| Dietary fructose, salt absorption and hypertension in metabolic syndrome: Toward a new paradigm. | |
| | |
MedLine Citation:
|
PMID: 20645932 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
|
Abstract The worldwide increase in the incidence of metabolic syndrome correlates with marked increase in total fructose intake in the form of high-fructose corn syrup, beverage and table sugar. Increased dietary fructose intake in rodents has been shown to recapitulate many aspects of metabolic syndrome by causing hypertension, insulin resistance, and hyperlipidemia. Recent studies demonstrated that increased dietary fructose intake stimulates salt absorption in the small intestine and kidney tubules, resulting in a state of salt overload and thus causing hypertension. The absorption of salt (sodium and chloride) in the small intestine is predominantly mediated via the chloride/base exchangers DRA (SLC26A3) and PAT1 (SLC26A6), and the Na(+)/H(+) exchanger NHE3 (SLC9A3). PAT1 and NHE3 also co-localize on the apical membrane of kidney proximal tubule. Luminal fructose stimulated salt absorption in the jejunum and kidney tubules, responses that were significantly diminished in PAT1 null mice. These studies further demonstrated that Glut5 (SLC2A5) is the major fructose-absorbing transporter in the small intestine (and kidney proximal tubule) and plays an essential role in the systemic homeostasis of fructose. Increased dietary fructose intake for several weeks upregulated the expression of NHE3, PAT1 and Glut5 in the intestine and resulted in hypertension in wild type mice, a response that was almost abolished in PAT1 null mice and abrogated in Glut5 null mice. This article will discuss the interaction of Glut5 with salt absorbing transporters and review the role of dietary fructose in enhanced salt absorption in intestine and kidney as it relates to the pathogenesis of hypertension in metabolic syndrome. |
| | |
Authors:
|
Manoocher Soleimani |
Publication Detail:
|
Type: JOURNAL ARTICLE Date: 2010-7-19 |
Journal Detail:
|
Title: Acta physiologica (Oxford, England) Volume: - ISSN: 1748-1716 ISO Abbreviation: - Publication Date: 2010 Jul |
Date Detail:
|
Created Date: 2010-7-21 Completed Date: - Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 101262545 Medline TA: Acta Physiol (Oxf) Country: - |
Other Details:
|
Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
|
Center on Genetics of Transport and Epithelial Biology and Department of Medicine, University of Cincinnati, Cincinnati, OH and Research Services, Veteran Administration Hospital in Cincinnati, OH. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: The combination of L-arginine and ischemic postconditioning at the onset of reperfusion limits myoca...
Next Document: The impact of maternal age on the effects of prenatal alcohol exposure on attention.