Abstract
The carotid bodies (CB) are peripheral chemoreceptors that sense changes in arterial blood O2, CO2, and pH levels. Hypoxia, hypercapnia, and acidosis activate the CB, which respond by increasing the action potential frequency in their sensory nerve, the carotid sinus nerve (CSN). CSN activity is integrated in the brain stem to induce a panoply of cardiorespiratory reflexes aimed, primarily, to normalize the altered blood gases, via hyperventilation, and to regulate blood pressure and cardiac performance, via sympathetic nervous system (SNS) activation. Besides its role in the cardiorespiratory control the CB has been proposed as a metabolic sensor implicated in the control of energy homeostasis and, more recently, in the regulation of whole body insulin sensitivity. Hypercaloric diets cause CB overactivation in rats, which seems to be at the origin of the development of insulin resistance and hypertension, core features of metabolic syndrome and type 2 diabetes. Consistent with this notion, CB sensory denervation prevents metabolic and hemodynamic alterations in hypercaloric feed animal. Obstructive sleep apnea (OSA) is another chronic disorder characterized by increased CB activity and intimately related with several metabolic and cardiovascular abnormalities. In this manuscript we review in a concise manner the putative pathways linking CB chemoreceptors deregulation with the pathogenesis of insulin resistance and arterial hypertension. Also, the link between chronic intermittent hypoxia (CIH) and insulin resistance is discussed. Then, a final section is devoted to debate strategies to reduce CB activity and its use for prevention and therapeutics of metabolic diseases with an emphasis on new exciting research in the modulation of bioelectronic signals, likely to be central in the future.
Highlights
Reviewed by: Giovanni Solinas, University of Gothenburg, Sweden J
We have demonstrated that insulin resistance and hypertension produced by hypercaloric diets are completely prevented by chronic bilateral carotid sinus nerve (CSN) resection, and these results strengthen the link between carotid bodies (CB) dysfunction and the development of insulin resistance (Ribeiro et al, 2013)
Gallego-Martin et al (2012) demonstrated that in intact CBs cultured during 1 day, but not in freshly isolated organs, 0 mM glucose media potentiates the release of CAs elicited by hypoxia and that chemoreceptor cells in culture become transiently more dependent on glycolysis suggesting that the scarcity of glucose leads the cells to acquire the ability to increase their neurosecretory response to hypoxia
Summary
EVIDENCES FOR A ROLE OF CAROTID BODY IN GLUCOSE HOMEOSTASIS The idea of a physiological role of the CB on the control of glucose metabolism was first suggested by Petropavlovskaya in the 50’s. In this pioneer study it was shown that the stimulation of the CB induces a reflex hyperglycemia, an effect that is mediated www.frontiersin.org
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