RESUMO
Overweight and obesity are a worldwide public health problem. Obesity prevalence has increased considerably, which indicates the need for more studies to better understand these diseases and related complications. Diet induced-obesity (DIO) animal models can reproduce human overweight and obesity, and there are many protocols used to lead to excess fat deposition. So, the purpose of this review was to identify the key points for the induction of obesity through diet, as well as identifying which are the necessary endpoints to be achieved when inducing fat gain. For this, we reviewed the literature in the last 6 years, looking for original articles that aimed to induce obesity through the diet. All articles evaluated should have a control group, in order to verify the results found, and had worked with Sprague-Dawley and Wistar rats, or with C57BL-/-6 mice strain. Articles that induced obesity by other methods, such as genetic manipulation, surgery, or drugs were excluded, since our main objective was to identify key points for the induction of obesity through diet. Articles in humans, in cell culture, in non-rodent animals, as well as review articles, articles that did not have obesity induction and book chapters were also excluded. Body weight and fat gain, as well as determinants related to inflammation, hormonal concentration, blood glycemia, lipid profile, and liver health, must be evaluated together to better determination of the development of obesity. In addition, to select the best model in each circumstance, it should be considered that each breed and sex respond differently to diet-induced obesity. The composition of the diet and calorie overconsumption are also relevant to the development of obesity. Finally, it is important that a non-obese control group is included in the experimental design.
RESUMO
The intestinal microbiota has come to be considered an additional risk factor for the development of metabolic diseases. Considering the potential role of antimicrobials as modulators of the intestinal microbiota, they have been investigated for use in the adjuvant treatment of obesity and insulin resistance (IR). In this regard, the present manuscript aimed to review the effect of regular use of antimicrobials on the treatment of obesity and/or IR, as well as its associated mechanisms. The regular use of antimicrobials does not seem to influence the body weight and adiposity of its consumer. Regarding IR, clinical trials did not observe positive effects, on the other hand, most of the experimental studies observed an increase in insulin sensitivity. The mechanisms used by antimicrobials that could lead to the improvement of insulin sensitivity are dependent on the modulation of the intestinal microbiota. This modulation would lead to a reduction in the stimulation of the immune system, as a consequence of improved intestinal barrier and/or the reduction of gram-negative bacteria in the microbiota. In addition, the secretion of glucagon-like peptide-1 would be modulated by metabolites produced by the intestinal microbiota, such as secondary bile acids and short-chain fatty acids. Based on the results obtained to date, more studies should be performed to elucidate the effect of these drugs on obesity and IR, as well as the mechanisms involved. In addition, the cost-benefit of the regular use of antimicrobials should be investigated, as this practice may lead to the development of antimicrobial-resistant microorganisms.
