†; Juliana C.N. Chan; Brian Tomlinson">
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Volume 52, Issue 3, Pages 338-343 (March 2003)


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The lipoprotein lipase gene HindIII polymorphism is associated with lipid levels in early-onset type 2 diabetic patients☆☆

Yan Qin Ma, G.Neil Thomas, Maggie C.Y. Ng, Julian A.J.H. Critchley, Juliana C.N. Chan, Brian Tomlinson

Received 1 June 2002; accepted 16 September 2002.

Abstract 

Lipoprotein lipase (LPL) plays a central role in triglyceride metabolism, and the LPL gene T495G HindIII polymorphism has been associated with variations in lipid levels and heart disease in Caucasians with the more common H+ allele being associated with adverse lipid profiles and increased risk of CHD. We investigated this polymorphism in 785 Chinese subjects with varying components of the metabolic syndrome, including 61.4% with early-onset type 2 diabetes (age at diagnosis ≤ 40 years), and 167 healthy control subjects using a polymerase chain reaction (PCR)-based restriction fragment length polymorphism (RFLP) method. The allele and genotype frequencies were similar in the patients and control subjects. When grouped above or below standard cutoffs for triglyceride levels, the H+ allele was more frequent in hypertriglyceridemic than that in normotriglyceridemic subjects in the total population (81.5% v 76.1%) and early-onset type 2 diabetics (84.4% v 77.4%, both P < .05). Moreover, H+H+ carriers had significantly higher plasma triglyceride and lower high-density lipoprotein (HDL)-cholesterol levels when compared to subjects with the H- allele in the total population, and in patients with early-onset diabetics (both P < .05). In the total population and the early-onset diabetic patients, this relationship was confined to males when gender was considered. We conclude that the H+ allele of the LPL gene HindIII polymorphism is associated with higher plasma triglyceride and lower HDL-cholesterol levels in Chinese patients with early-onset diabetes. Copyright 2003, Elsevier Science (USA). All rights reserved.

No full text is available. To read the body of this article, please view the PDF online.

From the Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong SAR. †Deceased

 Supported by a Direct Grant for Research (code no. 2040526) from the Medicine Panel, The Chinese University of Hong Kong and grants from Hong Kong Research Grants Council (no. CUHK 4095/00M and CUHK Strategic Research Program 9902).

☆☆ Address reprint requests to Dr G. Neil Thomas, Department of Community Medicine, 5/F Academic and Administration Block, Faculty of Medicine Building, University of Hong Kong, 21 Sassoon Rd, Hong Kong.

PII: S0026-0495(02)05269-1

doi:10.1053/meta.2003.50053


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