Evidence map›Paper›PMID 24892324›Full record

ReviewColombia medica (Cali, Colombia)2013

An approach to the etiology of metabolic syndrome.

Angélica M Muñoz Contreras, Gabriel Bedoya Berrío, Claudia M Velásquez R

Open access · greenAbstract readReview
In one paragraph

Review in Colombia medica (Cali, Colombia), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. 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

3 authors at 1 institution in 1 country.

Angélica M Muñoz ContrerasResearch Group on Food and Human Nutrition. Universidad de Antioquia, E-mail: angelicamariamc@yahoo.com.
Gabriel Bedoya BerríoFaculty of Exact and Natural Sciences, Group of Molecular Genetics -GENMOL. Universidad de Antioquia, E-mail: gbedoya@quimbaya.udea.edu.co.
Claudia M Velásquez RSchool of Nutrition and Diet, Research Group on Food and Human Nutrition. Universidad de Antioquia, E-mail: claudia.velasquez@siu.udea.edu.co.
Universidad de Antioquia · CO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased prevalence of obesity in the world, especially accumulation of abnormal amounts of visceral fat predisposes to insulin resistance, which is the central role of metabolic syndrome (MS). Obesity can deregulate the intracellular signaling of insulin due to the production of inflammatory substances, chemoattractant proteins, adipokines and molecules that trigger hormonal mediator potentials for destabilization of signal transduction, leading to metabolic disorders such as hyperglycemia, hypertension, and dyslipidemia. The complexity of the MS and of the genetic mechanisms involved in its etiology derives from the combination of variants on genes involved and environmental factors that predispose it. The purpose of this paper is to review the effects of obesity in molecular and biochemical responses that trigger insulin resistance and its relation to some candidate genes and the ancestral component of the population.

Indexed as

ancestrygeneticsinsulin resistanceMetabolic syndromeobesity

Identifiers

PMID24892324
PMCPMC4002015
OpenAlexW1604036316

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.