Abstract
This study was designed to determine the genotoxicity of a supraphysiological dose of triiodothyronine (T3) in both obese and calorie-restricted obese animals. Fifty male Wistar rats were randomly assigned to one of the two following groups: control (C; n = 10) and obese (OB; n = 40). The C group received standard food, whereas the OB group was fed a hypercaloric diet for 20 weeks. After this period, half of the OB animals (n = 20) were subjected to a 25%-calorie restriction of standard diet for 8 weeks forming thus a new group (OR), whereas the remaining OB animals were kept on the initial hypercaloric diet. During the following two weeks, 10 OR animals continued on the calorie restriction diet, whereas the remaining 10 rats of this group formed a new group (ORS) given a supraphysiological dose of T3 (25 µg/100 g body weight) along with the calorie restriction diet. Similarly, the remaining OB animals were divided into two groups, one that continued on the hypercaloric diet (OB, n = 10), and one that received the supraphysiological dose of T3 (25 µg/100 g body weight) along with the hypercaloric diet (OS, n = 10) for two weeks. The OB group showed weight gain, increased adiposity, insulin resistance, increased leptin levels and genotoxicity; T3 administration in OS animals led to an increase in genotoxicity and oxidative stress when compared with the OB group. The OR group showed weight loss and normalized levels of adiposity, insulin resistance, serum leptin and genotoxicity, thus having features similar to those of the C group. On the other hand, the ORS group, compared to OR animals, showed higher genotoxicity. Our results indicate that regardless of diet, a supraphysiological dose of T3 causes genotoxicity and potentiates oxidative stress.
Highlights
Obesity is a chronic metabolic disease, which is considered a public health problem that may lead to insulin resistance and increased serum leptin levels, affecting both developed and emerging countries [1]
The OR group showed a decrease in food ingestion and calorie intake when compared to the C and OB groups; the same occurred with the ORS group in comparison to the OS group
Serum concentrations of free T4 and TSH were similar for C and OB animals and significantly lower in OR animals
Summary
Obesity is a chronic metabolic disease, which is considered a public health problem that may lead to insulin resistance and increased serum leptin levels, affecting both developed and emerging countries [1]. It may be caused by several different factors, especially the increased availability and consumption of highly palatable diets as well as low energy expenditure [2]. Obesity causes an increase in the production of reactive oxygen species (ROS) [3], leading to redox system imbalance and an oxidative stress state. The administration of thyroid hormones, alone or in combination with a hypocaloric diet, occurs illicitly despite the fact that it is not accepted as an obesity treatment by federal health agencies
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