目前尚不清楚血脂异常对2型188bet在线平台网址 和相关特征的影响。欧美学者们对此开展了一项研究，结果表明，遗传变异与血脂和2型188bet在线平台网址 有关，但在利用孟德尔随机化方法得出确切的因果关系结论之前，还需进一步研究特定血脂变异潜在的遗传机制。论文5月6日在线发表于《188bet在线平台网址 》(Diabetes)杂志。

        研究者们利用回归模型和140项血脂相关的遗传变异体评估循环血高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)和甘油三酯与2型188bet在线平台网址 及其相关特征的关系。对每种遗传检测法进行变异体对其他两种血脂类型和肥胖倾向作用的校正。研究者们利用最大的数据集合，获取了来自DIAGRAM联盟的34840例2型188bet在线平台网址 病例和114981例对照者，以及来自MAGIC和GENESIS研究的133010例非188bet在线平台网址 个体。

        结果显示，在标称水平上，变异组和188bet在线平台网址 特征的8/21相关性是明显的，包括那些遗传决定的较低HDL-C和2型188bet在线平台网址 之间，以及遗传决定的较低LDL-C和2型188bet在线平台网址 之间。

        参考文献：Tove Fall,et al. Diabetes . Published online before print May 6, 2015, doi:10.2337/db14-1710

Using genetic variants to assess the relationship between circulating lipids and type 2 diabetes
1. Tove Fall*,1,
2. Weijia Xie*,2,
3. Wenny Poon3,
4. Hanieh Yaghootkar2,
5. Reedik Mägi4,
6. the GENESIS consortium,
7. Joshua W Knowles5,
8. Valeriya Lyssenko3,
9. Michael Weedon2,
10. Timothy M Frayling*,2⇑ and
11. Erik Ingelsson*,1
+Author Affiliations
1. 1Department of Medical Sciences, Molecular Epidemiology and Science for Life Laboratory, Uppsala University, Uppsala, Sweden
2. 2Genetics of Complex Traits, Peninsula College of Medicine and Dentistry, University of Exeter, UK.
3. 3Department of Clinical Sciences, Diabetes and Endocrinology, Lund University Diabetes Center, Malmö, Sweden.
4. 4Estonian Genome Center, University of Tartu, Estonia.
5. 5Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA
1. Corresponding author: Timothy M Frayling, Email:t.m.frayling@exeter.ac.uk

Abstract
The effects of dyslipidemia on the risk of type 2 diabetes (T2D) and related traits are not clear.
We used regression models and 140 lipid-associated genetic variants to estimate associations between circulating HDL-cholesterol, LDL-cholesterol and triglycerides, and T2D and related traits. Each genetic test was corrected for effects of variants on the other two lipid types and surrogates of adiposity. We used the largest datasets available – 34,840 T2D cases and 114,981 controls from the DIAGRAM consortium and up to 133,010 non-diabetic individuals for insulin secretion and sensitivity, from the MAGIC and GENESIS studies.
Eight out of 21 associations between groups of variants and diabetes traits were significant at the nominal level, including those between genetically determined lower HDL-C (β=-0.12, P=0.03) and T2D, and genetically determined lower LDL-C (β =-0.21, P=5x10-6) and T2D. While some of these may represent causal associations, we discuss why caution must be used when using Mendelian randomization in the context of circulating lipid levels and diabetes traits.
In conclusion, we found evidence of links between genetic variants associated with lipids and T2D, but deepened knowledge of the underlying genetic mechanisms of specific lipid variants is needed before drawing definite conclusions about causality using Mendelian randomization methodology.