增强子
生物
胰岛
小岛
内分泌学
等位基因
2型糖尿病
基因座(遗传学)
内科学
β细胞
基因
胰岛素
糖尿病
基因表达
遗传学
医学
作者
Tamara S. Roman,Maren E. Cannon,Swarooparani Vadlamudi,Martin L. Buchkovich,Brooke N. Wolford,Ryan Welch,Mario A. Morken,Grace Kwon,Arushi Varshney,Romy Kursawe,Ying Wu,Anne Jackson,Michael R. Erdos,Johanna Kuusisto,Markku Laakso,Laura J. Scott,Michael Boehnke,Francis S. Collins,Stephen C.J. Parker,Michael L. Stitzel
出处
期刊:Diabetes
[American Diabetes Association]
日期:2017-07-06
卷期号:66 (9): 2521-2530
被引量:70
摘要
Molecular mechanisms remain unknown for most type 2 diabetes genome-wide association study identified loci. Variants associated with type 2 diabetes and fasting glucose levels reside in introns of ADCY5, a gene that encodes adenylate cyclase 5. Adenylate cyclase 5 catalyzes the production of cyclic AMP, which is a second messenger molecule involved in cell signaling and pancreatic β-cell insulin secretion. We demonstrated that type 2 diabetes risk alleles are associated with decreased ADCY5 expression in human islets and examined candidate variants for regulatory function. rs11708067 overlaps a predicted enhancer region in pancreatic islets. The type 2 diabetes risk rs11708067-A allele showed fewer H3K27ac ChIP-seq reads in human islets, lower transcriptional activity in reporter assays in rodent β-cells (rat 832/13 and mouse MIN6), and increased nuclear protein binding compared with the rs11708067-G allele. Homozygous deletion of the orthologous enhancer region in 832/13 cells resulted in a 64% reduction in expression level of Adcy5, but not adjacent gene Sec22a, and a 39% reduction in insulin secretion. Together, these data suggest that rs11708067-A risk allele contributes to type 2 diabetes by disrupting an islet enhancer, which results in reduced ADCY5 expression and impaired insulin secretion.
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