Evidence map›Paper›PMID 25421524›Full record

ReviewDiabetologia2015

GLUT2, glucose sensing and glucose homeostasis.

Bernard Thorens

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 356 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
356citing papers in PubMed, 2 pooled it
23.2field-weighted citation impact, top 1% 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

356 citing papers in PubMed, 2 syntheses or guidelines pooled it, 708 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Morin counteracts KBrOMolecular and cellular biochemistry · 2026
    Article
  4. TheInternational journal of molecular sciences · 2026
    Article
  5. Article
  6. A Combination ofNutrients · 2026
    Article
  7. Review
  8. Nardilysin regulatesBiochemistry and biophysics reports · 2026
    Article
  9. Review
  10. Article
  11. Article
  12. Experimental models in diabetes research.Laboratory animal research · 2026
    Review
  13. Article
  14. Review
  15. Role of neddylation in diabetes metabolism: potential therapeutic target.Journal of diabetes and metabolic disorders · 2026
    Review
  16. Article
  17. Article
  18. Review
  19. Open veterinary journal · 2026
    Article
  20. Article

296 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

1 author at 1 institution in 1 country.

Bernard ThorensCenter for Integrative Genomics, University of Lausanne, Genopode Building, 1015, Lausanne, Switzerland, Bernard.Thorens@unil.ch.
University of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The glucose transporter isoform GLUT2 is expressed in liver, intestine, kidney and pancreatic islet beta cells, as well as in the central nervous system, in neurons, astrocytes and tanycytes. Physiological studies of genetically modified mice have revealed a role for GLUT2 in several regulatory mechanisms. In pancreatic beta cells, GLUT2 is required for glucose-stimulated insulin secretion. In hepatocytes, suppression of GLUT2 expression revealed the existence of an unsuspected glucose output pathway that may depend on a membrane traffic-dependent mechanism. GLUT2 expression is nevertheless required for the physiological control of glucose-sensitive genes, and its inactivation in the liver leads to impaired glucose-stimulated insulin secretion, revealing a liver-beta cell axis, which is likely to be dependent on bile acids controlling beta cell secretion capacity. In the nervous system, GLUT2-dependent glucose sensing controls feeding, thermoregulation and pancreatic islet cell mass and function, as well as sympathetic and parasympathetic activities. Electrophysiological and optogenetic techniques established that Glut2 (also known as Slc2a2)-expressing neurons of the nucleus tractus solitarius can be activated by hypoglycaemia to stimulate glucagon secretion. In humans, inactivating mutations in GLUT2 cause Fanconi-Bickel syndrome, which is characterised by hepatomegaly and kidney disease; defects in insulin secretion are rare in adult patients, but GLUT2 mutations cause transient neonatal diabetes. Genome-wide association studies have reported that GLUT2 variants increase the risks of fasting hyperglycaemia, transition to type 2 diabetes, hypercholesterolaemia and cardiovascular diseases. Individuals with a missense mutation in GLUT2 show preference for sugar-containing foods. We will discuss how studies in mice help interpret the role of GLUT2 in human physiology.

Indexed as

AnimalsDisease Models, AnimalGenome-Wide Association StudyGlucoseGlucose Transporter Type 2HomeostasisHumansHyperglycemiaInsulinMiceMutation, MissensePolymorphism, Single NucleotideSignal TransductionGlucoseGlucose Transporter Type 2InsulinSLC2A2 protein, humanSlc2a2 protein, mouse

Identifiers

PMID25421524
OpenAlexW2046120487

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.