Evidence map›Paper›PMID 18562324›Full record

ArticleThe Journal of biological chemistry2008

Lactaturia and loss of sodium-dependent lactate uptake in the colon of SLC5A8-deficient mice.

Henning Frank, Nicole Gröger, Martin Diener, Christoph Becker, Thomas Braun, Thomas Boettger

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

37 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. The role of lactate in cardiovascular diseases.Cell communication and signaling : CCS · 2023
    Review
  6. Article
  7. Review
  8. Article
  9. Urinary ketone body loss leads to degeneration of brain white matter in elderly SLC5A8-deficient mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020
    Article
  10. Lactate: Fueling the fire starter.Wiley interdisciplinary reviews. Systems biology and medicine · 2020
    Review
  11. Involvement of butyrate in electrogenic KPflugers Archiv : European journal of physiology · 2019
    Article
  12. Deficiency of Dietary Fiber inCanadian journal of gastroenterology & hepatology · 2019
    Article
  13. Role of Membrane Transporters in Intestinal Cancers.Cellular and molecular gastroenterology and hepatology · 2019
    Article
  14. Article
  15. Iodide Binding in Sodium-Coupled Cotransporters.Journal of chemical information and modeling · 2017
    Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
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

6 authors at 3 institutions in 1 country.

Henning FrankDepartment of Cardiac Development and Remodelling, Max-Planck-Institut fuer Herzund Lungenforschung, Parkstrasse 1, D-61231 Bad Nauheim, Germany.
Nicole Gröger
Martin Diener
Christoph Becker
Thomas Braun
Thomas Boettger
Max Planck Institute for Heart and Lung Research · DEJohannes Gutenberg University Mainz · DEUniversity of Giessen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SLC5A8 is a member of the sodium/glucose cotransporter family. It has been proposed that SLC5A8 might act as an apical iodide transporter in the thyroid follicular cells or as a transporter of short chain monocarboxylates. We have directly addressed the functional role of SLC5A8 in vivo by generation of SLC5A8 mutant mice. We found that SLC5A8 is responsible for the re-absorption of lactate at the apical membrane of the kidney proximal tubules and of serous salivary gland ducts. In addition, SLC5A8 mediated the uptake of lactate into colonocytes under physiological conditions. We did not find any evidence of SLC5A8 being essential for the apical iodide transport in the thyroid gland, even if the ion-cotransporter SLC26A4, causing the human Pendred syndrome, is missing. Because SLC5A8 is transcriptionally silenced in many tumors, it has been proposed that SLC5A8-mediated transport of butyrate suppresses tumor formation. Treatment of Slc5a8(-/-) mice with carcinogens and breeding to the Apc(min) mouse line did not reveal a higher incidence of tumor formation. We conclude that SLC5A8 is instrumental in preventing lactaturia and loss of sodium-dependent uptake of lactate in the colon but does not have any apparent role in the prevention of tumor formation and growth.

Indexed as

AnimalsButyratesCarcinogensCation Transport ProteinsCell Transformation, NeoplasticColonIntestinal AbsorptionKidney DiseasesLactic AcidMiceMice, KnockoutMonocarboxylic Acid TransportersNeoplasms, ExperimentalSodiumButyratesCarcinogensCation Transport ProteinsLactic AcidMonocarboxylic Acid TransportersSlc5a8 protein, mouseSodium

Identifiers

PMID18562324
PMCPMC3259809
OpenAlexW1979417681

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.