KCNQ1 变异对血脂谱和 2 型糖尿病的多效性影响：中国基于家系的研究。
Pleiotropic Effects of a KCNQ1 Variant on Lipid Profiles and Type 2 Diabetes: A Family-Based Study in China.
机构信息
Department of Epidemiology and Biostatistics, School of Public Health, Peking University Health Science Centre, Beijing, China.
Medical Informatics Center, Peking University Health Science Center, Beijing 100191, China.
出版信息
J Diabetes Res. 2020 Jan 13;2020:8278574. doi: 10.1155/2020/8278574. eCollection 2020.
OBJECTIVE
The genetic variant rs2237895, located in the Potassium Voltage-Gated Channel Subfamily Q Member 1 (KCNQ1) gene, has been replicated to be associated with type 2 diabetes mellitus (T2DM) susceptibility, but the relationship with lipids is conflicting. Furthermore, the common genetic predisposition to T2DM and lipids was not fully detected.
METHODS
In total, 5839 individuals (2220 were T2DM patients) across 2885 families were included. The effect of rs2237895 on T2DM and lipids was estimated using linear regression and logistic regression models after adjustment for multiple covariates. Mediation analysis was then used to test whether KCNQ1 participated in T2DM pathogenesis via lipid-mediated pathways.
RESULTS
Per allele-C of rs2237895 was associated with 17% (11-23%, < 0.001) increased T2DM risk. Moreover, it was correlated with 5% (1-9%, < 0.001) increased T2DM risk. Moreover, it was correlated with 5% (1-9%, < 0.001) increased T2DM risk. Moreover, it was correlated with 5% (1-9%, < 0.001) increased T2DM risk. Moreover, it was correlated with 5% (1-9%, < 0.001) increased T2DM risk. Moreover, it was correlated with 5% (1-9%, < 0.001) increased T2DM risk. Moreover, it was correlated with 5% (1-9%.
CONCLUSION
KCNQ1 had pleiotropic effects on lipids and T2DM, and the unexpected genetic effect on association of HDL-C with T2DM was observed, indicating the different pathways to lipids and T2DM. Further research studies are needed to verify potential biological mechanisms.
目的
位于钾电压门控通道亚家族 Q 成员 1（KCNQ1）基因中的遗传变异 rs2237895 已被复制与 2 型糖尿病（T2DM）易感性相关，但与脂质的关系存在冲突。此外，T2DM 和脂质的常见遗传易感性尚未完全检测到。
方法
共纳入 2885 个家系中的 5839 名个体（2220 名为 T2DM 患者）。使用线性回归和逻辑回归模型，在调整多个协变量后，估计 rs2237895 对 T2DM 和脂质的影响。然后使用中介分析来检验 KCNQ1 是否通过脂质介导途径参与 T2DM 的发病机制。
结果
rs2237895 的等位基因-C 与 17%（11-23%，<0.001）的 T2DM 风险增加相关。此外，它与 5%（1-9%，<0.001）的 T2DM 风险增加相关。此外，它与 5%（1-9%，<0.001）的 T2DM 风险增加相关。此外，它与 5%（1-9%，<0.001）的 T2DM 风险增加相关。此外，它与 5%（1-9%，<0.001）的 T2DM 风险增加相关。此外，它与 5%（1-9%，<0.001）的 T2DM 风险增加相关。此外，它与 5%（1-9%，<0.001）的 T2DM 风险增加相关。
结论
KCNQ1 对脂质和 T2DM 具有多效性作用，并且观察到 HDL-C 与 T2DM 关联的意外遗传效应，表明存在不同的脂质和 T2DM 途径。需要进一步的研究来验证潜在的生物学机制。
Zotero 插件