旧秩序阿米什人空腹血糖受损的表观遗传特征。

Journal of clinical epigenetics Pub Date : 2017-01-01 Epub Date: 2017-06-16 DOI:10.21767/2472-1158.100052
May E Montasser, Yu-Ching Cheng, Keith Tanner, Alan R Shuldiner, Jeffrey R O'Connell
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引用次数: 0

摘要

2型糖尿病(T2D)是一种常见的慢性疾病,具有巨大的疾病负担和经济影响。如果在早期发现,生活方式的改变可以显著改变疾病的进程。DNA甲基化特征可以作为早期检测T2D风险增加的生物标志物。设计:使用Illumina Infinium人甲基化450K芯片阵列对24名血糖正常的Old Order Amish (OOA)个体进行DNA甲基化分析,这些个体后来发展为空腹血糖受损(IFG)(病例),24名OOA个体在平均随访10年后仍保持正常血糖(对照组)。患者和对照组在年龄、性别、BMI、基线空腹血糖和75 g口服葡萄糖耐量试验(OGTT) 2小时后的血糖水平上相匹配。结果:关联分析发现,在病例和对照组之间,整体甲基化或单个探针甲基化没有显著差异,然而,前34个暗示显著的位点位于与T2D和血糖特征有有趣的生物学联系的基因上。这些基因包括BTC,在胰腺细胞增殖和胰岛素分泌中起作用,ITGA1是一种已知的骨密度基因,最近发现它也与T2D和血糖特征相关,并可能解释T2D和BMD之间的联系,RPTOR和TSC2都是胰岛素信号通路的一部分。结论:这些结果可能有助于揭示高血糖和T2D的发生和发展,并有助于识别高危个体进行早期干预;然而,需要进一步的研究来验证。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Epigenetic Signature of Impaired Fasting Glucose in the Old Order Amish.

Epigenetic Signature of Impaired Fasting Glucose in the Old Order Amish.

Introduction: Type 2 Diabetes (T2D) is a common chronic disease with substantial disease burden and economic impact. Lifestyle changes can significantly alter the course of the disease, if detected at an early stage. DNA methylation signature may serve as a biomarker for early detection of increased T2D risk.

Design: DNA methylation profiling was performed using the Illumina Infinium Human Methylation 450K Bead chip array in 24 normoglycemic Old Order Amish (OOA) individuals who later developed Impaired Fasting Glucose (IFG) (cases), and 24 OOA individuals who remained normoglycemic after an average follow up of 10 years (controls). Cases and controls were matched on age, sex, BMI, baseline fasting glucose, and glucose level after 2 h from 75 g Oral Glucose Tolerance Test (OGTT).

Results: Association analysis found no significant difference in either global methylation or individual probe methylation between cases and controls, however, the top 34 suggestive significant sites were located in genes with interesting biological links to T2D and glycemic traits. These genes include BTC that plays a role in pancreatic cell proliferation and insulin secretion, ITGA1 a known bone mineral density gene that was recently found to be associated also with T2D and glycemic traits, and may explain the link between T2D and BMD, and RPTOR and TSC2 both of which are part of insulin signaling pathway.

Conclusions: These results may shed light on the initiation and development of hyperglycemia and T2D and help to identify high risk individuals for early intervention; however, further studies are required for validation.

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