The authors declare that they have no competing interests.
All authors participated in the design, interpretation of the studies, analysis of the data and review of the manuscript; GSAF and ACA conducted the experiments; KEC, GTV and DCD induced the obesity; JAAF performed hormone assay; and GSAF, ACA and WDGK performed data analyses and wrote the manuscript. All authors read and approved the final manuscript.
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.
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.
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.
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.
WHO - World Health Organization: World Health Organization. Obesity: preventing and managing the global epidemic. 894. 2000, Geneva: WHO Technical Report Series, Part I: The problem of overweight and obesity
Bray GA: Obesity: historical development of scientific and cultural ideas. Int J Obes. 1990, 14 (11): 909-926. PubMed
Haffner SM, Valdez RA, Stern MP, Katz MS: Obesity, body fat distribution and sex hormones in men. Int J Obes Relat Metab Disord. 1993, 17 (11): 643-649. PubMed
Magnusdottir EV, Thorsteinsson T, Thorsteinsdottir S, Heimisdottir M, Olafsdottir K: Persistent organochlorines, sedentary occupation, obesity and human male subfertility. Human Reprod. 2005, 20 (1): 208-215. CrossRef
Mello MAR, Souza T, Braga LR, Santos W, Ribeiro IA, Gobatto CA: Glucose tolerance and insulin action in monosodium glutamate (MSG) obese exercise-trained rats. Physiol Chem Phys Med NMR. 2001, 33 (1): 63-71. PubMed
Cunha NV, Abreu SB, Panisb C, Grassiollia S, Guarnierb FA, Cecchinib R, Mazzucob TL, Pinge-Filho P, Martins-Pinge MC: Cox-2 inhibition attenuates cardiovascular and inflammatory aspects in monosodium glutamate-induced obese rats. Life Sci. 2010, 87: 375-381. 10.1016/j.lfs.2010.07.014. CrossRefPubMed
Lyon HN, Hirschhorn JN: Genetics of common forms of obesity: a brief overview. Am J Clin Nutr. 2005, 82 (1): 215S-217S. PubMed
Bueno AA, Oyama LM, Estadella D, Habitante CA, Bernardes BSS, Ribeiro EB, Oller CMN: Lipid metabolism of monosodium glutamate obese rats after partial removal of adipose tissue. Physiol Res. 2005, 54 (1): 57-65. PubMed
Dolnikoff M, Martin-Hidalgo A, Machado UF, Lima FB, Herrera E: Decreased lipolysis and enhanced glycerol and glucose utilization by adipose tissue prior to development of obesity in monosodium glutamate (MSG) treated-rats. Int J Obes Relat Metab Disord. 2001, 25 (3): 426-433. 10.1038/sj.ijo.0801517. CrossRefPubMed
Diemen VV, Trindade EN, Trindade MRM: Experimental model to induce obesity in rats. Acta Cir Bras. 2006, 21 (6): 425-429.
Hermo L, Robaire B: Epididymal cell types and their functions. The Epididymis – From Molecules to Clinical Practice. Edited by: Robaire B, Hinton BT. 2002, New York: sKluwer Academic / Plenum Publisher, 81-102. CrossRef
Fernandes GS, Arena AC, Fernandez CDB, Mercadante A, Barbisan LF, Kempinas WG: Reproductive effects in male rats exposed to diuron. ReprodToxicol. 2007, 23 (1): 106-112.
Weibel ER: Principles and methods for the morphometric study of the lung and other organs. Lab Invest. 1963, 12 (1): 131-155. PubMed
Kanarek RB, Marks-Kaufman R: Increased carbohydrate consumption induced by neonatal administration of monosodium glutamate to rats. Neuro behav Toxicol Teratol. 1981, 3 (3): 343-350.
Oida K, Nakai T, Hayashi T, Miyabo S, Takeda R: Plasma lipoproteins of monosodium glutamate-induced obese rats. Int J Obes. 1984, 8 (5): 385-391. PubMed
Papa PC, Vargas AM, Silva JLT, Nunes MT, Machado UF: GLUT4 protein is differently modulated during development of obesity in monosodium glutamate-treated mice. Life Sci. 2002, 71 (16): 1917-1928. 10.1016/S0024-3205(02)01948-3. CrossRef
Mozeš S, Sefeikov Z, Lenhardt L, Racek L: Effect of adrenalectomy on the activity of small intestine enzymes in monosodium glutamate obese rats. Physiol Res. 2004, 53 (4): 415-422. PubMed
Dawson R, Pelleymounter MA, Millard WJ, Liu S, Eppler B: Attenuation of leptin-mediated effects by monosodium glutamate-induced arcuate nucleus damage. Am J Physiol. 1997, 273 (1 Pt 1): E202-E206. PubMed
Nakagawa T, Ukai K, Ohyama T, Gomita Y, Okamura H: Effects of chronic administration of sibutramine on body weight, food intake and motor activity in neonatally monosodium glutamate-treated obese female rats: relationship of antiobesity effect with monoamines. Exp Anim. 2000, 49: 239-249. 10.1538/expanim.49.239. CrossRefPubMed
Zenick H, Clegg ED, Perreault SD, Klinefelter GR, Gray LE: Assessment of male reproductive toxicity: a risk assessment approach. Principles and Methods of Toxicology. Edited by: Hayes AW. 1994, New York: Raven, 937-988. 3
Gong SL, Xia FQ, Wei J, Li XY, Sun TH, Lu Z, Liu SZ: Harmful effects of MSG on function of hypothalamus-pituitary-target gland system. Biomed Environ Sci. 1995, 8 (4): 310-317. PubMed
Orth JM: Cell biology of testicular development in fetus and neonate. Cell and molecular biology of the testis. Edited by: Desjardins C, Ewing LL. 1993, New York: Oxford University Press, 3-42.
Berndtson WE, Igboeli G, Pickett BW: Relationship of absolute numbers of Sertoli cells to testicular size and spermatogenesis in young beef bulls. J AnimSci. 1987, 64 (1): 241-246.
França LR, Russell LD: The testis of domestic animals. Male reproduction: a multidisciplinary overview. Edited by: Martínez-Garcia F, Regadera J. 1998, Madrid: Churchill Communications Europe España, 197-219.
Kempinas WG, Klinefelter GR: The Epididymis as a Target for Toxicants. Comprehensive Toxicology. Edited by: Charlene A. 2010, McQueen: Oxford: Academic Press, 149-166. CrossRef
Fernandez CD, Bellentani FF, Fernandes GS, Perobelli JE, Favareto AP, Nascimento AF, Cicogna AC, Kempinas WD: Diet-induced obesity in rats leads to a decrease in sperm motility. Reprod Biol Endocrinol. 2011, 11: 9-32.
Magni P, Motta M, Martini L: Leptin: a possible link between food intake, energy expenditure, and reproductive function. Regul Pepti. 2000, 92 (1–3): 51-56. CrossRef
Barash IA, Cheung CC, Weigle DS, Ren H, Kabigting EB, Kuijper JL, Clifton DK, Steiner RA: Leptin is a metabolic signal to the reproductive system. Endocrinology. 1996, 137 (7): 3144-3147. 10.1210/en.137.7.3144. PubMed
- Glutamate-induced obesity leads to decreased sperm reserves and acceleration of transit time in the epididymis of adult male rats
Glaura SA Fernandes
Arielle C Arena
Kleber E Campos
Gustavo T Volpato
Janete A Anselmo-Franci
Débora C Damasceno
Wilma G Kempinas
- BioMed Central
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