Obesity has reached epidemic proportions worldwide contributing for the increase of the prevalence of several diseases associated with excess weight, including the metabolic syndrome, nonalcoholic fatty liver disease, diabetes mellitus type 2 (DM2), and some cancers. Excess body mass results primarily from an imbalance between caloric intake and energy expenditure comprising basal metabolism, physical activity, and diet-induced adaptive thermogenesis induced by food or cold. However, there are distinct and complex metabolic pathways involved in control of body weight which are mostly controlled by the central nervous system. Recent studies have shown that experimental obesity induced by consumption of high-fat diet is the result of the installation of an inflammatory process in the hypothalamus leading to resistance to anorexigenic hormones such as leptin and insulin, and finally to a defective regulation of food intake and energy expenditure. Chemokines are involved in the inflammation process hypothalamic which is observed within the first 24 hours of exposure to the diet rich in saturated fats, mainly by the action of monocyte recruitment to inflammatory phenotypic profile. The identification of inflammatory factors that play an important role in the recruitment of monocytes from the periphery contribute order to obtain advances in the understanding of pathophysiological mechanisms that lead to obesity. Thus, the present study aims at evaluating the expression of chemokines during the early stages of the installation of hypothalamic inflammation in obesity-induced experimental diet high in saturated fat.
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