Role of Tumor Necrosis Factor-a Promoter Polymorphism and Insulin Resistance in the Development of Non-alcoholic Fatty Liver Disease in Obese Children
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¾çÇý¶õ ( Yang Hye-Ran )
¼¿ï´ëÇб³ ÀÇ°ú´ëÇÐ ºÐ´ç¼¿ï´ëº´¿ø ¼Ò¾Æ°úÇб³½Ç
°íÀ缺 ( Ko Jae-Sung )
¼¿ï´ëÇб³ ÀÇ°ú´ëÇÐ ¼Ò¾Æ°úÇб³½Ç
¼Á¤±â ( Seo Jeong-Kee )
¼¿ï´ëÇб³ ÀÇ°ú´ëÇÐ ¼Ò¾Æ°úÇб³½Ç
KMID : 0816120120150010044
Abstract
Purpose: Tumor necrosis factor-Ձ (TNF-Ձ) 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-Ձ promoter polymorphisms and insulin resistance in the development of NAFLD in obese children.
Methods: A total of 111 obese children (M£ºF=74£º37; mean age, 11.1¡¾2.0 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-Ձ levels, homeostasis model assessment of insulin resistance (HOMA-IR), and TNF-Ձ -308 and -238 polymorphisms were evaluated.
Results: There were no differences in TNF-Ձ 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-Ձ 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.
Å°¿öµå
TNF-Ձ polymorphism; Insulin resistance; Fatty liver; Obesity; Child
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