Journal List > Korean J Pediatr Gastroenterol Nutr > v.10(2) > 1110190

Korean J Pediatr Gastroenterol Nutr. 2007 Sep;10(2):185-192. Korean.
Published online Sep 30, 2007.  https://doi.org/10.5223/kjpgn.2007.10.2.185
Copyright © 2007 The Korean Society of Pediatric Gastroenterology, Hepatology and Nutrition
The Role of Adipokines in the Pathogenesis of Non-alcoholic Fatty Liver Disease in Obese Children; the Relationship between Body Fat Distribution and Insulin Resistance
Hye Ran Yang, Jae Sung Ko and Jeong Kee Seo
Department of Pediatrics, Seoul National University College of Medicine, Seoul, Korea.
Abstract

PURPOSE

This study was conducted to evaluate the role of adiponectin, leptin, and tumor necrosis factor-α (TNF-α) in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) in obese children, and to elucidatethe relationship between these adipokines and insulin resistance.

METHODS

A total of 61 obese children (M : F=42 : 19, mean age 11.2±1.3 years) admitted to our facility between March 2004 and June 2005 were included in this study. Patients were divided into three groups based on their NAFLD status obese children without fatty liver (N=23); obese children with simple steatosis (N=20); and obese children with non-alcoholic steatohepatitis (NASH) (N=18). The serum levels of adiponectin, leptin, and TNF-α were measured, and insulin resistance determined by homeostasis model assessment (HOMA-IR) was calculated to estimate insulin resistance. In addition, the VSR (visceral-subcutaneous fat ratio) was estimated using abdominal computed tomography.

RESULTS

There was no difference in serum TNF-α and leptin levels observed between the 3 groups (22.13±6.37 vs. 21.35±6.95 vs. 25.17±9.30; p=0.342 & 20.29±8.57 vs. 16.42±6.85 vs. 20.10±7.86; p=0.330). However, the serum adiponectin level was significantly lower in children with non-alcoholic steatohepatitis (NASH) than in the other two groups (6.08±1.38 in children without steatosis vs. 5.69±0.79 in simple steatosis vs. 4.93±1.75 in NASH; p=0.026). In addition, the VSR was significantly increased in the NASH group (0.31±0.08 vs. 0.32±0.11 vs. 0.47±0.14; p=0.001), and HOMA-IR revealed a significant difference among the three groups (4.77±3.67 vs. 6.89±7.05 vs. 10.42±6.73; p=0.000). However, there was no significant correlation observed between the adiponectin levels and the HOMA-IR or the VSR (r=−0.117; p=0.450 & r=−0.106; p=0.499).

CONCLUSION

Insulin resistance may affect the development of hepatic steatosis and steatohepatitis in children, and the results of this study suggest that, of several adipokines evaluated, adiponectin is important in the progression of steatosis to steatohepatitis in obese children.

Keywords: Non-alcoholic fatty liver disease; Adiponectin; Insulin resistance; Obesity; Children