Open Access Research

Glutamate-induced obesity leads to decreased sperm reserves and acceleration of transit time in the epididymis of adult male rats

Glaura SA Fernandes1, Arielle C Arena2*, Kleber E Campos3, Gustavo T Volpato3, Janete A Anselmo-Franci4, Débora C Damasceno5 and Wilma G Kempinas2

Author Affiliations

1 Biological Sciences Center, State University of Londrina, UEL, Londrina, PR, Brazil

2 Department of Morphology, Institute of Biosciences, UNESP - UnivEstadualPaulista, Botucatu, SP, Brazil

3 Institute of Biological and Health Sciences, Federal University of Mato Grosso, UFMT, Barra do Garça, MT, Brazil

4 Department of Physiology, Ribeirão Preto Medical School, University of São Paulo, USP, Ribeirão Preto, SP, Brazil

5 Laboratory of Experimental Research on Gynecology and Obstetrics, Department of Gynecology and Obstetrics, Botucatu Medical School, UNESP - UnivEstadualPaulista, Botucatu, SP, Brazil

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Reproductive Biology and Endocrinology 2012, 10:105  doi:10.1186/1477-7827-10-105

Published: 5 December 2012

Abstract

Background

Given the established fact that obesity interferes with male reproductive functions, the present study aimed to evaluate sperm production in the testis and storage in the epididymis in a glutamate-induced model of obesity.

Methods

Male rats were treated neonatally with monosodium glutamate (MSG) at doses of 4 mg/kg subcutaneously, or with saline solution (control group), on postnatal days 2, 4, 6, 8 and 10. On day 120, obesity was confirmed by the Lee index in all MSG-treated rats. After this, all animals from the two experimental groups were anesthetized and killed to evaluate body and reproductive organ weights, sperm parameters, plasma hormone levels (FSH, LH and testosterone), testicular and epididymal histo-morphometry and histopathology.

Results

Significant reductions in absolute and relative weights of testis, epididymis, prostate and seminal vesicle were noted in MSG-treated animals. In these same animals plasma testosterone and follicle-stimulating hormone (FSH) concentrations were decreased, as well as sperm counts in the testis and epididymis and seminiferous epithelium height and tubular diameter. The sperm transit time was accelerated in obese rats. However, the number of Sertoli cells per seminiferous tubule and stereological findings on the epididymis were not markedly changed by obesity.

Conclusions

Neonatal MSG-administered model of obesity lowers sperm production and leads to a reduction in sperm storage in the epididymis of adult male rats. The acceleration of sperm transit time can have implications for the sperm quality of these rats.

Keywords:
Obesity; Monosodium glutamate; Epididymis; Testosterone; Sperm; Rat