Evidence map›Paper›PMID 15235769›Full record

ArticleDiabetologia2004

Single nucleotide polymorphisms of protein tyrosine phosphatase 1B gene are associated with obesity in morbidly obese French subjects.

S Kipfer-Coudreau, D Eberlé, M Sahbatou, A Bonhomme, B Guy-Grand, P Froguel, P Galan, A Basdevant, K Clément

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

16 citing papers in PubMed, 37 citations in OpenAlex.

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  12. Berberine Moderates Glucose and Lipid Metabolism through Multipathway Mechanism.Evidence-based complementary and alternative medicine : eCAM · 2011
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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

9 authors at 7 institutions in 2 countries.

S Kipfer-CoudreauINSERM Avenir and EA 3502, Nutrition Department, Paris VI University, Paris, France.
D EberléINSERM Avenir and EA 3502, Nutrition Department, Paris VI University, Paris, France.
M SahbatouCentre d'Etude du Polymorphisme Humain, Paris, France.
A BonhommeINSERM Avenir and EA 3502, Nutrition Department, Paris VI University, Paris, France.
B Guy-GrandINSERM Avenir and EA 3502, Nutrition Department, Paris VI University, Paris, France.
P FroguelCNRS UPRESA 80-90, Lille Institute of Biology, Pasteur Institute, Lille and Hammersmith Genome Centre, Imperial College, London, UK.
P GalanINSERM/INRA/CNAM, Institut Scientifique et Technique de la Nutrition et de l'Alimentation, ISTNA/CNAM, Paris, France.
A BasdevantINSERM Avenir and EA 3502, Nutrition Department, Paris VI University, Paris, France.
K ClémentINSERM Avenir and EA 3502, Nutrition Department, Paris VI University, Paris, France. karine.clement@htd.ap-hop-paris.fr.
Inserm · FRSorbonne Université · FRConservatoire National des Arts et Métiers · FRFondation Jean Dausset-CEPH · FRQueen Mary University of London · GBUniversité de Reims Champagne-Ardenne · FRUniversité Paris 8 · FR

Funding

Medical Research Council G0000477
6 · The paper itself

Abstract

aims/hypothesisThe development of insulin resistance may contribute to the occurrence and progression of the metabolic syndrome associated with obesity. Components contributing to the insulin pathway and its regulation are good candidates for the molecular study of metabolic syndrome pathogenesis. Protein tyrosine phosphatase 1B (PTP 1B) is an important negative regulator of insulin. We investigated whether PTP 1B SNPs are associated with obesity and obesity-related traits as well as global metabolic syndrome in morbidly obese subjects.

methodsUntranslated and coding regions of the PTP 1B gene were screened in groups of non-diabetic and diabetic obese subjects and in non-obese subjects. Unrelated morbidly obese ( n=711) and non-obese ( n=427) French Caucasian subjects were genotyped for a case-control study.

resultsSix SNPs were identified: two rare variants were located in 5'UTR (-109 C>T and -69 C>T), two in the intronic regions (IVS3+38 G>T and IVS5+3666delT) and two have been described previously (P303P in exon 8 and P387L in exon 9). A case-control study showed an association between the frequent IVS5+3666delT SNP and obesity ( p=0.02). In the obese group, associations between PTP 1B SNPs and features of dyslipidaemia were found. P303P was associated with lower apolipoprotein A1 levels ( p=0.05) whereas P387L was associated with higher triglyceride ( p=0.0003), apolipoprotein B ( p=0.09) and lipoprotein a concentrations ( p=0.006). CONCLUSIONS/

interpretationOur results support the hypothesis that the PTP 1B gene contributes to the polygenic basis of obesity. PTP 1B SNPs may interact with environmental factors to induce more severe phenotypes, e.g. atherogenic dyslipidaemia, in morbidly obese subjects.

Indexed as

CholesterolDNA PrimersFranceGenetic TestingGenetic VariationHumansObesity, MorbidPolymerase Chain ReactionPolymorphism, Single NucleotideProtein Tyrosine Phosphatase, Non-Receptor Type 1Protein Tyrosine PhosphatasesTriglyceridesCholesterolDNA PrimersProtein Tyrosine Phosphatase, Non-Receptor Type 1Protein Tyrosine PhosphatasesPTPN1 protein, humanTriglycerides

Identifiers

PMID15235769
OpenAlexW1971523035

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.