Obesity and type 2 diabetes are associated with activation of signaling pathways and increased inflammatory cytokine production. In turn, hypothalamic inflammation is associated with a lack of control of mechanisms of hunger and thermogenesis and consequently, with the development of obesity. Long chain saturated fatty acids leads to the activation of TLR4 signaling, ER stress and resistance to leptin in the hypothalamus, which are important pathways leading to hypothalamic inflammation. Autophagy is a cellular process in which proteins and organelles are degraded by lysosomal proteases and in the CNS is important for neuronal homeostasis and protein quality control and is closely attached to the immune system and inflammation. Alterations in the process of autophagy is associated with inflammation, type 2 diabetes and obesity, and in central nervous system with neurodegenerative diseases. Studies shows that increased inflammatory mediators may compromise neuronal homeostasis by negatively regulate the degradation and recycling of neuronal protein aggregates by autophagy inhibition. In this context, the objective of this work is to study this important pathway of cellular homeostasis in the hypothalamus of different animal models of obesity.
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