Obesity is nowadays a problem of public health worldwide and is determined by the accumulation of body fat mass. This fact is given by the loss of energy homeostasis, and the hypothalamus is the region of the brain responsible for coordinating food intake and energy expenditure by signaling peripheral hormones. It is known that this region suffers an inflammatory process during the development of obesity which is associated with activation of a cellular pathway related to the immune system, activation of TLR4 and also, with the induction of endoplasmic reticulum stress. Recently, it was also shown that change in the process of autophagy, important for the removal of dysfunctional proteins and organelles, can lead to changes in body because of the disruption of hypothalamic homeostasis. In peripheral tissues it was demonstrated that another type of autophagy, chaperone-mediated autophagy, is also decreased. This type of autophagy is responsible for the degradation of long-lived intracellular proteins and its failure causes the accumulation of dysfunctional proteins and formation of protein aggregates, which can direct the cell to apoptosis. Therefore, failure of chaperone-mediated autophagy may represent an important cellular dysfunction in the establishment of inflammation and cell death. The aim of this study is to investigate the modulation of chaperone-mediated autophagy in animals submitted to high-fat diet.
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