Evidence map›Paper›PMID 23801575›Full record

ArticleDiabetes2013

Impaired tethering and fusion of GLUT4 vesicles in insulin-resistant human adipose cells.

Vladimir A Lizunov, Jo-Ping Lee, Monica C Skarulis, Joshua Zimmerberg, Samuel W Cushman, Karin G Stenkula

Abstract read
In one paragraph

Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. GLUT4 On the move.The Biochemical journal · 2022
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Metabolic regulation through the endosomal system.Traffic (Copenhagen, Denmark) · 2019
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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 2 institutions in 2 countries.

Vladimir A LizunovProgram in Physical Biology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA.
Jo-Ping Lee
Monica C Skarulis
Joshua Zimmerberg
Samuel W Cushman
Karin G Stenkula
National Institutes of Health · USEunice Kennedy Shriver National Institute of Child Health and Human Development · US

Funding

Mechanisms and Intracellular Components in Exocytosis, Membrane Assembly and Repair, and Parasite ReplicationZIAHD001415 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI ZIMMERBERG, JOSHUA · 2009 to 2025
$26.0M
Biobehavioral Studies of Obesity, Weight loss and RecidivismZIADK075007 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI MUNIYAPPA, RANGANATH · 2009 to 2025
$13.8M
Regulation of Glucose Transport in Adipose CellsZIADK055118 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI CUSHMAN, SAMUEL · 2009 to 2013
$1.4M
Intramural NIH HHS
6 · The paper itself

Abstract

Systemic glucose homeostasis is profoundly influenced by adipose cell function. Here we investigated GLUT4 dynamics in living adipose cells from human subjects with varying BMI and insulin sensitivity index (Si) values. Cells were transfected with hemagglutinin (HA)-GLUT4-green fluorescent protein (GFP)/mCherry (red fluorescence), and were imaged live using total internal reflection fluorescence and confocal microscopy. HA-GLUT4-GFP redistribution to the plasma membrane (PM) was quantified by surface-exposed HA epitope. In the basal state, GLUT4 storage vesicle (GSV) trafficking to and fusion with the PM were invariant with donor subject Si, as was total cell-surface GLUT4. In cells from insulin-sensitive subjects, insulin augmented GSV tethering and fusion approximately threefold, resulting in a corresponding increase in total PM GLUT4. However, with decreasing Si, these effects diminished progressively. All insulin-induced effects on GLUT4 redistribution and trafficking correlated strongly with Si and only weakly with BMI. Thus, while basal GLUT4 dynamics and total cell-surface GLUT4 are intact in human adipose cells, independent of donor Si, cells from insulin-resistant donors show markedly impaired GSV tethering and fusion responses to insulin, even after overnight culture. This altered insulin responsiveness is consistent with the hypothesis that adipose cellular dysfunction is a primary contributor to systemic metabolic dysfunction.

Indexed as

AdipocytesCells, CulturedGlucose Transporter Type 4HumansInsulinMicroscopy, FluorescenceProtein TransportGlucose Transporter Type 4Insulin

Identifiers

PMID23801575
PMCPMC3749349
OpenAlexW2151540881

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.