Abstract
The carotid body (CB) is responsible for the peripheral chemoreflex by sensing blood gases and pH. The CB also appears to act as a peripheral sensor of metabolites and hormones, regulating the metabolism. CB malfunction induces aberrant chemosensory responses that culminate in the tonic overactivation of the sympathetic nervous system. The sympatho-excitation evoked by CB may contribute to the pathogenesis of metabolic syndrome, inducing systemic hypertension, insulin resistance and sleep-disordered breathing. Several molecular pathways are involved in the modulation of CB activity, and their pharmacological manipulation may lead to overall benefits for cardiometabolic diseases. In this review, we will discuss the role of the CB in the regulation of metabolism and in the pathogenesis of the metabolic dysfunction induced by CB overactivity. We will also explore the potential pharmacological targets in the CB for the treatment of metabolic syndrome.
Highlights
Metabolic syndrome affects approximately one-fifth of the US adult population [1,2,3]
In sustained exposure to hypoxia observed at high altitude, carotid body (CB) plays a fundamental role in the development of cellular and neurochemical rearrangements that culminate in hypoxic ventilatory acclimatization (HVA) [33]
Considering that leptin exerts multiple functions, regulating the metabolic rate and energy expenditure [154,155,156], and that leptin resistance is often observed in obese patients [13,16,17], we propose that the pharmacological blockade of the transient receptor potential melastatin 7 (TRPM7) channels in the CB could be a potential and more feasible therapy for metabolic syndrome
Summary
Metabolic syndrome affects approximately one-fifth of the US adult population [1,2,3]. Investigators proposed that there is a single peripheral sensor for multiple metabolic parameters [9], dysfunction of which may lead to metabolic dysregulation and the impaired blood–brain barrier transport of metabolites in obese subjects [10,11,12,13,14,15,16,17]. Multiple investigators attributed this peripheral sensing function to the carotid body (CB). We will provide insights into new potential pharmacological targets in the CB for the treatment of cardiometabolic dysfunction
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