期刊
DIABETOLOGIA
卷 57, 期 6, 页码 1154-1158出版社
SPRINGER
DOI: 10.1007/s00125-014-3198-8
关键词
DNAmethylation; Epigenetics; High-fat overfeeding; Insulin resistance; Low birthweight; Skeletal muscle; Type 2 diabetes
资金
- Danish Council for Independent Research-Medical Sciences (FSS)
- Danish Council for Strategic Research
- Programme Commission on Food and Health (FOSU)
- Danish Diabetes Association
- European Foundation for the Study of Diabetes (EFSD)
- EU
- Augustinus Fonden
- Novo Nordisk Foundation
- Aase and Ejnar Danielsen Foundation
Aims/hypothesis The association between low birthweight (LBW) and risk of developing type 2 diabetes may involve epigenetic mechanisms, with skeletal muscle being a prime target tissue. Differential DNA methylation patterns have been observed in single genes in muscle tissue from type 2 diabetic and LBW individuals, and we recently showed multiple DNA methylation changes during short-term high-fat overfeeding in muscle of healthy people. In a randomised crossover study, we analysed genome-wide DNA promoter methylation in skeletal muscle of 17 young LBW men and 23 matched normal birthweight (NBW) men after a control and a 5 day high-fat overfeeding diet. Methods DNA methylation was measured using Illumina's Infinium BeadArray covering 27,578 CpG sites representing 14,475 different genes. Results After correction for multiple comparisons, DNA methylation levels were found to be similar in the LBW and NBW groups during the control diet. Whereas widespread DNA methylation changes were observed in the NBW group in response to high-fat overfeeding, only a few methylation changes were seen in the LBW group (chi(2), p < 0.001). Conclusions/interpretation Our results indicate lower DNA methylation plasticity in skeletal muscle from LBW vs NBW men, potentially contributing to understanding the link between LBW and increased risk of type 2 diabetes.
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