| pubmed-article:19091748 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19091748 | lifeskim:mentions | umls-concept:C0020538 | lld:lifeskim |
| pubmed-article:19091748 | lifeskim:mentions | umls-concept:C0021853 | lld:lifeskim |
| pubmed-article:19091748 | lifeskim:mentions | umls-concept:C0000854 | lld:lifeskim |
| pubmed-article:19091748 | lifeskim:mentions | umls-concept:C0016745 | lld:lifeskim |
| pubmed-article:19091748 | lifeskim:mentions | umls-concept:C1420176 | lld:lifeskim |
| pubmed-article:19091748 | lifeskim:mentions | umls-concept:C0079411 | lld:lifeskim |
| pubmed-article:19091748 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
| pubmed-article:19091748 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:19091748 | pubmed:dateCreated | 2009-2-16 | lld:pubmed |
| pubmed-article:19091748 | pubmed:abstractText | The identity of the transporter responsible for fructose absorption in the intestine in vivo and its potential role in fructose-induced hypertension remain speculative. Here we demonstrate that Glut5 (Slc2a5) deletion reduced fructose absorption by approximately 75% in the jejunum and decreased the concentration of serum fructose by approximately 90% relative to wild-type mice on increased dietary fructose. When fed a control (60% starch) diet, Glut5(-/-) mice had normal blood pressure and displayed normal weight gain. However, whereas Glut5(+/+) mice showed enhanced salt absorption in their jejuna in response to luminal fructose and developed systemic hypertension when fed a high fructose (60% fructose) diet for 14 weeks, Glut5(-/-) mice did not display fructose-stimulated salt absorption in their jejuna, and they experienced a significant impairment of nutrient absorption in their intestine with accompanying hypotension as early as 3-5 days after the start of a high fructose diet. Examination of the intestinal tract of Glut5(-/-) mice fed a high fructose diet revealed massive dilatation of the caecum and colon, consistent with severe malabsorption, along with a unique adaptive up-regulation of ion transporters. In contrast to the malabsorption of fructose, Glut5(-/-) mice did not exhibit an absorption defect when fed a high glucose (60% glucose) diet. We conclude that Glut5 is essential for the absorption of fructose in the intestine and plays a fundamental role in the generation of fructose-induced hypertension. Deletion of Glut5 results in a serious nutrient-absorptive defect and volume depletion only when the animals are fed a high fructose diet and is associated with compensatory adaptive up-regulation of ion-absorbing transporters in the colon. | lld:pubmed |
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| pubmed-article:19091748 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19091748 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19091748 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19091748 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19091748 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19091748 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:19091748 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:19091748 | pubmed:author | pubmed-author:SoleimaniMano... | lld:pubmed |
| pubmed-article:19091748 | pubmed:author | pubmed-author:ZuoJianJ | lld:pubmed |
| pubmed-article:19091748 | pubmed:author | pubmed-author:SeidlerUrsula... | lld:pubmed |
| pubmed-article:19091748 | pubmed:author | pubmed-author:MEOLL | lld:pubmed |
| pubmed-article:19091748 | pubmed:author | pubmed-author:KimCharlesC | lld:pubmed |
| pubmed-article:19091748 | pubmed:author | pubmed-author:WuXudongX | lld:pubmed |
| pubmed-article:19091748 | pubmed:author | pubmed-author:AmlalHassaneH | lld:pubmed |
| pubmed-article:19091748 | pubmed:author | pubmed-author:BaroneSharonS | lld:pubmed |
| pubmed-article:19091748 | pubmed:author | pubmed-author:YuYilingY | lld:pubmed |
| pubmed-article:19091748 | pubmed:author | pubmed-author:SinghAnurag... | lld:pubmed |
| pubmed-article:19091748 | pubmed:author | pubmed-author:FussellStacey... | lld:pubmed |
| pubmed-article:19091748 | pubmed:author | pubmed-author:LucasFredF | lld:pubmed |
| pubmed-article:19091748 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:19091748 | pubmed:day | 20 | lld:pubmed |
| pubmed-article:19091748 | pubmed:volume | 284 | lld:pubmed |
| pubmed-article:19091748 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19091748 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19091748 | pubmed:pagination | 5056-66 | lld:pubmed |
| pubmed-article:19091748 | pubmed:dateRevised | 2010-9-23 | lld:pubmed |
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| pubmed-article:19091748 | pubmed:meshHeading | pubmed-meshheading:19091748... | lld:pubmed |
| pubmed-article:19091748 | pubmed:meshHeading | pubmed-meshheading:19091748... | lld:pubmed |
| pubmed-article:19091748 | pubmed:meshHeading | pubmed-meshheading:19091748... | lld:pubmed |
| pubmed-article:19091748 | pubmed:meshHeading | pubmed-meshheading:19091748... | lld:pubmed |
| pubmed-article:19091748 | pubmed:meshHeading | pubmed-meshheading:19091748... | lld:pubmed |
| pubmed-article:19091748 | pubmed:meshHeading | pubmed-meshheading:19091748... | lld:pubmed |
| pubmed-article:19091748 | pubmed:meshHeading | pubmed-meshheading:19091748... | lld:pubmed |
| pubmed-article:19091748 | pubmed:meshHeading | pubmed-meshheading:19091748... | lld:pubmed |
| pubmed-article:19091748 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19091748 | pubmed:articleTitle | Slc2a5 (Glut5) is essential for the absorption of fructose in the intestine and generation of fructose-induced hypertension. | lld:pubmed |
| pubmed-article:19091748 | pubmed:affiliation | Center on Genetics of Transport and Epithelial Biology and the Department of Medicine, University of Cincinnati, Cincinnati, Ohio 45267, USA. | lld:pubmed |
