-fat diet 10% (B), and high-fat diet 60% (C). * Represents significant differences between the experimental group and the control group. ** Represents p < 0.05.

Figure 2

Serum testosterone levels in Wistar rats Under different dietary regimens: balanced meal, high-fat diet (10%), and high-fat diet (60%). Values (n = 6) are expressed as mean ± standard deviation (SD). Statistical analysis indicates a significant difference between the balanced meal and the high-fat diet 60% groups (p < 0.05). * Represents significant differences between the experimental group and the control group.

Figure 3

Capacitated sperm cells, as determined by the chlortetracycline (CTC) assay, after a 6-h incubation period in a capacitation medium. Data (n = 6) are expressed as average ± standard deviation (SD). Different letters (a, b, c) indicate significant differences. Specifically, a significant difference was observed between the high-fat diet 10% (HFD10) and high-fat diet 60% (HFD60) groups (p < 0.05). * Represents significant differences between the experimental group and the control group.

Figure 4

Phosphatidylserine externalization in sperm cells from high-fat diet Wistar rats, presented as average ± SD. Different letters (a, b, c) indicate significant differences. Specifically, a statistically significant difference was observed between the high-fat diet 10% (HFD10) and high-fat diet 60% (HFD60) groups (p < 0.05) (n = 6). * Represents significant differences between the experimental group and the control group.