Evidence map›Paper›PMID 8784789›Full record

ArticleMolecular medicine (Cambridge, Mass.)1996

Insulin-stimulated glucose uptake involves the transition of glucose transporters to a caveolae-rich fraction within the plasma membrane: implications for type II diabetes.

J Gustavsson, S Parpal, P Strålfors

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In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

25 citing papers in PubMed, 103 citations in OpenAlex.

  1. Statin Use and Hyperglycemia: Do Statins Cause Diabetes?Current atherosclerosis reports · 2024
    Review
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  8. Mechanisms of statin-induced new-onset diabetes.Journal of cellular physiology · 2019
    Review
  9. Article
  10. Cholesterol-enriched membrane microdomains are needed for insulin signaling and proliferation in hepatic cells.American journal of physiology. Gastrointestinal and liver physiology · 2018
    Article
  11. Article
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  15. Dissociation of the insulin receptor and caveolin-1 complex by ganglioside GM3 in the state of insulin resistance.Proceedings of the National Academy of Sciences of the United States of America · 2007
    Article
  16. Article
  17. Spatial and temporal regulation of GLUT4 translocation by flotillin-1 and caveolin-3 in skeletal muscle cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2006
    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

3 authors at 1 institution in 1 country.

J GustavssonDepartment of Cell Biology, Faculty of Health Sciences, University of Linköping, Sweden.
S Parpal
P Strålfors
Linköping University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAdipose and muscle tissues express an insulin-sensitive glucose transporter (GLUT4). This transporter has been shown to translocate from intracellular stores to the plasma membrane following insulin stimulation. The molecular mechanisms signalling this event and the details of the translocation pathway remain unknown. In type II diabetes, the cellular transport of glucose in response to insulin is impaired, partly explaining why blood-glucose levels in patients are not lowered by insulin as in normal individuals. MATERIALS AND

methodsIsolated rat epididymal adipocytes were stimulated with insulin and subjected to subcellular fractionation and to measurement of glucose uptake. A caveolae-rich fraction was isolated from the plasma membranes after detergent solubilization and ultracentrifugal floatation in a sucrose gradient. Presence of GLUT4 and caveolin was determined by immunoblotting after SDS-PAGE.

resultsIn freshly isolated adipocytes, insulin induced a rapid translocation of GLUT4 to the plasma membrane fraction, which was followed by a slower transition of the transporter into a detergent resistant caveolae-rich region of the plasma membrane. The insulin-stimulated appearance of transporters in the caveolae-rich fraction occurred in parallel with enhanced glucose uptake by cells. Treatment with isoproterenol plus adenosine deaminase rapidly inhibited insulin-stimulated glucose transport by 40%, and at the same time GLUT4 disappeared from the caveolae-rich fraction and from plasma membranes as a whole.

conclusionsInsulin stimulates glucose uptake in adipocytes by rapidly translocating GLUT4 from intracellular stores to the plasma membrane. This is followed by a slower transition of GLUT4 to the caveolae-rich regions of the plasma membrane, where glucose transport appears to take place. These results have implications for an understanding of the defect in glucose transport involved in type II diabetes.

Indexed as

Muscle ProteinsAdenosine DeaminaseAdipocytesAnimalsBiological TransportCell FractionationCell MembraneCells, CulturedDeoxyglucoseDiabetes Mellitus, Type 2EpididymisGlucoseGlucose Transporter Type 4InsulinIsoproterenolKineticsAdenosine DeaminaseDeoxyglucoseGlucoseGlucose Transporter Type 4InsulinIsoproterenolMonosaccharide Transport ProteinsMuscle ProteinsSlc2a4 protein, rat

Identifiers

PMID8784789
PMCPMC2230151
OpenAlexW1583163003

What OpenQuestion holds

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Registered trials

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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.