Evidence map›Paper›PMID 9410892›Full record

ArticleThe Journal of clinical investigation1997

Angiotensin II inhibits insulin signaling in aortic smooth muscle cells at multiple levels. A potential role for serine phosphorylation in insulin/angiotensin II crosstalk.

F Folli, C R Kahn, H Hansen, J L Bouchie, E P Feener

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed
6.1field-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

112 citing papers in PubMed, 425 citations in OpenAlex.

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  16. Hypertension and Type 2 Diabetes-The Novel Treatment Possibilities.International journal of molecular sciences · 2022
    Review
  17. Angiotensin II Inhibits Insulin Receptor Signaling in Adipose Cells.International journal of molecular sciences · 2022
    Article
  18. The Role of the Gut Microbiota in the Pathogenesis of Diabetes.International journal of molecular sciences · 2022
    Review
  19. Article
  20. Article

52 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

5 authors at 2 institutions in 1 country.

F FolliDepartment of Medicine I, I.R.C.C.S.H. San Raffaele, Milano, Italy.
C R Kahn
H Hansen
J L Bouchie
E P Feener
Harvard University Press · USJoslin Diabetes Center · US

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI ROHIT N. KULKARNI · 1986 to 2026
$50.5M
Insulin Receptor Substrates and Insulin ActionR01DK033201 · NIDDK · JOSLIN DIABETES CENTER · PI KAHN, C RONALD · 1986 to 2016
$10.6M
VASOACTIVE HORMONE INDUCED GENES IN DIABETIC VASCULATURER29DK048358 · NIDDK · JOSLIN DIABETES CENTER · PI FEENER, EDWARD P · 1995 to 1999
–
NIDDK NIH HHS DK 33201NIDDK NIH HHS DK 36836NIDDK NIH HHS DK 48358
6 · The paper itself

Abstract

To investigate potential interactions between angiotensin II (AII) and the insulin signaling system in the vasculature, insulin and AII regulation of insulin receptor substrate-1 (IRS-1) phosphorylation and phosphatidylinositol (PI) 3-kinase activation were examined in rat aortic smooth muscle cells. Pretreatment of cells with AII inhibited insulin-stimulated PI 3-kinase activity associated with IRS-1 by 60%. While AII did not impair insulin-stimulated tyrosine phosphorylation of the insulin receptor (IR) beta-subunit, it decreased insulin-stimulated tyrosine phosphorylation of IRS-1 by 50%. AII inhibited the insulin-stimulated association between IRS-1 and the p85 subunit of PI 3-kinase by 30-50% in a dose-dependent manner. This inhibitory effect of AII on IRS-1/PI 3-kinase association was blocked by the AII receptor antagonist saralasin, but not by AT1 antagonist losartan or AT2 antagonist PD123319. AII increased the serine phosphorylation of both the IR beta-subunit and IRS-1. In vitro binding experiments showed that autophosphorylation increased IR binding to IRS-1 from control cells by 2.5-fold versus 1.2-fold for IRS-1 from AII-stimulated cells, suggesting that AII stimulation reduces IRS-1's ability to associate with activated IR. In addition, AII increased p85 serine phosphorylation, inhibited the total pool of p85 associated PI 3-kinase activity, and decreased levels of the p50/p55 regulatory subunit of PI 3-kinase. These results suggest that activation of the renin-angiotensin system may lead to insulin resistance in the vasculature.

Indexed as

Angiotensin IIAnimalsAortaCells, CulturedInsulinInsulin Receptor Substrate ProteinsMuscle, Smooth, VascularPhosphatidylinositol 3-KinasesPhosphoproteinsPhosphoserinePhosphotyrosineRatsRats, Sprague-DawleyReceptor, InsulinReceptors, AngiotensinReceptors, Platelet-Derived Growth FactorAngiotensin IIInsulinInsulin Receptor Substrate ProteinsIrs1 protein, ratPhosphatidylinositol 3-KinasesPhosphoproteinsPhosphoserinePhosphotyrosineReceptor, InsulinReceptors, AngiotensinReceptors, Platelet-Derived Growth FactorTetradecanoylphorbol Acetate

Identifiers

PMID9410892
PMCPMC508410
OpenAlexW1984633752

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.