Fig. 2
From: Immunity and the carotid body: implications for metabolic diseases
Postulated link between diet-induced dysmetabolism and the brain-carotid body axis: Hypercaloric diets generate a dysmetabolic state characterized by hyperleptinemia, hyperinsulinemia and inflammation, transduced by an overexpression of inflammatory cytokines. These key mediators contribute to carotid body (CB) dysfunction that is in the genesis of metabolic diseases since all these mediators are able to activate the CB, by acting on respective receptors within the organ, and modulate its function, e.g. via the release of neurotransmitters. Carotid sinus nerve (CSN) transmit this information from CB to the central nervous system, namely to the nucleus tractus solitarii (NTS), leading to the activation of both sympathetic and parasympathetic nervous systems to the efferent organs to modulate metabolism. Also, CSN information integrated in the NTS will impair satiety control and food intake, aggravating hyperphagia. All together, these afferent stimuli (metabolic vs inflammation) and intensity of reflexes stimulation may contribute to the activation or to different degrees of activation of different pathways contributing to dysmetabolic states