The gut-brain axis and sodium appetite : can inflammation-related signaling influence the control of sodium intake?
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Date
2022
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Abstract
Sodium is the main cation present in the extracellular fluid. Sodium and water content in the body are
responsible for volume and osmotic homeostasis through mechanisms involving sodium and water excretion and
intake. When body sodium content decreases below the homeostatic threshold, a condition termed sodium
deficiency, highly motivated sodium seeking, and intake occurs. This is termed sodium appetite. Classically,
sodium and water intakes are controlled by a number of neuroendocrine mechanisms that include signaling
molecules from the renin-angiotensin-aldosterone system acting in the central nervous system (CNS). However,
recent findings have shown that sodium and water intakes can also be influenced by inflammatory agents and
mediators acting in the CNS. For instance, central infusion of IL-1β or TNF-α can directly affect sodium and water
consumption in animal models. Some dietary conditions, such as high salt intake, have been shown to change the
intestinal microbiome composition, stimulating the immune branch of the gut-brain axis through the production
of inflammatory cytokines, such as IL-17, which can stimulate the brain immune system. In this review, we
address the latest findings supporting the hypothesis that immune signaling in the brain could produce a
reduction in thirst and sodium appetite and, therefore, contribute to sodium intake control.
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Keywords
Gut microbiome, Cytokines, Neuroinflammation, Interleukins
Citation
FREITAS, F. E. D. A. et al. The gut-brain axis and sodium appetite: can inflammation-related signaling influence the control of sodium intake? Appetite, v. 175, artigo 106050, 2022. Disponível em: <https://www.sciencedirect.com/science/article/pii/S0195666322001416>. Acesso em: 11 out. 2022.