Obesity as a factor in spermatogenesis disorders (experimental study)

Abstract

<jats:p><jats:bold><jats:italic>Intr</jats:italic></jats:bold><jats:bold><jats:italic>oduction.</jats:italic></jats:bold><jats:bold><jats:italic> </jats:italic></jats:bold><jats:italic>In recent years, the effects of obesity on male fertility have been extensively investigated. The results of existing studies are extremely contradictory.</jats:italic></jats:p><jats:p><jats:bold><jats:italic>The study objective </jats:italic></jats:bold><jats:italic>was</jats:italic><jats:italic> </jats:italic><jats:italic>to determine the effect of obesity on the male reproductive system using the biological model of laboratory rats as an example.</jats:italic></jats:p><jats:p><jats:bold><jats:italic>Materials and methods. </jats:italic></jats:bold><jats:italic>In vivo modeling of diet-induced obesity. The study was conducted on 22 laboratory sexually mature white rats weighing 140–160 g. The animals were divided into two groups: 1 control (10 animals) and 2 rats with diet-induced obesity (12 animals). After 12 weeks, the animals were removed from the experiment. All rats underwent: calculation of the Lee index (body mass index in rats), determination of the concentration and viability of spermatozoa in a suspension of sperm from the epididymis, determination of glucose level of total cholesterol and triglycerides in the blood, study of sperm DNA fragmentation, histological examination testis: calculating the crosssectional area of the seminiferous tubule; determination of the number of non-functioning tubules and tubules with desquamated spermiogenic epithelium; determination of the average spermatogenesis index.</jats:italic></jats:p><jats:p><jats:bold><jats:italic>Results. </jats:italic></jats:bold><jats:italic>In the study groups there were no differences in glucose and total cholesterol levels. However, a statistically significant, significant difference in the level of triglycerides in the blood was revealed. The concentration of sperm and their viability in the studied groups did not differ. The level of sperm DNA fragmentation in the experimental group is significantly higher than in the control group (31.5 ± 10.1 and ± 1.4 %, respectively, p &lt;0.05). Morphometric evaluation of histological preparations did not establish differences in the cross-sectional area of the seminiferous tubules and the average spermatogenesis index in the studied groups. In rats with obesity, compared with the control group, significantly more non-functioning tubules (2.9 ± 0.3 and 8.4 ± 0.3; p &lt;0.05) and tubules with desquamated spermatogenic epithelium (1.8 ± 0.3 and 8.8 ± 0.5; p &lt;0.05).</jats:italic></jats:p><jats:p><jats:bold><jats:italic>Conclusion. </jats:italic></jats:bold><jats:italic>Diet-induced obesity causes impaired spermatogenesis, and damage to the sperm genetic material in male white rats.</jats:italic></jats:p>