Evidence map›Paper›PMID 29077558›Full record

ArticleDevelopmental period medicine

[The genetics of obesity - pathogenetic, clinical and diagnostic aspects].

Artur Barczyk, Anna Kutkowska-Kaźmierczak, Jennifer Castañeda, Ewa Obersztyn

Open access · greenAbstract read
In one paragraph

Article in Developmental period medicine. 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
0.7field-weighted citation impact, top 23% 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. Review
  2. Review
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

4 authors at 1 institution in 1 country.

Artur BarczykZakład Genetyki Medycznej, Instytut Matki i Dziecka, Warszawa, Polska.
Anna Kutkowska-KaźmierczakZakład Genetyki Medycznej, Instytut Matki i Dziecka, Warszawa, Polska.
Jennifer CastañedaZakład Genetyki Medycznej, Instytut Matki i Dziecka, Warszawa, Polska.
Ewa ObersztynZakład Genetyki Medycznej, Instytut Matki i Dziecka, Warszawa, Polska.
Instytut Matki i Dziecka · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Due to its prevalence and its health-related, economic and social consequences, childhood and adult obesity is a complex, medical and civilizational problem, which has been on the increase in the last decade. The results of multi-center investigations reveal that genetic factors play an essential role in the etiopathogenesis of obesity, particularly in the case of extreme cases with very early onset. The Body Mass Index (BMI) is one of the most frequently used indicators of obesity and shows a strong genetic component with a 40-70% degree of heritability. The three types of genetically conditioned obesity are: (1) isolated (nonsyndromic) monogenic obesity, (2) syndromic monogenic obesity associated with dysmorphic features and/or congenital defects, caused by mutations in specific gene(s), (3) chromosomal aberrations, including submicroscopic changes. The most prevalent common (complex) obesity is linked to the presence of various changes in different genomic loci, which are subject to interactions and modifications by environmental (ethnic, dietary, lifestyle, bacterial flora, oxidative stress), as well as epigenetic (i.e., associated with DNA methylation, histone modification) and epistatic (gene-gene interaction) factors. Recent investigations using the modern methods of genome-wide association studies (GWAS), bioinformatics and proteomics, have made it possible to elucidate 8 key genes among the 97 genes most likely to play significant roles in the metabolic effects of obesity. The results of investigations on the pathogenesis of complex obesity do not as yet clarify the potential pathogenic significance of these genomic changes in humans. This article discusses the neuro-endocrinological regulation of the sensation of hunger and thirst, the clinical consequences of mutations in genes associated with the melanocortin pathway, and the features of the most common obesity syndromes, including syndromes conditioned by genomic imprinting. A diagnostic algorithm for cases of suspected syndromic obesity is proposed.

Indexed as

AdultChildEpigenomicsGenetic Predisposition to DiseaseGenetic TestingHumansLeptinObesityPediatric ObesityPhenotypeLeptingeneticshuman obesitymonogenic obesitymultifactorial obesityobesitysyndromic obesity

Identifiers

PMID29077558
PMCPMC8522950
OpenAlexW3025842848

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.