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1 Department of Pharmacology & Toxicology, University of Tuebingen, Tuebingen, Germany
2 Department of Physiology, University of Tuebingen, Tuebingen, Germany
3 Department of Internal Medicine, University of Tuebingen, United States
4 Department of Physiology, University of Tuebingen, United States
5 Department of Physiology, University of Tuebiingen, United States
6 Department of Clinical Neurobiology, University Hospital of Neurology, Heidelberg, Germany
7 Department of Biology, Chemistry, and Pharmacy, Free University Berlin, Berlin, Germany
8 Departments of Medicine & Pharmacology, University of California San Diego & VASDHCS, San Diego, California, United States
* To whom correspondence should be addressed. E-mail: florian.lang{at}uni-tuebingen.de.
Mineralocorticoids enhance expression and insulin stimulates activity of the serum and glucocorticoid inducible kinase SGK1 which activates the renal epithelial Na+ channel ENaC. Under salt deficient diet SGK1 knockout mice (sgk1-\-) excrete significantly more NaCl than their wild type littermates (sgk1+/+) and become hypotensive. The present experiments explored whether SGK1 participates in the hypertensive effects of high-fat-diet and high-salt-intake. Renal SGK1 protein abundance of sgk1+/+ mice were significantly elevated following high fat diet. Under control diet fluid intake, blood pressure, urinary flow rate and urinary Na+, K+, Cl- excretion were similar in sgk1-/- and sgk1+/+ mice. Under standard diet, high-salt-intake (1% NaCl in drinking water for 25 days) increased fluid intake, urinary flow rate and urinary Na+, K+, Cl- excretion similarly in sgk1-/- and sgk1+/+ mice without significantly altering blood pressure. High-fat-diet alone (17 weeks) did not significantly alter fluid intake, urinary flow rate, urinary Na+, K+, Cl- excretion or plasma aldosterone levels, but increased plasma insulin, total cholesterol, triglyceride concentrations and systolic blood pressure to the same extent in both genotypes. Additional high-salt-intake (1% NaCl in drinking water for 25 days) on top of high-fat-diet did not affect hyperinsulinemia nor hyperlipidemia but increased fluid intake, urinary flow rate and urinary NaCl excretion significantly more in sgk1-/- than in sgk1+/+ mice. Furthermore, in animals receiving high fat diet, additional salt intake increased blood pressure only in sgk1+/+ mice (to 132±3 mmHg) but not in sgk1-/- mice (120±4 mmHg). Thus, lack of SGK1 protects against the hypertensive effects of combined high-fat-diet/high-salt-intake.
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