| 저자(한글) |
Na, Yeon Kyung,Hong, Hae Sook,Lee, Won Kee,Kim, Young Hun,Kim, Dong Sun |
| 저자(영문) |
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| 소속기관 |
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| 소속기관(영문) |
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| 출판인 |
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| 간행물 번호 |
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| 발행연도 |
2015-01-01 |
| 초록 |
Obesity is the fifth leading risk for death globally, and a significant challenge to global health. It is a common, complex, non-malignant disease and develops due to interactions between the genes and the environment. DNA methylation can act as a downstream effector of environmental signals; analysis of this process therefore holds substantial promise for identifying mechanisms through which genetic and environmental factors jointly contribute to disease risk. To assess the effects of excessive weight and obesity on gene-specific methylation levels of promoter regions, we determined the methylation status of four genes involved in inflammation and oxidative stress [interleukin 6 (IL6), tumor necrosis factor ${ alpha}$ ( $TNF{ alpha}$ ), mitochondrial transcription factor A (TFAM), and glucose transport 4 (GLUT4)] in blood cell-derived DNA from healthy women volunteers with a range of body mass indices (BMIs) by methylation-specific PCR. Interestingly, the samples from obese individuals ( $BMI{ geq}30kg/m^2$ ) showed significantly increased hypermethylation for IL6 gene compared to normal weight ( $BMI /TEX gt; 23kg/m^2$ ) and overweight sample ( $23kg/m^2{ leq}BMI /TEX gt; 30kg/m^2$ ) (P = 0.034 and P = 0.026). However there was no statistically significant difference in promoter methylation of the other 3 genes between each group. These findings suggest that aberrant DNA methylation of IL6 gene promoter may play an important role in the etiology and pathogenesis of obesity and IL6 methylation could be used as molecular biomarker for obesity risk assessment. Further studies are required to elucidate the potential mechanisms underlying this relationship. |
| 원문URL |
http://click.ndsl.kr/servlet/OpenAPIDetailView?keyValue=03553784&target=NART&cn=JAKO201517058945488 |
| 첨부파일 |
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