ABSTRACT
To study the prevalence of metabolic syndrome [MS], insulin resistance [IR] and non-alcoholic fatty liver disease [NAFLD] in overweight/obese children with clinical hepatomegaly and/or raised alanine aminotransferase [ALT]. Thirty-three overweight and obese children, aged 2-13 years, presenting with hepatomegaly and/or raised ALT, were studied for the prevalence of MS, IR and NAFLD. Laboratory analysis included fasting blood glucose, serum insulin, serum triglycerides [TG], total cholesterol, high-density lipoprotein cholesterol [HDL-c], low-density lipoprotein cholesterol [LDL-c] and liver biochemical profile, in addition to liver ultrasound and liver biopsy. Twenty patients [60.6%] were labeled with MS. IR was present in 16 [48.4%]. Fifteen [44%] patients had biopsy-proven NAFLD. Patients with MS were more likely to have NAFLD by biopsy [P=0.001]. Children with NAFLD had significantly higher body mass index, waist circumference, ALT, total cholesterol, LDL-c, TG, fasting insulin, and lower HDL-c compared to patients with normal liver histology [P<0.05] and fitted more with the criteria of MS [80% vs. 44%]. IR was significantly more common among NAFLD patients [73% vs. 28%]. There is a close association between obesity, MS, IR and NAFLD. Obese children with clinical or biochemical hepatic abnormalities are prone to suffer from MS, IR and NAFLD
ABSTRACT
Polymorphisms in the promoter of microsomal triglyceride transfer protein [MTP] lead to decreased MTP transcription, less export of triglyceride from hepatocytes, and greater intracellular triglyceride accumulation. Therefore, functional polymorphisms in MTP may be involved in determining susceptibility to nonalcoholic steatohepatitis [NASH]. The aim of this study is to examine the effect of some genetic influences among a group of obese Egyptian children. A cross-sectional study was conducted on 76 overweight and obese children presenting to the Pediatric Endocrinology Unit, Cairo University Children's Hospital, Egypt, as well as on 20 healthy controls. Anthropometric measurements were taken for all the patients and they underwent clinical examination, ultrasonographic examination of the liver, and liver biopsy when appropriate. Liver functions, blood glucose, serum insulin, C-peptide, and lipid profile were assessed and HOMA-IR calculated. Blood samples from biopsy-proven NASH patients and controls were analyzed by polymerase chain reaction [PCR] and restriction fragment length polymorphism for the -493 G/T polymorphism in the promoter of MTP and the 1183 T/C polymorphism in the mitochondrial targeting sequence of manganese superoxide dismutase [MnSOD]. Eight had biopsy-proven simple steatosis and 7 had NASH. NASH patients had a much higher incidence of the MTP G/G genotype [P = 0.002, CI: 2.9-392] compared with the controls. NASH patients also had a 100% prevalence of the MnSOD T/T genotype. Certain genotypes in MTP and MnSOD are significantly more prevalent among obese children with NASH and may be responsible for such a phenotype