| BackgroudNonalcoholic fatty liver disease (NAFLD) was first described in diabetic, middle-aged femalewithout a history of significant alcohol use with liver histology consistent with alcoholic hepatitis in 1980. It is a clinicopathologic syndrome with the spectrum of conditions ranges from simple steatosis to steatohepatitis(NASH), fibrosis and end stage liver disease. Diagnostic criteria of NAFLD included clinical diagnostic criteria and histological diagnostic criteria which is the golden criteria. At present, a two-hit theory which consists of the accumulation of excessive hepatic fat and insulin resistance and oxidative stress induced inflammation and cell apoptosis describes the progression from simple steatosis to NASH, fibrosis, or cirrhosis. Various cytokines take part in both two hits, and the second hit may play role in the occurrence of NASH. As the children obesity growing, recently, condition about obesity children with NAFLD was increasingly taken people's attention. NAFLD may present as young as 4 years old and fibrosis is often found in liver biopsy. Moreover cirrhosis has been reported. However, the incidence of NAFLD in obesity children is still unclear, and the pathology of children NAFLD has not been studied systematically.Adiponectin, described recently is specifically secreted by adipocytes. Human adiponectin consists of 244 amino acids. It is believed to modulate glucose transport, increase insulin sensitivity, anti-inflammatory and anti-atherogenic in adults. Therefore, we speculated that it may play a protective role in both of two hits. ObjectiveThe aim of this study is to investigate the prevalence of clinical NAFLD in obese children through clinical survey, and study the association between serum adiponectin and NAFLD through animalexperiment. Subjects1. In this clinical survey, 113 cases of obesity children aged from 6 to 16 years in our unit were enrolled from July 2003 to August 2005. Obesity was defined as weight over 97 percentile of the children with same age and gender which investigated in 9 cities in 1995 without endocrine, genetic metabolic and kidney disease. All these obesity cases included 78 males and 35 females. In order to controlling the age, gender and sex development, 37 cases of healthy normal weight children control (control group) were selected randomly according the matching of age, gender and sex development, weight within 25 to 75 percentile of the children with same age and gender. All subjects had no history of alcohol using, long time drugs using, liver disease, and the result of tests for hepatitis virus and TORCH were negative.2. In this animal experiment, 32 aged one month healthy male New Zealand rabbits were randomly divided into control group and model group. Control group were fed with regular diet and model group were fed with high fat diet. According to the feed time, model group was divided into two subgroups again, one named S weeks group, the other 12 weeks group. The directions for high fat diet refer to the non-alcoholic steatohepatitis model of SD rats, regular diet plus lOOg/kg lard and 20g/kg cholesterol.Methods1. Height, weight, gender, age and tanner stage were examined and BMI were calculated. Biochemical indicator included serum total cholesterol (TC), triglyceride (TG), alanine aminotransferase (ALT), plasma HDL-cholesterol (HDL-C) and LDL-cholesterol (LDL-C). Serum levels of adiponectin were all assayed by an enzyme linked immunosorbent assay. According to the results of liver ultrasonic image and liver function, obesity children were divided into 3 groups. Obese group 1 was defined as obese children without any liver abnormality. Obese group 2 was defined as obese children just with fatty liver in ultrasonic appearance, but without liver function abnormality. Obese group 3 was defined as obese children with both fatty liver in ultrasonic appearance and liver function abnormality.2. Animal experiment: When finished the feeding at 8 weeks and 12 weeks, rabbits were fasted more than 10 hours and killed. Biochemical indicator included serum total cholesterol (TC), triglyceride (TG), alanine aminotransferase (ALT) and asparagine aminotransferase (AST). Serumlevels of adiponectin were all measured by an enzyme linked immunosorbent assay. Weight liver and calculate liver index. Take a little piece of liver tissue sunk into 10% formaldehyde solution prepare to do pathological observation.3.Statistic: Statistical analyses were conducted by using SPSS software (versionl 1.5). Differences were considered statistically significant at P<0.05. Fisher test was used to measure the enumeration data between subgroups. Skewed data were transformed logarithmically before performing a statistical analysis. Quantitative data were presented as mean±SD. The statistical significance between means was estimated by one-way ANOVA. Stepwise multiple linear regression models were used to examine the determinant of serum adiponectin levels. Results Clinical survey1. Compared with control, higher serum TC, TG, ALT, LDL-C and lower HDL-C were found in obese children (all P< 0.005). Moreover, the adiponectin level in obese children was significantly lower than that of controls (P <0.001).2. In all the 113 obese children, NAFLD was found in 63 cases (55.75%), including 22 cases in obese group 2 and 41 cases in obese group 3. Age, gender and sex development were not significantly different (all p>0.05). BMI in obese group 1 was significantly lower than that of obese group 2 and group3 (i'>0.05). Serum adiponectin level in obese 1 group were significantly higher than that of obese group 2 and obese group 3 (P<0.05), and no difference were found between obese group 2 and obese group 3 (p>0.05). Other biochemical markers, such as HDL-C, LDL-C, TC, TG were no difference among these groups (allp>0.05).3. Gender, BMI, NAFLD and HDL-C were the independent determinants of serum adiponectin levels in children, which explained 33.7% of variance. Serum adiponectin levels were inversely associated with BMI, gender (male) and NAFLD (P...
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