Evidence map›Paper›PMID 17464498›Full record

ArticleDiabetologia2007

A German genome-wide linkage scan for type 2 diabetes supports the existence of a metabolic syndrome locus on chromosome 1p36.13 and a type 2 diabetes locus on chromosome 16p12.2.

K Hoffmann, M Mattheisen, S Dahm, P Nürnberg, C Roe, J Johnson, N J Cox, H E Wichmann, T F Wienker, J Schulze and 2 more

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In one paragraph

Article in Diabetologia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

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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

14 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. The Values and Perspectives of Organoids in the Field of Metabolic Syndrome.International journal of molecular sciences · 2023
    Review
  3. Article
  4. Microfibril-associated glycoproteins MAGP-1 and MAGP-2 in disease.Matrix biology : journal of the International Society for Matrix Biology · 2018
    Review
  5. Article
  6. The microfibril-associated glycoproteins (MAGPs) and the microfibrillar niche.Matrix biology : journal of the International Society for Matrix Biology · 2015
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Prostasin: a possible candidate gene for human hypertension.American journal of hypertension · 2008
    Article
  13. Genetics of metabolic syndrome.Current diabetes reports · 2008
    Review
  14. 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

12 authors at 9 institutions in 2 countries.

K HoffmannInstitute of Medical Genetics, Charité, University Medical School, Humboldt University, Berlin, Germany.
M Mattheisen
S Dahm
P Nürnberg
C Roe
J Johnson
N J Cox
H E Wichmann
T F Wienker
J Schulze
P E Schwarz
T H Lindner
University Hospital Carl Gustav Carus · DEUniversity of Bonn · DEUniversity of Chicago · USAdvocate Illinois Masonic Medical Center · USCharité - Universitätsmedizin Berlin · DEInstitute of Groundwater Ecology · DEMax Delbrück Center · DENuremberg Hospital · DEUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisThe aim was to identify type 2 diabetes susceptibility regions in 250 German families. SUBJECTS AND

methodsWe conducted a genome-wide linkage scan using 439 short tandem repeat polymorphisms at an average resolution of 7.76 +/- 3.80 cM (Marshfield). In an affected-only-design (affected sib pairs), we performed nonparametric multipoint linkage analyses. Conditional analyses were applied where linkage signals were found in the baseline analyses.

resultsWe identified two loci with nominal evidence for linkage on chromosomes 1p36.13 and 16p12.2 (D1S3669, 37.05 cM, logarithmic odds ratio [LOD] = 1.49, p = 0.004; D16S403, 43.89 cM, LOD = 1.85, p = 0.002). D16S403 crossed the empirically obtained threshold of genome-wide suggestive significance of LOD = 1.51. Positive findings in those regions have been reported by the following other linkage studies on: (1) symptomatic/clinical gall bladder disease with type 2 diabetes in Mexican Americans from the San Antonio Family Diabetes/Gallbladder Study (LOD = 3.7, D1S1597-D1S407, 29.93-33.75 cM); (2) body size-adiposity in another Mexican American population (D1S1597, LOD = 2.53, 29.93 cM); (3) lipid abnormalities (LOD = 3.1, D1S2826-D1S513, 41.92-60.01 cM); and (4) hypertension in Australian sib pairs (LOD = 3.1, D1S2834-D1S2728, 31.02-33.75 cM); as well as (5) a meta-analysis of four European type 2 diabetes-related genome scans (LOD = 1.09, D16S412, 42.81 cM). In linkage analyses conditional on evidence for linkage at D16S403 we identified a LOD increase (Delta LOD) of 1.55 (p = 0.0075) at D17S2180. Similar conditioning on D17S2180 revealed evidence for interaction with D1S3669 (Delta LOD = 1.67, p = 0.0055), D16S403 (Delta LOD = 1.48, p = 0.0091) and another locus on chromosome 1 where several genome scans have reported evidence for linkage ( approximately 200 cM, Delta LOD = 1.60, p = 0.0066). CONCLUSIONS/

interpretationOur results and the findings of other studies are consistent with the presence of a locus for a complex metabolic syndrome on chromosome 1p36.13.

Indexed as

Chromosomes, Human, Pair 1Chromosomes, Human, Pair 16Genetic LinkageGenomicsChromosome MappingDiabetes Mellitus, Type 2FemaleGenetic Predisposition to DiseaseGenome, HumanGermanyHumansMaleMetabolic SyndromeOdds RatioPolymorphism, Genetic

Identifiers

PMID17464498
OpenAlexW2061825805

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Registered trials

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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.