Our study demonstrates that neonatal treatment with MSG alters the epididymal parameters by reducing sperm storage and accelerating sperm transit time. Furthermore, the present data confirm previous results showing that neonatal treatment with MSG is able to induce obesity (high Lee index, small corporal weight and naso-anal length) [32–36] although few control rats also presented obesity status by Lee index, related to aging . Thus, neonatal treatment with MSG caused a cessation of growth and development with a concomitant accumulation of body fat leading to a decrease in body weight in relation to control group. Neonatal MSG treatment is a model of obesity in rodents which causes alterations in hypothalamic arcuate nucleus (ARC) and impairs leptin and insulin signaling in this region [37–39] resulting in hyperleptinemia and hyperinsulinemia. When the hypothalamic ventromedial nucleus and arcuate nucleus are destroyed in rats by treatment with MSG in the neonatal stage, obesity occurs as the rats grow .
Wet-weight alterations in the reproductive organs constitute a parameter for indicating changes in sex hormone levels . In this study, the significant reduction in the weights of all analyzed organs in obese rats corroborate with the reduction of testosterone levels. As mentioned previously, the obesity induced by glutamate is obtained through a hypothalamic injury that disrupts the secretion of hormones including the gonadotrophins (FSH and LH) [42, 43]. According to França et al. , in this obesity model, significant diminutions in the testosterone and FSH levels are related to disrupted HPG axis development due to the hyperleptinemia. In the same manner, Tena-Sempere et al.  reported that a possible cause for this severe reduction in the testosterone levels in animals neonatally treated with glutamate may have been due to an increase in plasma leptin levels. However, despite the decreased testosterone and FSH levels, the LH levels (hormone directly involved in regulating testosterone secretion) were unchanged by MSG treatment. This result can be related with severe ARC lesions [24, 45, 46] and so we suggest that MSG specifically leads to lesions in FSH neurons. Moreover, it is important to emphasize that the hormonal profile of obese men is characterized by decreased total and, often, free testosterone levels, diminished gonadotropin levels, and increased circulating estrogen levels .
The number of spermatids present in the testis and the total DSP are important indicators of male fertility potential . In the present study, the reduction in sperm production led by MSG-induced obesity was associated with reduced testicular weight, seminiferous tubular diameter, testicular seminiferous epithelium height and testosterone and FSH levels. On the other hand, França et al.  showed unchanged sperm production, testis weight and seminiferous tubular diameter in obese adult rats after neonatal glutamate-induced obesity. In this sense, it is known that the number of Sertoli cells, established during the prepubertal period, determines the final testicular size and the magnitude of sperm production in sexually mature animals [48–50]. In the present study the number of Sertoli cells did not change in the obese rats, as well as the efficiency of the spermatogenic process, as evidenced by results of DSP per gram of testis that were similar between the experimental groups. It is possible that the disturbance in the HPG axis due to MSG treatment compromises the real significance of reduced FSH plasma levels observed in the present model. Evaluation of inhibin B levels in MSG rats could provide additional information regarding Sertoli cell function . Thus, this experimental model may produces lightly different results between different research groups, as disclosed in the literature.
The reduction in sperm count in the epididymis in obese rats was probably responsible by the decrease of the epididymal weight and contributed for the acceleration of the sperm transit time through the epididymis. Acceleration in sperm transit time can impair sperm maturation and reduce the number of gametes available for ejaculation and fertility . These alteration were independent of epididymal components (epithelium, stroma and lumen) since they are unaffected by glutamate-induced obesity.
It is very known that in obesity conditions there is an excess of leptin which is secreted by the adipocytes . Studies show that the plasma leptin concentrations were significantly elevated in both humans [52, 53] and in rodent obesity models [54, 55], and directly proportional to the amount of fat. Leptin is important for the regulation of food intake, energy metabolism and reproductive function [55–58]. It has been proposed that a specific narrow leptin concentration range is necessary to maintain normal reproductive function, and levels below or above these thresholds are critical to this peptide’s influence on the function of the hypothalamus-pituitary-gonadal (HPG) axis [57, 58] by acting on hypothalamic receptors and also by promoting peripheral effects . However, the relationship between high leptin levels and the male reproductive system is not clear.