Influência do hormônio tireoidiano e da restrição alimentar sobre dano de DNA em animais obesos

Abstract

Introduction: Obesity is a chronic and multifactorial disease which increases the risk of developing other health conditions. It is usually considered a disease related to a lifestyle in which a wrong diet is chosen and no physical activity is carried out. The most common practice to treat obesity is caloric restriction. The increase in calories intake and a diet rich in fat are significant determinants to Deoxyribonucleic Acid (DNA) damage. Several studies have shown that the DNA damage decreases in animals submitted to caloric restriction because such restriction reduces the free radicals formation. Physiological concentrations of thyroid hormones do not produce genetic damages. On the other hand, inappropriate concentrations of such hormones can cause DNA damage. Objective: To verify the interaction between obesity, supraphysiological dose of thyroid hormone and food restriction on DNA damage. Methodology: Male Wistar rats, with 30 days of age supplied by Sao Paulo State University Animal Centre Universidade Estadual Paulista (UNESP), Botucatu, SP. Brazil were divided into two groups: Control (C) and Obese (OB). The control group were fed on either a normal diet, while obese group was submitted to a process of obesity induction and received a hypercaloric diet, standardized by Agroceres, during 20 weeks. Later, 20 animals in OB group were submitted to food restriction (RC) receiving 75% of the amount eaten by the C group, with standard diet, during eight weeks, while remaining rats continuously received the hypercaloric diet until the end of the experiment. Hence, these groups had a food restriction of 25%. After this period, 10 animals in RC group were maintained in food restriction while 10 remaining animals, besides food restriction, also received a supraphysiological dose of HT (RCS) of 25μg/100g of animal body weight. The same procedure was carried out in OB group, where 10 animals continuously received a hypercaloric diet while 10 remaining animals, besides hypercaloric diet, also received a supraphysiological dose of HT (RCS) of 25μg/100g of animal body weight, during two weeks. At the end of the experiment, 10 animals in each group suffered euthanasia. The euthanasia was carried out in order to biochemical exams, hormonal levels and Single Cell Gel Electrophoresis could be accomplished. Results: Animals in OB group presented weight gain, adiposity, DNA damage, alterations in lipidic and glicemic profiles, increase in leptin and plasmatic insulin and decrease in repair system, while the OBS group, treated with T3 presented an increase in DNA damage and a decrease in repair system when compared to animals in OB group. The animals in RC group presented weight loss, adiposity, DNA damage, increase in repair system, improved lipidic and glicemic profiles and normal levels of leptin and insulin, with values similar to C group. The RCS group, treated with T3, presented increase in DNA damage and decrease in repair system, when compared to RC group. Conclusion: The diet adopted in this study, rich in AGl, caused obesity and induced DNA damage. The supraphysiological dose of T3, provided to OB group reduced body weight and adiposity, but highlighted the production of DNA damage. The food restriction minimized the effects of obesity, decreasing weight, adiposity and DNA damages in the group treated with saline solution. However, it was not efficient in reducing the damages caused by the administration of triiodotironina, showing that the thyroid hormone in high levels leads to DNA damage, independently the treatment.