Evidence map›Paper›PMID 19091748›Full record

ArticleThe Journal of biological chemistry2009

Slc2a5 (Glut5) is essential for the absorption of fructose in the intestine and generation of fructose-induced hypertension.

Sharon Barone, Stacey L Fussell, Anurag Kumar Singh, Fred Lucas, Jie Xu, Charles Kim, Xudong Wu, Yiling Yu, Hassane Amlal, Ursula Seidler and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers.

0numbers the graph read from it
0cells of the map it votes in
132citing papers in PubMed
4.0field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

132 citing papers in PubMed, 233 citations in OpenAlex.

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  4. bioRxiv : the preprint server for biology · 2026
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  19. Handling the sugar rush: the role of the renal proximal tubule.American journal of physiology. Renal physiology · 2024
    Review
  20. Review

72 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

Sharon BaroneCenter on Genetics of Transport and Epithelial Biology and the Department of Medicine, University of Cincinnati, Cincinnati, Ohio 45267, USA.
Stacey L Fussell
Anurag Kumar Singh
Fred Lucas
Jie Xu
Charles Kim
Xudong Wu
Yiling Yu
Hassane Amlal
Ursula Seidler
Jian Zuo
Manoocher Soleimani
Veterans Health Administration · USSt. Jude Children's Research Hospital · USMedizinische Hochschule Hannover · DEUniversity of Cincinnati · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
GENETIC ANALYSIS OF MAMMALIAN HEARING SENSITIVITYR01DC006471 · NIDCD · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI ZUO, JIAN · 2004 to 2013
$3.5M
Apical CI/OH-/HCO3-exchanger in kidney and GI tractR01DK062809 · NIDDK · UNIVERSITY OF CINCINNATI · PI SOLEIMANI, MANOOCHER · 2004 to 2007
$1.5M
Apical Chloride/Bicarbonate Exchangers in Small Intestine and KidneyR56DK062809 · NIDDK · UNIVERSITY OF CINCINNATI · PI SOLEIMANI, MANOOCHER · 2009 to 2009
$461k
NCI NIH HHS CA21765NIDCD NIH HHS DC06471NIDDK NIH HHS DK 62809
6 · The paper itself

Abstract

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.

Indexed as

AnimalsBlood PressureChlorocebus aethiopsCOS CellsDietFructoseGlucoseGlucose Transporter Type 5Glucose Transport Proteins, FacilitativeHumansHypertensionIntestinal AbsorptionIntestinal MucosaIon TransportMiceMice, KnockoutFructoseGlucoseGlucose Transporter Type 5Glucose Transport Proteins, FacilitativeSLC2A5 protein, humanSlc2a5 protein, mouseStarchSweetening Agents

Identifiers

PMID19091748
PMCPMC2643499
OpenAlexW2039222039

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.