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Aldosterone-induced salt appetite requires HSD2 neurons. | LitMetric

AI Article Synopsis

  • Excessive production of aldosterone is linked to serious health risks, including heart disease, stroke, dementia, and increased mortality, primarily by promoting sodium retention and consumption.
  • Researchers identified specific neurons in the human brain that are sensitive to aldosterone and express a genetic regulator called HSD2, which play a crucial role in salt intake.
  • Experimental studies in mice confirmed that these HSD2 neurons are essential for aldosterone-induced salt consumption, suggesting they could be a potential target for treatments aimed at controlling dietary sodium intake.

Article Abstract

Excessive aldosterone production increases the risk of heart disease, stroke, dementia, and death. Aldosterone increases both sodium retention and sodium consumption, and increased sodium consumption may worsen end-organ damage in patients with aldosteronism. Preventing this increase could improve outcomes, but the behavioral mechanisms of aldosterone-induced sodium appetite remain unclear. In rodents, we previously identified aldosterone-sensitive neurons, which express the mineralocorticoid receptor and its prereceptor regulator, 11-β-hydroxysteroid dehydrogenase 2 (HSD2). In the present study, we identified HSD2 neurons in the human brain and then used a mouse model to evaluate their role in aldosterone-induced salt intake. First, we confirmed that dietary sodium deprivation increases aldosterone production, salt intake, and HSD2 neuron activity. Next, we showed that continuous chemogenetic stimulation of HSD2 neurons causes a large and specific increase in salt intake. Finally, we used dose-response studies and genetically targeted ablation of HSD2 neurons to show that these neurons are necessary for aldosterone-induced salt intake. Identifying HSD2 neurons in the human brain and establishing their necessity for aldosterone-induced salt intake in mice improves our understanding of appetitive circuits and highlights this small cell population as a therapeutic target for moderating dietary sodium.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11623954PMC
http://dx.doi.org/10.1172/jci.insight.175087DOI Listing

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