Evidence map›Paper›PMID 24748926›Full record

ReviewWorld journal of diabetes2014

Recent advances in the molecular genetics of type 2 diabetes mellitus.

Antonio Brunetti, Eusebio Chiefari, Daniela Foti

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in World journal of diabetes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 4 pooled it
14.7field-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

50 citing papers in PubMed, 4 syntheses or guidelines pooled it, 128 citations in OpenAlex.

  1. Pooled it
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  14. Insulin Resistance and Cancer: In Search for a Causal Link.International journal of molecular sciences · 2021
    Review
  15. Significant association ofJournal of diabetes and metabolic disorders · 2021
    Article
  16. Role of Wnt signaling pathways in type 2 diabetes mellitus.Molecular and cellular biochemistry · 2021
    Review
  17. Article
  18. Review
  19. Article
  20. Identification of Hub Genes in Type 2 Diabetes Mellitus Using Bioinformatics Analysis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020
    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.

Antonio BrunettiAntonio Brunetti, Eusebio Chiefari, Daniela Foti, Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Eusebio ChiefariAntonio Brunetti, Eusebio Chiefari, Daniela Foti, Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Daniela FotiAntonio Brunetti, Eusebio Chiefari, Daniela Foti, Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Magna Graecia University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes mellitus (T2DM) is a complex disease in which both genetic and environmental factors interact in determining impaired β-cell insulin secretion and peripheral insulin resistance. Insulin resistance in muscle, liver and fat is a prominent feature of most patients with T2DM and obesity, resulting in a reduced response of these tissues to insulin. Considerable evidence has been accumulated to indicate that heredity is a major determinant of insulin resistance and T2DM. It is believed that, among individuals destined to develop T2DM, hyperinsulinemia is the mechanism by which the pancreatic β-cell initially compensates for deteriorating peripheral insulin sensitivity, thus ensuring normal glucose tolerance. Most of these people will develop T2DM when β-cells fail to compensate. Despite the progress achieved in this field in recent years, the genetic causes of insulin resistance and T2DM remain elusive. Candidate gene association, linkage and genome-wide association studies have highlighted the role of genetic factors in the development of T2DM. Using these strategies, a large number of variants have been identified in many of these genes, most of which may influence both hepatic and peripheral insulin resistance, adipogenesis and β-cell mass and function. Recently, a new gene has been identified by our research group, the HMGA1 gene, whose loss of function can greatly raise the risk of developing T2DM in humans and mice. Functional genetic variants of the HMGA1 gene have been associated with insulin resistance syndromes among white Europeans, Chinese individuals and Americans of Hispanic ancestry. These findings may represent new ways to improve or even prevent T2DM.

Indexed as

Candidate geneGenetic variantsGenome-wide association studyHigh-mobility group A1Insulin resistant diabetes

Identifiers

PMID24748926
PMCPMC3990314
OpenAlexW169987683

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.