Evidence map›Paper›PMID 8649419›Full record

ArticleMolecular and cellular biology1996

Insulin signalling and insulin actions in the muscles and livers of insulin-resistant, insulin receptor substrate 1-deficient mice.

T Yamauchi, K Tobe, H Tamemoto, K Ueki, Y Kaburagi, R Yamamoto-Honda, Y Takahashi, F Yoshizawa, S Aizawa, Y Akanuma and 3 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

66 citing papers in PubMed, 289 citations in OpenAlex.

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  9. Insulin signaling in health and disease.The Journal of clinical investigation · 2021
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6 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

13 authors at 5 institutions in 3 countries.

T YamauchiThird Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
K Tobe
H Tamemoto
K Ueki
Y Kaburagi
R Yamamoto-Honda
Y Takahashi
F Yoshizawa
S Aizawa
Y Akanuma
N Sonenberg
Y Yazaki
T Kadowaki
The University of Tokyo · JPIwate Prefectural Morioka Agricultural High School · JPKumamoto University · JPMcGill University · CAThird Way · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We and others recently generated mice with a targeted disruption of the insulin receptor substrate 1 (IRS-1) gene and demonstrated that they exhibited growth retardation and had resistance to the glucose-lowering effect of insulin. Insulin initiates its biological effects by activating at least two major signalling pathways, one involving phosphatidylinositol 3-kinase (PI3-kinase) and the other involving a ras/mitogen-activated protein kinase (MAP kinase) cascade. In this study, we investigated the roles of IRS-1 and IRS-2 in the biological action in the physiological target organs of insulin by comparing the effects of insulin in wild-type and IRS-1-deficient mice. In muscles from IRS-1-deficient mice, the responses to insulin-induced PI3-kinase activation, glucose transport, p70 S6 kinase and MAP kinase activation, mRNA translation, and protein synthesis were significantly impaired compared with those in wild-type mice. Insulin-induced protein synthesis was both wortmannin sensitive and insensitive in wild-type and IRS-1 deficient mice. However, in another target organ, the liver, the responses to insulin-induced PI3-kinase and MAP kinase activation were not significantly reduced. The amount of tyrosine-phosphorylated IRS-2 (in IRS-1-deficient mice) was roughly equal to that of IRS-1 (in wild-type mice) in the liver, whereas it only 20 to 30% of that of IRS-1 in the muscles. In conclusion, (i) IRS-1 plays central roles in two major biological actions of insulin in muscles, glucose transport and protein synthesis; (ii) the insulin resistance of IRS-1-deficient mice is mainly due to resistance in the muscles; and (iii) the degree of compensation for IRS-1 deficiency appears to be correlated with the amount of tyrosine-phosphorylated IRS-2 (in IRS-1-deficient mice) relative to that of IRS-1 (in wild-type mice).

Indexed as

Adaptor Proteins, Signal TransducingAnimalsBiological Transport, ActiveCalcium-Calmodulin-Dependent Protein KinasesGlucoseGRB2 Adaptor ProteinInsulinInsulin Receptor Substrate ProteinsInsulin ResistanceIntracellular Signaling Peptides and ProteinsLiverMaleMiceMice, KnockoutMuscle, SkeletalPhosphatidylinositol 3-KinasesAdaptor Proteins, Signal TransducingCalcium-Calmodulin-Dependent Protein KinasesGlucoseGRB2 Adaptor ProteinGrb2 protein, mouseInsulinInsulin Receptor Substrate ProteinsIntracellular Signaling Peptides and ProteinsIrs1 protein, mouseIrs2 protein, mousePhosphatidylinositol 3-KinasesPhosphoproteinsPhosphotransferases (Alcohol Group Acceptor)ProteinsProtein Serine-Threonine KinasesReceptor, InsulinRibosomal Protein S6 KinasesTranscription FactorsTyrosine

Identifiers

PMID8649419
PMCPMC231302
OpenAlexW2108544809

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.