Adiponectin and adiponectin receptors in obese and owerweight children with nonalcholic fatty liver

Obesity and fatty liver disease are one of the important increasing the frequency of healthy problem in our country. Studies have been carried out for many years to understand the role of adiponectin and adiponectin receptors in the patogenesis of obesity, insulin resistance and nonalcoholic liver disease. There aren't any studies about soluble adiponectin receptor level. This studies, aim to investigate of adiponectin and adiponectin receptors in nonalcoholic fatty liver disease (NAFLD) to child. Children admitted to pediatric department in our hospital or had been determined liver steatosis in liver ultrasonography in any reason were re-evaluated with weight and height measurement, insulin resistance, lipid profile and liver enzymes. Children were divided into groups according to liver enzymes and whether they were obese or not. Children who had increased level of liver enzymes were evaluated as steatohepatitis (NASH). In our study, 51 patient had fatty liver in ultrasonography. As a control group, 10 healthy obese children who had no fatty liver and 10 healthy owerweigtht children who had no fatty liver were included. No significant difference in ages and antropometric measurement were detected between patient and control group. Insulin resistance were detected as positive in almost all children who had either simple fatty liver (15/25) or steatohepatitis (5/6). Insulin resistance is the most important step in the patogenesis of fatty liver as emphasized before. There were no significant difference in adiponectin levels between patient with fatty liver and control group, but adiponectin levels were found under the normal level in two groups. The reason of no difference in two groups is that adiponectin starts to fall at early stages of steatosis evenmore as a early stage of gaining weight without steatosis. Another reason might be that whatever no fatty liver had been detected in ultrasonography in children included to control group, perhaps fatty liver would be found under microscopy. Adiponectin receptor 2 is an important molecule in steatosis and expressed especially in liver. In comparison of adipoR2 levels in obese children with fatty liver and without fatty liver, adipoR2 was significantly higher in the fatty liver group (p<0,001). In early stages of steatosis, adipoR2 increases to compensate decreasing level of adiponectin. Tissue adipoR2 levels detected less than normal level research of adult with liver inflamation and fibrosis. For this reason, at early stages of steatosis, adipoR2 increases to compansate to reducing level of adiponectin, in later stages with fibrosis, adipoR2 becomes desensitized and then adipoR2 level decreases with adiponectin. In conclusion, the child adipoR2 levels use identification of liver inflamation and fibrosis. This technique is alternative of biopsi and noninvasive procedure. İn the future NAFLD treatment will be increased adiponectin levels or adiponectin receptor 2 sensitivity.