High salt intake reprioritizes osmolyte and energy metabolism for body fluid conservation
| Autor: | Janet D. Klein, Daisuke Nakano, Friedrich C. Luft, Raymond C. Harris, Jeff M. Sands, Tetyana V. Pedchenko, Agnes Schröder, Jonathan Jantsch, Dominik N. Müller, Lauren M. LaRocque, Akira Nishiyama, Jens Titze, Anna Dikalova, Adriana Marton, Manfred Rauh, Steffen Daub, Sergey Dikalov, Patrick Neubert, Natalia Rakova, Kento Kitada, Louise Lantier, David G. Harrison, David H. Wasserman, Yahua Zhang |
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| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Male medicine.medical_specialty Renal urea handling 030204 cardiovascular system & hematology Kidney Natriuresis Excretion 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine Internal medicine Extracellular fluid medicine Animals Urea Salt intake Sodium Chloride Dietary Muscle Skeletal Chemistry Sodium Kidney metabolism General Medicine Water-Electrolyte Balance 030104 developmental biology Endocrinology Liver Cardiovascular and Metabolic Diseases Energy Metabolism Homeostasis Research Article |
| Popis: | Natriuretic regulation of extracellular fluid volume homeostasis includes suppression of the renin-angiotensin-aldosterone system, pressure natriuresis, and reduced renal nerve activity, actions that concomitantly increase urinary Na+ excretion and lead to increased urine volume. The resulting natriuresis-driven diuretic water loss is assumed to control the extracellular volume. Here, we have demonstrated that urine concentration, and therefore regulation of water conservation, is an important control system for urine formation and extracellular volume homeostasis in mice and humans across various levels of salt intake. We observed that the renal concentration mechanism couples natriuresis with correspondent renal water reabsorption, limits natriuretic osmotic diuresis, and results in concurrent extracellular volume conservation and concentration of salt excreted into urine. This water-conserving mechanism of dietary salt excretion relies on urea transporter–driven urea recycling by the kidneys and on urea production by liver and skeletal muscle. The energy-intense nature of hepatic and extrahepatic urea osmolyte production for renal water conservation requires reprioritization of energy and substrate metabolism in liver and skeletal muscle, resulting in hepatic ketogenesis and glucocorticoid-driven muscle catabolism, which are prevented by increasing food intake. This natriuretic-ureotelic, water-conserving principle relies on metabolism-driven extracellular volume control and is regulated by concerted liver, muscle, and renal actions. |
| Databáze: | OpenAIRE |
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