Evidence map›Paper›PMID 16870829›Full record

ArticleAmerican journal of physiology. Cell physiology2007

Potentiation of insulin-stimulated glucose transport by the AMP-activated protein kinase.

Jeong-Sun Ju, Michael A Gitcho, Carter A Casmaer, Pankaj B Patil, Dae-Gyue Han, Susan A Spencer, Jonathan S Fisher

Abstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Vav3, a GEF for RhoA, Plays a Critical Role under High Glucose Conditions.Endocrinology and metabolism (Seoul, Korea) · 2014
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. A role for AMPK in increased insulin action after serum starvation.American journal of physiology. Cell physiology · 2010
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. 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

7 authors at 1 institution in 1 country.

Jeong-Sun JuDepartment of Biology, Saint Louis University, 3507 Laclede Avenue, St. Louis, MO 63103, USA.
Michael A Gitcho
Carter A Casmaer
Pankaj B Patil
Dae-Gyue Han
Susan A Spencer
Jonathan S Fisher
Saint Louis University · US

Funding

ARK5 AMP-activated protein kinase and glucose transportK01DK066330 · NIDDK · SAINT LOUIS UNIVERSITY · PI FISHER, JONATHAN S · 2004 to 2007
$373k
NIDDK NIH HHS K01 DK 066330NIDDK NIH HHS K01 DK066330
6 · The paper itself

Abstract

Data from the use of activators and inhibitors of the AMP-activated protein kinase (AMPK) suggest that AMPK increases sensitivity of glucose transport to stimulation by insulin in muscle cells. We assayed insulin action after adenoviral (Ad) transduction of constitutively active (CA; a truncated form of AMPKalpha(1)) and dominant-negative (DN; which depletes endogenous AMPKalpha) forms of AMPKalpha (Ad-AMPKalpha-CA and Ad-AMPKalpha-DN, respectively) into C(2)C(12) myotubes. Compared with control (Ad-green fluorescent protein), Ad-AMPK-CA increased the ability of insulin to stimulate glucose transport. The increased insulin action in cells expressing AMPK-CA was suppressed by compound C (an AMPK inhibitor). Exposure of cells to 5-aminoimidazole-4-carboxamide-1beta-D-ribofuranoside (an AMPK activator) increased insulin action in uninfected myotubes and myotubes transduced with green fluorescent protein but not in Ad-AMPK-DN-infected myotubes. In Ad-AMPK-CA-transduced cells, serine phosphorylation of insulin receptor substrate 1 was decreased at a mammalian target of rapamycin (or p70 S6 kinase) target site that has been reported to be associated with insulin resistance. These data suggest that, in myotubes, activated AMPKalpha(1) is sufficient to increase insulin action and that the presence of functional AMPKalpha is required for 5-aminoimidazole-4-carboxamide-1beta,D-ribofuranoside-related increases in insulin action.

Indexed as

Aminoimidazole CarboxamideAMP-Activated Protein KinasesAnimalsBiological TransportCells, CulturedDrug SynergismEnzyme ActivatorsGenes, DominantGlucoseGreen Fluorescent ProteinsHypoglycemic AgentsInsulinInsulin Receptor Substrate ProteinsIsoenzymesLuminescent AgentsMiceAICA ribonucleotideAminoimidazole CarboxamideAMP-Activated Protein KinasesEnzyme ActivatorsGlucoseGreen Fluorescent ProteinsHypoglycemic AgentsInsulinInsulin Receptor Substrate ProteinsIrs1 protein, mouseIsoenzymesLuminescent AgentsmTOR protein, mouseMultienzyme ComplexesPhosphoproteinsProtein KinasesProtein Serine-Threonine KinasesRibonucleotidesTOR Serine-Threonine Kinases

Identifiers

PMID16870829
PMCPMC1868576
OpenAlexW2107627105

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.