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Abstract
Non-alcoholic fatty liver disease (NAFLD) is a chronic condition characterized by fat accumulation combined with low-grade inflammation in the liver. A large body of clinical and experimental data shows that an increased flux of free fatty acids from increased visceral adipose tissue can lead to NAFLD and insulin resistance. Thus, patients with obesity, insulin resistance, and dyslipidemia are at the greatest risk for NAFLD. Many people believe NAFLD is one of the phenotypes of metabolic syndrome or insulin resistance.
In the United States, NAFLD prevalence was reported to be approximately 34% in the adult population. In previous studies performed in Korea, NAFLD prevalence varied from 17.9% to 27.4%, depending on the study populations and diagnostic methods. Prevalence of NAFLD confirmed by liver biopsy was 51.4% in living liver donors in Korea. Recent data showed that NAFLD prevalence was 27.3% (38.3% in men and 12.6% in women) among 161,891 Seoul and Gyeonggi-province residents receiving a health examination from January 2009 to December 2010.
Insulin resistance is a major feature and pathogenic factor of NAFLD. Theoretically, genetic variation in candidate genes related to insulin resistance may contribute to the pathogenesis of NAFLD. A recent genetic study using the significance analysis of microarrays method reported that 21 candidate genes, from a pool containing thousands of genes, were involved in NAFLD and insulin resistance. Comprehensive investigation of common genes that are potentially pathogenic in the development of NAFLD is warranted.
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Table 1.
Candidate Genes related with fatty liver
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