Evidence map›Paper›PMID 14673082›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2003

Glucose transporter-1-deficient mice exhibit impaired development and deformities that are similar to diabetic embryopathy.

Charles W Heilig, Thomas Saunders, Frank C Brosius, Kelle Moley, Kathleen Heilig, Raymond Baggs, LiRong Guo, David Conner

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 115 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. The role of SLC transporters for brain health and disease.Cellular and molecular life sciences : CMLS · 2021
    Review
  11. Review
  12. Review
  13. Glucose transporters in cardiovascular system in health and disease.Pflugers Archiv : European journal of physiology · 2020
    Review
  14. Glucose transporters in brain in health and disease.Pflugers Archiv : European journal of physiology · 2020
    Review
  15. Review
  16. Therapeutic strategies for glucose transporter 1 deficiency syndrome.Annals of clinical and translational neurology · 2019
    Review
  17. Article
  18. Article
  19. Article
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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

8 authors at 5 institutions in 1 country.

Charles W HeiligJohns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD 21205, USA. cheilig@jhmi.edu
Thomas Saunders
Frank C Brosius
Kelle Moley
Kathleen Heilig
Raymond Baggs
LiRong Guo
David Conner
Harvard University · USUniversity of Michigan–Ann Arbor · USHenry Ford Health System · USJohns Hopkins University · USUniversity of Rochester · US

Funding

GLUTS AND GLUCOSE TRANSPORT IN THE MOUSE BLASTOCYSTR01HD040390 · NICHD · WASHINGTON UNIVERSITY · PI MOLEY, KELLE H · 2002 to 2012
$2.6M
THE CELLULAR RESPONSE TO IRON STARVATION AND INTOXICATION IN YEASTZ01DK054507 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI PHILPOTT, CAROLINE C. · 1998 to 2008
$617k
REGULATION OF MESANGIAL CELL ECM SYNTHESIS BY GLUT1R01DK054507 · NIDDK · UNIVERSITY OF ROCHESTER · PI HEILIG, CHARLES W · 1998 to 2002
$499k
Intramural NIH HHS Z01 DK054507NICHD NIH HHS R01 HD040390NIDDK NIH HHS R01 DK54507
6 · The paper itself

Abstract

The hyperglycemia of maternal diabetes suppresses the glucose transporter-1 (GLUT1) facilitative glucose transporter 49-66% in preimplantation embryos. Glucose uptake is reduced and apoptosis is activated. We hypothesized that the reduction of embryonic GLUT1 may play a key role in the malformations of diabetic embryopathy. Therefore, we produced GLUT1-deficient transgenic mice [i.e., antisense-GLUT1 (GT1AS)] to determine whether GLUT1 deficiency alone could reproduce the growth defects. Early cell division of fertilized mouse eggs injected with GT1AS was markedly impaired, P < 0.001 vs. controls. Two populations of preimplantation embryos obtained from GT1AS x GT1AS heterozygote matings exhibited reduction of the 2-deoxyglucose uptake rate: one by 50% (presumed heterozygotes, P < 0.001 vs. control) and the other by 95% (presumed homozygotes, P < 0.001 vs. heterozygotes). Embryonic GLUT1 deficiency in the range reported with maternal diabetes was associated with growth retardation and developmental malformations similar to those described in diabetes-exposed embryos: intrauterine growth retardation (31.1%), caudal regression (9.8%), anencephaly with absence of the head (6.6%), microphthalmia (4.9%), and micrognathia (1.6%). Reduced body weight (small embryos, <70% of the nontransgenic body weight) was accompanied by other malformations and a 56% reduction of GLUT1 protein, P < 0.001 vs. nonsmall embryos (body weight >or=70% normal). The heart, brain, and kidneys of embryonic day 18.5 GT1AS embryos exhibited 24-51% reductions of GLUT1 protein. The homozygous GT1AS genotype was lethal during gestation. Reduced embryonic GLUT1 was associated with the appearance of apoptosis. Therefore, GLUT1 deficiency may play a role in producing embryonic malformations resulting from the hyperglycemia of maternal diabetes. Late gestational macrosomia was absent, apparently requiring a different mechanism.

Indexed as

Animalsbeta-GalactosidaseBiological TransportCongenital AbnormalitiesCrosses, GeneticDeoxyglucoseDiabetes MellitusDNA, AntisenseFemaleGlucose Transporter Type 1Litter SizeMaleMiceMice, TransgenicMonosaccharide Transport ProteinsPregnancybeta-GalactosidaseDeoxyglucoseDNA, AntisenseGlucose Transporter Type 1Monosaccharide Transport ProteinsSlc2a1 protein, mouse

Identifiers

PMID14673082
PMCPMC307616
OpenAlexW1994602446

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.