Studies show that the consumption of a diet rich in saturated fatty acids in a very short period activates inflammatory pathways in the hypothalamus, showing that inflammatory processes play a role in the development of metabolic disorders that are associated with hypothalamic activity. Nicotinic acetylcholine receptors (nAChRs) are widely expressed in the central nervous system and recent studies show that an important feature of α7nAChR receptors is their ability to activate signal transduction pathways that result in inhibition of inflammatory cytokine transcription. This mechanism is called the cholinergic anti-inflammatory reflex. A study from our laboratory showed that the consumption of a high-fat diet for three days can reduce the expression of the α7nAChR receptor and make the hypothalamus more susceptible to inflammatory damage. The expression and activity of the α7nAChR receptor depends on several cellular mechanisms that can act by stimulating or inhibiting the expression of the Chrna7 gene or by controlling the presence and activity of the receptor in the membrane, such as methylation, the ubiquitin-proteasome system and maturation involving chaperone proteins (mechanisms pre-transcriptional and post-translational). Although studies have sought to investigate the effects of inflammatory processes on cellular activity, the role of the α7nAChR receptor in this context has not been much investigated.