Effects of diet-induced obesity on the development of testicle in Sprague Dawley rats / 中华临床营养杂志

ABSTRACT

ObjectiveTo investigate the effects of diet-induced obesity on the developmental process of testes in pubertal Sprague Dawley (SD) rats and explore the possible reversibility. MethodsSixty one-month-old male SD rats were randomly divided into a control group ( n =10) and a model group ( n =50 ), which were fed on a normal diet and a high-fat diet, respectively. After 8 weeks, all the rats in the control group and 10 rats randomly picked out from the model group were killed. The serum testosterone and estradiol levels were measured by enzymelinked inununosorbent assay. Their left testes sections were stained by HE method, and the histology was observed under optical microscope and the spermatogenic activity was evaluated by Johnsen scoring system. The remaining 40 rats in the model group were further randomly divided into 3 subgroups continued high-fat diet subgroup ( n =13), resume normal diet subgroup (n =13), and weight-loss subgroup (n =14). The continued high-fat diet subgroup was fed by high-fat diet, while the other two subgroups were fed by normal diet. Rats in weight-loss group took normal diet with running 20 min/d. After 6 weeks, the same parameters were assessed using the same methods. ResultsAfter 8 weeks, compared with the control group, the testosterone level of the model group significantly decreased (P =0.024) and the estradiol level significantly increased ( P =0. 017). The result of HE staining showed that the spermatogenic cell layers decreased, with part of seminiferous tubule experiencing atrophy.The number of Leydig cell also decreased and lipo vacuole was seen in the interstitial tissue of testis. The Johnsen score of the model group was significantly lower than that of the control group (P =0.000). The testosterone level was significantly lower in the continued high-fat diet subgroup than that in resume normal diet subgroup ( P =0.001 ) and weight-loss subgroup ( P =0.000), and was significantly lower in resume normal diet subgroup than that in weight-loss subgroup ( P =0.001 ). The estradiol level was significantly higher in continued high-fat diet subgroup than that in resume normal diet subgroup ( P =0.001 ) and weight-loss group ( P =0.000 ), and was significantly higher in resume normal diet subgroup than that in weight-loss group ( P =0.001 ). HE staining showed that, pathological changes aggravating and worsening compared with the control group, the model group had significantly decreased seminiferous tubule cell layers, with some seminiferous tubules experiencing atrophy.The Johnsen score was significantly higher in weight-loss subgroup than that in the other two subgroups ( P =0.000and 0.001, respectively). The Johnsen score was negatively correlated with body weight ( r =- 0.962, P =0.000), and positively correhted with the serum testosterone level ( r =0.916, P =0.000 ). Conclusions High-fat diet can induce pubertal obesity in male SD rats, which is featured by testicular hypoplasia, decreased spermatogenesis, and endocrine dysfunction. Physical exercise may improve the conditions. The degree of obesity may be negatively correlated with the spermatogenic function.