Evidence mapPaperPMID 32389340Full record

ReviewThe Canadian journal of cardiology2020

Role of Hyperinsulinemia and Insulin Resistance in Hypertension: Metabolic Syndrome Revisited.

Alexandre A da Silva, Jussara M do Carmo, Xuan Li, Zhen Wang, Alan J Mouton, John E Hall

Open access · greenAbstract readReview
In one paragraph

Review in The Canadian journal of cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 242 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
242citing papers in PubMed, 6 pooled it
22.4field-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.

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

242 citing papers in PubMed, 6 syntheses or guidelines pooled it, 376 citations in OpenAlex.

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182 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

6 authors at 1 institution in 1 country.

Alexandre A da SilvaDepartment of Physiology and Biophysics, Mississippi Center for Obesity Research, and Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, Mississippi, USA. Electronic address: asilva@umc.edu.
Jussara M do CarmoDepartment of Physiology and Biophysics, Mississippi Center for Obesity Research, and Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Xuan LiDepartment of Physiology and Biophysics, Mississippi Center for Obesity Research, and Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Zhen WangDepartment of Physiology and Biophysics, Mississippi Center for Obesity Research, and Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Alan J MoutonDepartment of Physiology and Biophysics, Mississippi Center for Obesity Research, and Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, Mississippi, USA.
John E HallDepartment of Physiology and Biophysics, Mississippi Center for Obesity Research, and Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, Mississippi, USA.
University of Mississippi Medical Center · US

Funding

STRUCTURAL VASCULAR ADAPTATION OF THE MICROCIRCULATIONP01HL051971 · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · 1993 to 2005
$11.3M
Tracking and Evaluation CoreU54GM115428 · UNIVERSITY OF MISSISSIPPI MED CTR · 2025 to 2025
$3.6M
Project 003 - Lorena AmaralP20GM121334 · UNIVERSITY OF MISSISSIPPI MED CTR · 2025 to 2025
$2.6M
NHLBI NIH HHS P01 HL051971NIDDK NIH HHS R00 DK113280NIDDK NIH HHS R01 DK121411NIGMS NIH HHS P20 GM104357NIGMS NIH HHS U54 GM115428
6 · The paper itself

Abstract

Hyperinsulinemia and insulin resistance were proposed more than 30 years ago to be important contributors to elevated blood pressure (BP) associated with obesity and the metabolic syndrome, also called syndrome X. Support for this concept initially came from clinical and population studies showing correlations among hyperinsulinemia, insulin resistance, and elevated BP in individuals with metabolic syndrome. Short-term studies in experimental animals and in humans provided additional evidence that hyperinsulinemia may evoke increases in sympathetic nervous system (SNS) activity and renal sodium retention that, if sustained, could increase BP. Although insulin infusions may increase SNS activity and modestly raise BP in rodents, chronic insulin administration does not significantly increase BP in lean or obese insulin-resistant rabbits, dogs, horses, or humans. Multiple studies in humans and experimental animals have also shown that severe insulin resistance and hyperinsulinemia may occur in the absence of elevated BP. These observations question whether insulin resistance and hyperinsulinemia are major factors linking obesity/metabolic syndrome with hypertension. Other mechanisms, such as physical compression of the kidneys, activation of the renin-angiotensin-aldosterone system, hyperleptinemia, stimulation of the brain melanocortin system, and SNS activation, appear to play a more critical role in initiating hypertension in obese subjects with metabolic syndrome. However, the metabolic effects of insulin resistance, including hyperglycemia and dyslipidemia, appear to interact synergistically with increased BP to cause vascular and kidney injury that can exacerbate the hypertension and associated injury to the kidneys and cardiovascular system.

Indexed as

AnimalsHumansHyperinsulinismHypertensionInsulin ResistanceKidneyLeptinMetabolic SyndromeObesityRenin-Angiotensin SystemSodiumSympathetic Nervous SystemLeptinSodium

Identifiers

PMID32389340
PMCPMC7219403
OpenAlexW3006318956

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.