Evidence map›Paper›PMID 22822162›Full record

ArticleEndocrinology2012

Glucose transporter 8 (GLUT8) regulates enterocyte fructose transport and global mammalian fructose utilization.

Brian J DeBosch, Maggie Chi, Kelle H Moley

Abstract read
In one paragraph

Article in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

44 citing papers in PubMed, 71 citations in OpenAlex.

  1. Trial
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  9. Early Embryonic Development in Agriculturally Important Species.Animals : an open access journal from MDPI · 2024
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  12. Article
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  15. Article
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  19. Glucose transporters in the small intestine in health and disease.Pflugers Archiv : European journal of physiology · 2020
    Review
  20. Review
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

3 authors at 2 institutions in 1 country.

Brian J DeBoschDepartment of Pediatrics, Washington University in St. Louis School of Medicine, 660 South Euclid Avenue, St. Louis, Missouri 63110, USA.
Maggie Chi
Kelle H Moley
Washington University in St. Louis · USUniversity of Missouri–St. Louis · US

Funding

Pediatric Scientist Development Program (PSDP) [K12]K12HD000850 · NICHD · YALE UNIVERSITY · PI Sallie R. Permar · 1987 to 2026
$44.1M
WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI Jennifer Lynn Powers Carson · 2013 to 2026
$27.1M
TRANSGENICS COREP60DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI SCHAFFER, JEAN E. · 1986 to 2012
$25.2M
GLUTS AND GLUCOSE TRANSPORT IN THE MOUSE BLASTOCYSTR01HD040390 · NICHD · WASHINGTON UNIVERSITY · PI MOLEY, KELLE H · 2002 to 2012
$2.6M
NICHD NIH HHS 5K12HD000850-27NICHD NIH HHS K12 HD000850NICHD NIH HHS R01 HD040390NICHD NIH HHS R01HD040390-07NIDDK NIH HHS P30 DK020579NIDDK NIH HHS P60 DK020579
6 · The paper itself

Abstract

Enterocyte fructose absorption is a tightly regulated process that precedes the deleterious effects of excess dietary fructose in mammals. Glucose transporter (GLUT)8 is a glucose/fructose transporter previously shown to be expressed in murine intestine. The in vivo function of GLUT8, however, remains unclear. Here, we demonstrate enhanced fructose-induced fructose transport in both in vitro and in vivo models of enterocyte GLUT8 deficiency. Fructose exposure stimulated [(14)C]-fructose uptake and decreased GLUT8 protein abundance in Caco2 colonocytes, whereas direct short hairpin RNA-mediated GLUT8 knockdown also stimulated fructose uptake. To assess GLUT8 function in vivo, we generated GLUT8-deficient (GLUT8KO) mice. GLUT8KO mice exhibited significantly greater jejunal fructose uptake at baseline and after high-fructose diet (HFrD) feeding vs. wild-type mice. Strikingly, long-term HFrD feeding in GLUT8KO mice exacerbated fructose-induced increases in blood pressure, serum insulin, low-density lipoprotein and total cholesterol vs. wild-type controls. Enhanced fructose uptake paralleled with increased abundance of the fructose and glucose transporter, GLUT12, in HFrD-fed GLUT8KO mouse enterocytes and in Caco2 cultures exposed to high-fructose medium. We conclude that GLUT8 regulates enterocyte fructose transport by regulating GLUT12, and that disrupted GLUT8 function has deleterious long-term metabolic sequelae. GLUT8 may thus represent a modifiable target in the prevention and treatment of malnutrition or the metabolic syndrome.

Indexed as

AnimalsBiological TransportCaco-2 CellsEnterocytesFructoseGlucose Transport Proteins, FacilitativeHumansMiceMice, KnockoutMicroscopy, ConfocalFructoseGlucose Transport Proteins, FacilitativeSLC2A8 protein, humanSlc2a8 protein, mouse

Identifiers

PMID22822162
PMCPMC3423610
OpenAlexW2149411284

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.