학술논문
Association of lipoprotein lipase S447X, apolipoprotein E exon 4, and apoC3 -455T>C polymorphisms on the susceptibility to diabetic nephropathy
Document Type
Author abstract
Author
Source
Clinical Genetics. July, 2006, Vol. 70 Issue 1, p20, 9 p.
Subject
Language
English
ISSN
0009-9163
Abstract
To purchase or authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1399-0004.2006.00628.x Byline: MCY Ng (a), JCN Chan (a), L Baum (a), W-Y So (a), VKL Lam (a), Y Wang (a), E Poon (a), B Tomlinson (a), S Cheng (b), K Lindpaintner (c) Keywords: diabetic nephropathy; genotype; lipids; polymorphism Abstract: Diabetic nephropathy (DN) is the leading cause of end-stage renal disease. In DN patients, triglyceride (TG) level is elevated and lipoprotein lipase (LPL) activity, which hydrolyzes TG, is decreased. The LPL S447X and apolipoprotein E (APOE) exon 4 polymorphisms affect TG levels, and the APOC3-455T>C polymorphism affects LPL activity. Our aim was to examine the association of these polymorphisms with nephropathy in type 2 diabetes. We examined these polymorphisms in a case-control study of type 2 diabetic patients including 374 with DN and 392 without DN. LPL 447X-containing genotypes (447X+) were significantly decreased in DN patients [18.6 vs 25.6%, odds ratio (OR) = 0.66, p = 0.02], as were APOE?3/?3 genotypes (64.8 vs 73.1%, OR = 0.68, p = 0.01). In addition, combinations of genotypes [APOE?3/?3 and LPL 447X+ (OR = 0.56), APOC3 CC and LPL 447X+ (OR = 0.31), APOE?3/?3 and APOC3 CC (OR = 0.61] were protective for DN compared with the most common combination of the respective polymorphisms. Our findings suggest the importance of interactions among lipid genes in modulating the risk of DN. Author Affiliation: (a)Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Shatin, Hong Kong, (b)Department of Human Genetics, Roche Molecular Systems, Alameda, CA, USA, and (c)Roche Center for Medical Genomics, F. Hoffmann-La Roche, AG, Basel, Switzerland Article History: Received 10 February 2006, revised and accepted for publication 20 April 2006 Article note: (*) Prof Juliana C. N. Chan, Department of Medicine and Therapeutics, Chinese University of Hong Kong, Shatin, Hong Kong. , Tel.: +852 2632 3138; , fax: +852 2632 3108; , e-mail: jchan@cuhk.edu.hk