Evidence map›Paper›PMID 10444069›Full record

ArticleThe Journal of cell biology1999

Two compartments for insulin-stimulated exocytosis in 3T3-L1 adipocytes defined by endogenous ACRP30 and GLUT4.

J S Bogan, H F Lodish

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of cell biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

46 citing papers in PubMed, 174 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. CaJournal of cell science · 2019
    Article
  7. The Mechanism of Phillyrin from the Leaves ofBioMed research international · 2019
    Article
  8. Article
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  10. Article
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  12. Article
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  16. Ficus deltoidea: A Potential Alternative Medicine for Diabetes Mellitus.Evidence-based complementary and alternative medicine : eCAM · 2012 · on this map
    Article
  17. Article
  18. Article
  19. Adipokines as novel biomarkers and regulators of the metabolic syndrome.Annals of the New York Academy of Sciences · 2010
    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

2 authors at 2 institutions in 1 country.

J S BoganWhitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142-1479, USA.
H F Lodish
Massachusetts General Hospital · USWhitehead Institute for Biomedical Research · US

Funding

Lincs and miRs that regulate brown fat formation and functionR01DK047618 · NIDDK · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI LODISH, HARVEY F · 1994 to 2016
$6.3M
ADIPOCYTE PROTEIN SECRETION AND INSULIN ACTIONR37DK047618 · NIDDK · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI LODISH, HARVEY F · 1998 to 2007
$4.8M
NIDDK NIH HHS DK02371NIDDK NIH HHS DK47618NIDDK NIH HHS R01 DK047618NIDDK NIH HHS R37 DK047618
6 · The paper itself

Abstract

Insulin stimulates adipose cells both to secrete proteins and to translocate the GLUT4 glucose transporter from an intracellular compartment to the plasma membrane. We demonstrate that whereas insulin stimulation of 3T3-L1 adipocytes has no effect on secretion of the alpha3 chain of type VI collagen, secretion of the protein hormone adipocyte complement related protein of 30 kD (ACRP30) is markedly enhanced. Like GLUT4, regulated exocytosis of ACRP30 appears to require phosphatidylinositol-3-kinase activity, since insulin-stimulated ACRP30 secretion is blocked by pharmacologic inhibitors of this enzyme. Thus, 3T3-L1 adipocytes possess a regulated secretory compartment containing ACRP30. Whether GLUT4 recycles to such a compartment has been controversial. We present deconvolution immunofluorescence microscopy data demonstrating that the subcellular distributions of ACRP30 and GLUT4 are distinct and nonoverlapping; in contrast, those of GLUT4 and the transferrin receptor overlap. Together with supporting evidence that GLUT4 does not recycle to a secretory compartment via the trans-Golgi network, we conclude that there are at least two compartments that undergo insulin-stimulated exocytosis in 3T3-L1 adipocytes: one for ACRP30 secretion and one for GLUT4 translocation.

Indexed as

Intercellular Signaling Peptides and ProteinsMuscle ProteinsProteins3T3 CellsAdaptor Protein Complex gamma SubunitsAdipocytesAdiponectinAnimalsBlood ProteinsCoatomer ProteinCollagenEndoplasmic ReticulumExocytosisFluorescent Antibody TechniqueGlucose Transporter Type 4Golgi ApparatusAdaptor Protein Complex gamma SubunitsAdiponectinBlood ProteinsCoatomer ProteinCollagenendoplasminGlucose Transporter Type 4InsulinIntercellular Signaling Peptides and ProteinsMembrane GlycoproteinsMembrane ProteinsMicrotubule-Associated ProteinsMonosaccharide Transport ProteinsMuscle ProteinsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProteinsReceptors, TransferrinSlc2a4 protein, mouse

Identifiers

PMID10444069
PMCPMC2150549
OpenAlexW2124376410

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.