Role of Tumor Necrosis Factor-alpha Promoter Polymorphism and Insulin Resistance in the Development of Non-alcoholic Fatty Liver Disease in Obese Children.
10.5223/pghn.2012.15.1.44
- Author:
Hye Ran YANG
1
;
Jae Sung KO
;
Jeong Kee SEO
Author Information
1. Department of Pediatrics, Seoul National University Bundang Hospital, Korea.
- Publication Type:Original Article
- Keywords:
TNF-alpha polymorphism;
Insulin resistance;
Fatty liver;
Obesity;
Child
- MeSH:
Adult;
Child;
Fatty Liver;
Genotype;
Homeostasis;
Humans;
Insulin;
Insulin Resistance;
Obesity;
Tumor Necrosis Factor-alpha
- From:Pediatric Gastroenterology, Hepatology & Nutrition
2012;15(1):44-51
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Tumor necrosis factor-alpha (TNF-alpha) polymorphism has been suggested to play an important role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) in obese adults, and known to be a mediator of insulin resistance. In this study, we evaluated the role of TNF-alpha promoter polymorphisms and insulin resistance in the development of NAFLD in obese children. METHODS: A total of 111 obese children (M:F=74:37; mean age, 11.1+/-2.0 yrs) were included. The children were divided into 3 groups: controls (group I, n=61), children with simple steatosis (group II, n=17), and children with non-alcoholic steatohepatitis (group III, n=33). Serum TNF-alpha levels, homeostasis model assessment of insulin resistance (HOMA-IR), and TNF-alpha -308 and -238 polymorphisms were evaluated. RESULTS: There were no differences in TNF-alpha polymorphism at the -308 or the -238 loci between group I and group II + III (p=0.134 and p=0.133). The medians of HOMA-IR were significantly different between group I and group II + III (p=0.001), with significant difference between group II and group III (p=0.007). No difference was observed in the HOMA-IR among the genotypes at the -308 locus (p=0.061) or the -238 locus (p=0.207) in obese children. CONCLUSION: TNF-alpha promoter polymorphisms at the -308 and -238 loci were not significantly associated with the development of NAFLD in children; nevertheless, insulin resistance remains a likely essential factor in the pathogenesis of NAFLD in obese children, especially in the progression to NASH.
