Skip Navigation


Human Molecular Genetics Advance Access originally published online on April 5, 2007
Human Molecular Genetics 2007 16(11):1343-1350; doi:10.1093/hmg/ddm084
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
16/11/1343    most recent
ddm084v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (4)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Meirhaeghe, A.
Right arrow Articles by Amouyel, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Meirhaeghe, A.
Right arrow Articles by Amouyel, P.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Association between the T-381C polymorphism of the brain natriuretic peptide gene and risk of type 2 diabetes in human populations

Aline Meirhaeghe1,*, Manjinder S. Sandhu2,3, Mark I. McCarthy4, Pascal de Groote5, Dominique Cottel1, Dominique Arveiler6, Jean Ferrières7, Christopher J. Groves4, Andrew T. Hattersley8, Graham A. Hitman9, Mark Walker10, Nicholas J. Wareham3 and Philippe Amouyel1

1 INSERM, U744, Lille; Institut Pasteur de Lille, Lille; Université de Lille 2, UMR-5744, Lille, France, 2 Department of Public Health and Primary Care, Institute of Public Health, University of Cambridge, Strangeways Research Laboratory, Cambridge, UK, 3 MRC Epidemiology Unit, Strangeways Research Laboratory, Cambridge, UK, 4 Diabetes Research Laboratories, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Oxford, UK, 5 Service de Cardiologie C, Hôpital Cardiologique, CHRU Lille, Lille, France, 6 Department of Epidemiology and Public Health, Faculty of Medicine, Strasbourg, France, 7 INSERM, U558, Faculté de Médecine, Toulouse, France, 8 Department of Diabetes and Vascular Medicine, Peninsula Medical School, Exeter, UK, 9 Department of Diabetes and Metabolic Medicine, Barts and the London, Queen Mary’s School of Medicine and Dentistry, University of London, London, UK and 10 Department of Medicine, School of Medicine, Newcastle University, Newcastle upon Tyne, UK

* To whom correspondence should be addressed at: INSERM, U744, Institut Pasteur de Lille, 1 rue du Pr. Calmette, BP 245, 59019 Lille Cedex, France. Tel: +33 320877391; Fax: +33 320877894; Email: aline.meirhaeghe-hurez{at}pasteur-lille.fr

Received January 23, 2007; Accepted March 27, 2007

Brain natriuretic peptide (BNP/NPPB) is a member of the natriuretic family involved in the regulation of blood pressure and blood volume as well as lipolysis control in human fat cells. Thus BNP may play a role in energy metabolism and metabolic diseases. We therefore assessed the association between the BNP promoter T-381C polymorphism and risk of type 2 diabetes and metabolic and BNP expression traits in several population samples. In French population-based samples (n = 3216), we found that individuals bearing the -381CC genotype had lower (P = 0.005) fasting glucose levels than -381TC or -381TT individuals. Moreover, the -381CC genotype was less frequent in individuals with type 2 diabetes (n = 280, 13.6%) or with impaired fasting glucose (n = 248, 12.9%) compared with normoglycaemic individuals (n = 2485, 17.8%). The adjusted odds ratio (OR) (95% CI) of type 2 diabetes for -381CC individuals was 0.69 (0.47–1.00), P = 0.05, when compared with -381T allele bearers. We replicated this association in four additional case–control studies for type 2 diabetes. The overall OR (95% CI) of type 2 diabetes was 0.85 (0.76–0.96), P = 0.008, (under a recessive model) (3593 cases and 6646 controls in total). We also found that the -381C allele was associated with higher plasma BNP concentrations (P = 0.015, n = 634) and higher BNP promoter activity in reporter gene assays. Collectively, these data suggest that relatively high BNP expression may protect against type 2 diabetes in humans.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
J. Physiol.Home page
J. Gutkowska, T. L. Broderick, D. Bogdan, D. Wang, J.-M. Lavoie, and M. Jankowski
Downregulation of oxytocin and natriuretic peptides in diabetes: possible implications in cardiomyopathy
J. Physiol., October 1, 2009; 587(19): 4725 - 4736.
[Abstract] [Full Text] [PDF]


Home page
Hum Mol GenetHome page
H. Choquet, C. Cavalcanti-Proenca, C. Lecoeur, C. Dina, S. Cauchi, M. Vaxillaire, S. Hadjadj, F. Horber, N. Potoczna, G. Charpentier, et al.
The T-381C SNP in BNP gene may be modestly associated with type 2 diabetes: an updated meta-analysis in 49 279 subjects
Hum. Mol. Genet., July 1, 2009; 18(13): 2495 - 2501.
[Abstract] [Full Text] [PDF]


Home page
Clin. Chem.Home page
C. Vassalle and M. G. Andreassi
Genetic Polymorphisms of the Natriuretic Peptide System in the Pathogenesis of Cardiovascular Disease: What Lies on the Horizon?
Clin. Chem., May 1, 2009; 55(5): 878 - 887.
[Abstract] [Full Text] [PDF]


Home page
Eur Heart JHome page
C. Christoffersen, I. Hunter, A. L. Jensen, and J. P. Goetze
Diabetes and the endocrine heart
Eur. Heart J., October 2, 2007; 28(20): 2427 - 2429.
[Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.