Evidence mapPaperPMID 8074198Full record

ReviewThe American journal of physiology1994

Hemodynamic actions of insulin.

A D Baron

4 registry-linked trialsAbstract readReview
PubMed Publisher
In one paragraph

Review in The American journal of physiology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 4 registered trials, which are not on this map. Cited by 150 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
150citing papers in PubMed, 3 pooled it
16.4field-weighted citation impact, top 1% 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.

NCT02633488 nacompletedstarted 2014, after this paper: background citation

Effect of Metformin on Insulin Sensitivity and Pan-Arterial Vascular Function in Adults With Metabolic Syndrome

Ran2014Enrolled19Registered outcomes1Posted comparisons1ConditionsInsulin Sensitivity, Metabolic SyndromeArmsMetformin, Placebos
Open the trial in the graph
NCT04133922 early_phase1withdrawnstarted 2019, after this paper: background citation

Effect of GLP-1 on Microvascular Insulin Responses in Type 1 Diabetes

Ran2019Enrolled0Registered outcomes5Posted comparisons0ConditionsInsulin Sensitivity/Resistance, Type 1 DiabetesArmsDextrose 20 % in Water, GLP-1, Insulin
Open the trial in the graph
NCT02490124 completednot on this mapstarted 2014, after this paper: background citation

The Effect of Type 1 Diabetes on Pan-Arterial Vascular Function and Insulin Sensitivity in Humans

TypeobservationalSponsorUniversity of VirginiaRan2014 to 2015Enrolled7ConditionsDiabetes Type 1
NCT03174288 nacompletednot on this mapstarted 2015, after this paper: background citation

The Impact of Fitness and Mineralocorticoid Receptor Blockade on Vascular Dysfunction in Adults With Type 1 Diabetes

TypeinterventionalSponsorUniversity of VirginiaRan2015 to 2019Enrolled32ConditionsType 1 DiabetesArmsExercise, Spironolactone
3 · Its place in the literature

Who cites it

150 citing papers in PubMed, 3 syntheses or guidelines pooled it, 604 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. Trial
  7. Trial
  8. Trial
  9. Trial
  10. Trial
  11. Trial
  12. Trial
  13. Trial
  14. Trial
  15. Trial
  16. Trial
  17. Trial
  18. Trial
  19. Review
  20. Review

90 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

1 author at 1 institution in 1 country.

A D BaronDepartment of Medicine, Indiana University School of Medicine, Indianapolis 46202-5124.
Indiana University – Purdue University Indianapolis · US

Funding

ROLE OF HEMODYNAMICS IN IN VIVO INSULIN RESISTANCER37DK042469 · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · 1999 to 2003
$1.1M
ROLE OF HEMODYNAMICS IN IN VIVO INSULIN RESISTANCER01DK042469 · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · 1995 to 1998
ROLE OF HEMODYNAMICS IN IN VIVO INSULIN RESISTANCER29DK042469 · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · 1990 to 1994
NIDDK NIH HHS DK-42469
6 · The paper itself

Abstract

There is accumulating evidence that insulin has a physiological role to vasodilate skeletal muscle vasculature in humans. This effect occurs in a dose-dependent fashion within a half-maximal response of approximately 40 microU/ml. This vasodilating action is impaired in states of insulin resistance such as obesity, non-insulin-dependent diabetes, and elevated blood pressure. The precise physiological role of insulin-mediated vasodilation is not known. Data indicate that the degree of skeletal muscle perfusion can be an important determinant of insulin-mediated glucose uptake. Therefore, it is possible that insulin-mediated vasodilation is an integral aspect of insulin's overall action to stimulate glucose uptake; thus defective vasodilation could potentially contribute to insulin resistance. In addition, insulin-mediated vasodilation may play a role in the regulation of vascular tone. Data are provided to indicate that the pressor response to systemic norepinephrine infusions is increased in obese insulin-resistant subjects. Moreover, the normal effect of insulin to shift the norepinephrine pressor dose-response curve to the right is impaired in these patients. Therefore, impaired insulin-mediated vasodilation could further contribute to the increased prevalence of hypertension observed in states of insulin resistance. Finally, data are presented to indicate that, via a yet unknown interaction with the endothelium, insulin is able to increase nitric oxide synthesis and release and through this mechanism vasodilate. It is interesting to speculate that states of insulin resistance might also be associated with a defect in insulin's action to modulate the nitric oxide system.(ABSTRACT TRUNCATED AT 250 WORDS)

Indexed as

AnimalsBlood PressureCardiac OutputHemodynamicsHumansInsulinModels, BiologicalMusclesRegional Blood FlowVascular ResistanceVasodilationVasomotor SystemInsulin

Identifiers

PMID8074198
OpenAlexW1782741946

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

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.