Variants in the SIRT1 Gene May Affect Diabetes Risk in Interaction With Prenatal Exposure to Famine

被引：47

作者：

Botden, Ilse P. G. ^{[1
]}

Zillikens, M. Carola ^{[1
]}

de Rooij, Susanne R. ^{[2
]}

Langendonk, Janneke G. ^{[1
]}

Danser, A. H. Jan ^{[1
]}

Sijbrands, Eric J. G. ^{[1
]}

Roseboom, Tessa J. ^{[2
,3
]}

机构：

[1] Erasmus Univ, Med Ctr, Dept Internal Med, Rotterdam, Netherlands

[2] Univ Amsterdam, Acad Med Ctr, Dept Clin Epidemiol Biostat & Bioinformat, NL-1105 AZ Amsterdam, Netherlands

[3] Univ Amsterdam, Acad Med Ctr, Dept Obstet & Gynecol, NL-1105 AZ Amsterdam, Netherlands

来源：

DIABETES CARE | 2012年 / 35卷 / 02期

关键词：

GLUCOSE-METABOLISM; BETA-CELLS; APOPTOSIS; OBESITY; DISEASE; LIFE;

D O I：

10.2337/dc11-1203

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

OBJECTIVE-To investigate whether SIRT1, a nutrient-sensing histone deacetylase, influences fetal programming during malnutrition. RESEARCH DESIGN AND METHODS-In 793 individuals of the Dutch Famine Birth Cohort, we analyzed the interaction between three SIRT1 single nucleotide polymorphisms (SNPs) and prenatal exposure to famine on type 2 diabetes risk. RESULTS-In the total population (exposed and unexposed), SIRT1 variants were not associated with type 2 diabetes. A significant interaction was found between two SIRT1 SNPs and exposure to famine in utero on type 2 diabetes risk (P = 0.03 for rs7895833; P = 0.01 for rs1467568). Minor alleles of these SNPs were associated with a lower prevalence of type 2 diabetes only in individuals who had been exposed to famine prenatally (odds ratio for rs7895833 0.50 [95% CI 0.24-1.03], P = 0.06; for rs1467568 0.48 [0.25-0.91], P = 0.02). CONCLUSIONS-SIRT1 may be an important genetic factor involved in fetal programming during malnutrition, influencing type 2 diabetes risk later in life.

引用

页码：424 / 426

页数：3

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