Diet-induced Obesity In Rats Leads To A Decrease In Sperm Motility.

Obesity is rapidly becoming a worldwide epidemic that affects children and adults. Some studies have shown a relationship between obesity and infertility, but until now it remains controversial. Thus, the aim of the present study was to investigate the effect of high-fat diet-induced obesity on male reproductive parameters. In a first experiment, male Wistar rats were fed a high-fat diet (HFD) or standard chow (SD) for 15, 30 or 45 weeks, after which they were evaluated by adiposity index, serum leptin levels, reproductive organ weights and sperm counts. In a second experiment, rats received HFD or SD only for 15 weeks, long enough to cause obesity. Sexual hormones and sexual behavior were evaluated in these animals, as well as fertility after natural mating. Another group of rats was submitted to motility analysis and fertility evaluation after in utero insemination. After 15, 30 or 45 weeks, HFD-fed animals presented significant increases in obesity index and serum leptin levels. Reproductive organ weights and sperm counts in the testis and epididymis were similar between the two groups at all timepoints studied. Sexual behavior was not altered by the diet regimen, and HFD fertility after natural mating was also similar to SD-fed animals. Intergroup testosterone levels were also comparable, but estradiol levels were increased in HFD rats. Furthermore, sperm quality was reduced in HFD animals as evidenced by their decreased percentage of sperm with progressive movement. This altered motility parameter was followed by a trend toward reduction in fertility potential after artificial in utero insemination. The results reported herein showed that obesity can affect sperm quality, by reducing sperm motility, without affecting other sperm parameters. The low sperm quality caused a slight reduction in fertility potential, showing that obesity may lead to impairment in male fertility.93

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

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.National Council for Scientific and Technological Development (CNPq)National Council for Scientific and Technological Development (CNPq

A high fat diet during adolescence in male rats negatively programs reproductive and metabolic function which is partially ameliorated by exercise

An interaction between obesity, impaired glucose metabolism and sperm function in adults has been observed but it is not known whether exposure to a diet high in fat during the peri-pubertal period can have longstanding programmed effects on reproductive function and gonadal structure. This study examined metabolic and reproductive function in obese rats programmed by exposure to a high fat (HF) diet during adolescence. The effect of physical training (Ex) in ameliorating this phenotype was also assessed. Thirty-day-old male Wistar rats were fed a HF diet (35% lard w/w) for 30 days then subsequently fed a normal fat diet (NF) for a 40-day recovery period. Control animals were fed a NF diet throughout life. At 70 days of life, animals started a low frequency moderate exercise training that lasted 30 days. Control animals remained sedentary (Se). At 100 days of life, biometric, metabolic and reproductive parameters were evaluated. Animals exposed to HF diet showed greater body weight, glucose intolerance, increased fat tissue deposition, reduced VO 2max and reduced energy expenditure. Consumption of the HF diet led to an increase in the number of abnormal seminiferous tubule and a reduction in seminiferous epithelium height and seminiferous tubular diameter, which was reversed by moderate exercise. Compared with the NF-Se group, a high fat diet decreased the number of seminiferous tubules in stages VII-VIII and the NF-Ex group showed an increase in stages XI-XIII. HF-Se and NF-Ex animals showed a decreased number of spermatozoa in the cauda epididymis compared with animals from the NF-Se group. Animals exposed to both treatments (HF and Ex) were similar to all the other groups, thus these alterations induced by HF or Ex alone were partially prevented. Physical training reduced fat pad deposition and restored altered reproductive parameters. HF diet consumption during the peri-pubertal period induces long-term changes on metabolism and the reproductive system, but moderate and low frequency physical training is able to recover adipose tissue deposition and reproductive system alterations induced by high fat diet. This study highlights the importance of a balanced diet and continued physical activity during adolescence, with regard to metabolic and reproductive health

Ejaculatory dysfunction in streptozotocin-induced diabetic rats: the role of testosterone

