Analysis of common PTPN1gene variants in type 2 diabetes, obesity and associated phenotypes in the French population View Full Text


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Article Info

DATE

2006-12

AUTHORS

Claire Cheyssac, Cécile Lecoeur, Aurélie Dechaume, Amina Bibi, Guillaume Charpentier, Beverley Balkau, Michel Marre, Philippe Froguel, Fernando Gibson, Martine Vaxillaire

ABSTRACT

BACKGROUND: The protein tyrosine phosphatase-1B, a negative regulator for insulin and leptin signalling, potentially modulates glucose and energy homeostasis. PTP1B is encoded by the PTPN1 gene located on chromosome 20q13 showing linkage with type 2 diabetes (T2D) in several populations. PTPN1 gene variants have been inconsistently associated with T2D, and the aim of our study was to investigate the effect of PTPN1 genetic variations on the risk of T2D, obesity and on the variability of metabolic phenotypes in the French population. METHODS: Fourteen single nucleotide polymorphisms (SNPs) spanning the PTPN1 locus were selected from previous association reports and from HapMap linkage disequilibrium data. SNPs were evaluated for association with T2D in two case-control groups with 1227 cases and 1047 controls. Association with moderate and severe obesity was also tested in a case-control study design. Association with metabolic traits was evaluated in 736 normoglycaemic, non-obese subjects from a general population. Five SNPs showing a trend towards association with T2D, obesity or metabolic parameters were investigated for familial association. RESULTS: From 14 SNPs investigated, only SNP rs914458, located 10 kb downstream of the PTPN1 gene significantly associated with T2D (p = 0.02 under a dominant model; OR = 1.43 [1.06-1.94]) in the combined sample set. SNP rs914458 also showed association with moderate obesity (allelic p = 0.04; OR = 1.2 [1.01-1.43]). When testing for association with metabolic traits, two strongly correlated SNPs, rs941798 and rs2426159, present multiple consistent associations. SNP rs2426159 exhibited evidence of association under a dominant model with glucose homeostasis related traits (p = 0.04 for fasting insulin and HOMA-B) and with lipid markers (0.02 = p = 0.04). Moreover, risk allele homozygotes for this SNP had an increased systolic blood pressure (p = 0.03). No preferential transmission of alleles was observed for the SNPs tested in the family sample. CONCLUSION: In our study, PTPN1 variants showed moderate association with T2D and obesity. However, consistent associations with metabolic variables reflecting insulin resistance and dyslipidemia are found for two intronic SNPs as previously reported. Thus, our data indicate that PTPN1 variants may modulate the lipid profile, thereby influencing susceptibility to metabolic disease. More... »

PAGES

44

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/1471-2350-7-44

DOI

http://dx.doi.org/10.1186/1471-2350-7-44

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1022272835

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/16677372


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301 Imperial College Genome Centre and Section of Genomic Medicine, Hammersmith campus, Imperial College, W2 0NN, London, UK
302 rdf:type schema:Organization
303 https://www.grid.ac/institutes/grid.7452.4 schema:alternateName Paris Diderot University
304 schema:name INSERM U695, Faculté de Médecine Xavier Bichat, Paris, France
305 rdf:type schema:Organization
 




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