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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
8
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pubmed:dateCreated |
2009-2-16
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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.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-10371369,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-10926838,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-11172478,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-12399260,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-12748858,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-1439534,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-15460079,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-1695905,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-17001077,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-17222166,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-17443803,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-17851562,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-17921363,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-17964915,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-18301272,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-18393659,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-18417103,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-1910333,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-1918368,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-2189777,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-6326095,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-7946527,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-8213607,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-8261594,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-8333543,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-8650183,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-8662294,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-8884571,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-8927690,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-9124564,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-9662405,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19091748-9806880
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0021-9258
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pubmed:author |
pubmed-author:AmlalHassaneH,
pubmed-author:BaroneSharonS,
pubmed-author:FussellStacey LSL,
pubmed-author:KimCharlesC,
pubmed-author:LucasFredF,
pubmed-author:MEOLL,
pubmed-author:SeidlerUrsulaU,
pubmed-author:SinghAnurag KumarAK,
pubmed-author:SoleimaniManoocherM,
pubmed-author:WuXudongX,
pubmed-author:YuYilingY,
pubmed-author:ZuoJianJ
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pubmed:issnType |
Print
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pubmed:day |
20
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pubmed:volume |
284
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5056-66
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pubmed:dateRevised |
2010-9-23
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pubmed:meshHeading |
pubmed-meshheading:19091748-Animals,
pubmed-meshheading:19091748-Blood Pressure,
pubmed-meshheading:19091748-COS Cells,
pubmed-meshheading:19091748-Cercopithecus aethiops,
pubmed-meshheading:19091748-Diet,
pubmed-meshheading:19091748-Fructose,
pubmed-meshheading:19091748-Glucose,
pubmed-meshheading:19091748-Glucose Transport Proteins, Facilitative,
pubmed-meshheading:19091748-Glucose Transporter Type 5,
pubmed-meshheading:19091748-Humans,
pubmed-meshheading:19091748-Hypertension,
pubmed-meshheading:19091748-Intestinal Absorption,
pubmed-meshheading:19091748-Intestines,
pubmed-meshheading:19091748-Ion Transport,
pubmed-meshheading:19091748-Mice,
pubmed-meshheading:19091748-Mice, Knockout,
pubmed-meshheading:19091748-Starch,
pubmed-meshheading:19091748-Sweetening Agents
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pubmed:year |
2009
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pubmed:articleTitle |
Slc2a5 (Glut5) is essential for the absorption of fructose in the intestine and generation of fructose-induced hypertension.
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pubmed:affiliation |
Center on Genetics of Transport and Epithelial Biology and the Department of Medicine, University of Cincinnati, Cincinnati, Ohio 45267, USA.
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