IFIBYNE   05513
INSTITUTO DE FISIOLOGIA, BIOLOGIA MOLECULAR Y NEUROCIENCIAS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Obesity impacts the ovary at several levels
Autor/es:
ELIA EVELIN MARIEL
Reunión:
Simposio; XVII Annual Symposium of the Frontiers in Reproduction; 2014
Resumen:
Obesity constitutes a health problem of increasing worldwide prevalence and presents a major public health concern. In addition to the myriad health detriments caused by obesity, reproduction is also compromised. Most obese women are not infertile; however, obesity and its negative impact upon fecundity and fertility are well documented. However, the mechanisms by which body fat excess interferes with reproductive function are still not fully understood. Besides, significant evidence suggests that excess body fat negatively affects reproductive functions in females not only in human but also in many models of obesity . A number of animal models have been described for the study of obesity. In particular, the model of obesity developed in rodents that more closely reflects Western diet habits is the cafeteria diet. It avoids the use of very high intakes of a particular type or source of fat while inducing persistent hyperphagia and increased energy intake as a result of the variety and novelty of the foods available. It has been shown that cafeteria diet can impact upon metabolic function; however little is specifically known about the ovarian metabolism. In light of the above, the aim of the present study was to study whether obesity induced by cafeteria diet affect reproductive function in female rats and to contribute in the understanding of the mechanisms involved in this disruption. For that purpose, female Wistar rats were fed ad libitum with two different diets: (a) control group was fed with a standard diet, and (b) obese group was offered with food that was periodically changed: chocolate chip cookies, peanuts, sausages, etc. We found that cafeteria diet induced in rats both obesity and hyperglycemia, without altering triglycerides, cholesterol nor protein C reactive serum levels. Moreover, this diet altered the ovarian function since animals showed prolonged diestro phases and decreased estradiol serum levels in the morning of the estro. However, obesity did not alter the number of follicles in different stages of development, although we detected an increase in the number of antral atretic follicles as well as the presence of cystic follicles and follicles showing multiple oocytes in those animals. By immunohistochemistry, we analyzed the expression of both: Anti-Mullerian hormone (AMH), a marker of ovarian reserve and Ciclo-oxygenase type 2 (COX-2), a key enzyme involved in the follicular rupture. We found a decreased in the number of AMH immunoreactive pre-antral follicles in the obese group respect o controls, as well as a decreased in the number of COX-2 positive antral and preovulatory follicles. In view of the above, we conclude that cafeteria diet induced not only obesity but it also altered ovarian function by reducing the ovarian reserve as well as the serum estradiol levels and, probably, by complicating ovulation. Obesity is a serious epidemiological problem worldwide that represents one of the biggest challenges in public health around the XXI century. Our results are indicating that obesity has a negative effect on the reproductive function, altering ovarian physiology by several mechanisms. These could generate an effect on the offspring, which would represent a long-term increase in the prevalence of the disease. Therefore we consider that the study of this pathology is essential to facilitate the development of a potential therapeutic in reproductive medicine.