Hyperglycemic and hypoinsulinemic states caused by diabetes mellitus are usually related to some type of sexual dysfunction, resulting in infertility in humans and experimental models, mostly due to their effects on ejaculatory function. This study aimed to evaluate the possible role of testosterone in the restoration of normal ejaculatory function in diabetic rats. Male Wistar rats were randomly allocated into 3 experimental groups: control, diabetic (streptozotocin), and diabetic with testosterone supplementation (streptozotocin plus testosterone). The following parameters were assessed at the end of the experiment: body weight, circulating testosterone levels, number of spermatozoa ejaculated in the uterus through natural mating, and weight and in vitro isometric contractions of the vas deferens. Diabetic rats showed reduced plasma testosterone levels and ejaculatory dysfunction as observed by a lack in the spermatozoa ejaculated into the uterus of receptive females. In these diabetic rats, no difference was observed in the sensitivity of the vas deferens to norepinephrine, with or without the presence of the cocktail (cocaine plus propranolol). In spite of this, an increased sensitivity to methoxamine through the alpha(1)-adrenoceptor was observed. Testosterone supplementation did not restore these parameters to control values. We conclude that, in this experimental model, the lack of testosterone was not directly related to the diabetes-induced ejaculatory dysfunction.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq

Ejaculatory Dysfunction In Streptozotocin-induced Diabetic Rats: The Role Of Testosterone.

Hyperglycemic and hypoinsulinemic states caused by diabetes mellitus are usually related to some type of sexual dysfunction, resulting in infertility in humans and experimental models, mostly due to their effects on ejaculatory function. This study aimed to evaluate the possible role of testosterone in the restoration of normal ejaculatory function in diabetic rats. Male Wistar rats were randomly allocated into 3 experimental groups: control, diabetic (streptozotocin), and diabetic with testosterone supplementation (streptozotocin plus testosterone). The following parameters were assessed at the end of the experiment: body weight, circulating testosterone levels, number of spermatozoa ejaculated in the uterus through natural mating, and weight and in vitro isometric contractions of the vas deferens. Diabetic rats showed reduced plasma testosterone levels and ejaculatory dysfunction as observed by a lack in the spermatozoa ejaculated into the uterus of receptive females. In these diabetic rats, no difference was observed in the sensitivity of the vas deferens to norepinephrine, with or without the presence of the cocktail (cocaine plus propranolol). In spite of this, an increased sensitivity to methoxamine through the α1-adrenoceptor was observed. Testosterone supplementation did not restore these parameters to control values.We conclude that, in this experimental model, the lack of testosterone was not directly related to the diabetes-induced ejaculatory dysfunction.63130-

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

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

Can vitamins C and E restore the androgen level and hypersensitivity of the vas deferens in hyperglycemic rats?

Diabetic neuropathy can affect the male reproductive system. The aim of this study was therefore to evaluate whether antioxidant (vitamins C and/or E) treatment could attenuate reproductive dysfunctions in hyperglycemic adult male rats. The animals were randomly assigned to one of four experimental groups: hyperglycemic control (Hy), hyperglycemic + 150 mg/day vitamin C (HyC), hyperglycemic + 100 mg/day vitamin E (HyE) or hyperglycemic + vitamins C and E (HyCE). The normoglycemic group (n = 10) received only the vehicles. The testosterone level and noradrenergic response of the vas deferens were analyzed. Both vitamins significantly decreased the TBARS (thiobarbituric acid reactive species) level in the hyperglycemic groups. There was a significant reduction in the testosterone level in the Hy and HyE groups when compared to the normoglycemic group. However, the testosterone levels were partially recovered in the HyC and HyCE groups. In addition, an increased sensitivity of the alpha-1 adrenoceptor in the vas deferens of the hyperglycemic control group was observed. Treatment with vitamins partially restored (vitamin E or in combination with vitamin C) or totally (vitamin C alone) this dysfunction. Moreover, the maximum response values to norepinephrine were similar among all groups. Thus, we concluded that vitamin C is more efficient than vitamin E in attenuating the effects of hyperglycemia on the male reproductive system of adult rats.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP