Journal
KIDNEY INTERNATIONAL
Volume 74, Issue 4, Pages 438-447Publisher
ELSEVIER SCIENCE INC
DOI: 10.1038/ki.2008.184
Keywords
salt absorption; increased fructose intake; small intestine; kidney; metabolic syndrome
Categories
Funding
- NIDDK NIH HHS [R01 DK062809, DK 62809] Funding Source: Medline
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Increased dietary fructose in rodents recapitulates many aspects of the Metabolic Syndrome with hypertension, insulin resistance and dyslipidemia. Here we show that fructose increased jejunal NaCl and water absorption which was significantly decreased in mice whose apical chloride/base exchanger Slc26a6 (PAT1, CFEX) was knocked out. Increased dietary fructose intake enhanced expression of this transporter as well as the fructose-absorbing transporter Slc2a5 (Glut5) in the small intestine of wild type mice. Fructose feeding decreased salt excretion by the kidney and resulted in hypertension, a response almost abolished in the knockout mice. In parallel studies, a chloride-free diet blocked fructose-induced hypertension in Sprague Dawley rats. Serum uric acid remained unchanged in animals on increased fructose intake with hypertension. We suggest that fructose-induced hypertension is likely caused by increased salt absorption by the intestine and kidney and the transporters Slc26a6 and Slc2a5 are essential in this process.
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