Alterations in the spermatic function generated by obesity in rats

Abstract

In order to assess the effect of obesity on epididymal and germinal epithelia in control rats and obese rats induced by a high fat diet, we evaluated the epididymal and testicular morphologies, lipid peroxidation in the epididymis, leptin serum levels, steroid hormones, insulin, cholesterol, triglycerides, glycemia and some spermatobioscopic parameters. No significant difference was observed in the levels of insulin, glucose, cholesterol and triglycerides between the two groups. Nonetheless, in the obese rats, circulating leptin and estradiol levels showed a significant increase and there was a decline in the testosterone levels. The same group showed an increase in the lipid peroxidation of the epididymis and reduced spermatobioscopic parameters. The heads of the epididymis showed morphological differences in obese rats. No significant difference was observed between the testes of both groups. There is a clear evidence of an effect on sperm in obese rats and this seems to occur in the epididymis.

Introduction

Obesity (Ob) and overweight are the most frequent chronic medical problems (Sitorius, 1998) and are characterized by excessive storage of adipose tissue in the organism (Pascuali, 2006). They are recognized by WHO (1997) as a worldwide public health problem (Brito, 1999; Halabe, 1999, Aguilar, 2000; Ventriglia, 2001). According to the 2006 National Health and Nutrition Examination Survey, one of the three countries with the largest number of Ob and overweight subjects is Mexico (Olaiz et al., 2006).

The health consequences of Ob have been emphasized in different reports. Recently, Ob has been reported to affect fertility by decreasing the quantity of spermatozoids (Jensen et al., 2004; Magnusdottir et al., 2005; Hammound et al., 2008). Furthermore, it has been seen that obese males frequently show a low hormonal profile for testosterone and a high profile for estradiol (Schneider et al., 1979; Strain et al., 1982; Zumoff et al., 1990; Haffner et al., 1993; Giagulli et al., 1994; Tsai et al., 2004; Pauli et al., 2008). This pattern is proportional to the degree of Ob (Zumoff et al., 1990; Giagulli et al., 1994; Osuna et al., 2006; Sallmen et al., 2006; Nguyen et al., 2007).

It has been determined that the reduction in testosterone levels associated with Ob is accompanied by enough intratesticular decrease of this hormone to alter spermatozoids and reduce the quantity of the same in obese subjects (Hammound et al., 2008). Pauli et al. (2008) observed a reduction in inhibin B level in obese males, which suggests that spermatogenesis is affected since inhibin B is a good marker for spermatogenesis (Myers et al., 2008).

It is also known that morphological and functional integrity of the epididymis are androgen-dependent. With androgen regulation, the epididymal epithelia cells produce different proteins, glycoproteins, glycolipids and phospholipids – components of the epididymal fluid which are needed for maturation and survival of spermatozoids. The products of secretion are liberated in the lumen (Bilinska et al., 2006). In obese patients, a large amount of fat is deposited in the scrotum, and this, or its products, can cause oxidative stress (OS) (Bouloumie et al., 1999; Yamagishi et al., 2001; Dandona et al., 2005; Davi and Falco, 2005) and oxidize lipids, amino acids and carbohydrates, as well as damage DNA by altering the epididymis itself, or the spermatozoids stored there (Kasturi et al., 2008).

There are few data on reproductive outcomes in the obese male. The mechanism that makes Ob influence fertility is unknown. In this work, we evaluate the possible site of injury of Ob in the testes or epididymidis in rats.

Obese rodent models are valuable tools for studying the underlying biological processes that contribute to the development of obesity in humans. The model of diet-induced obesity in rodents is particularly suited to this task, as diet-induced obesity in rats shares several features with human obesity, including polygenic inheritance (Levin et al., 2003).