Paper Title
Hepatic Lactotransferrinregulates Hepatic Steatosis in Non-Alcoholic Fatty Liver Disease Induced by Hormone Disturbance

Abstract
Non-alcoholic fatty liver disease (NAFLD) is a globally emerging metabolic disease which even could developto hepatic cirrhosis and hepatoma. Although many studies suggested treatment to slow down the progression of NALFD, there are few treatments to prevent hepatic lipid accumulation, an initial step of NAFLD. To investigate the endogenous factor regulating hepatic lipid accumulation, we established IR (ionizing radiation)-induced fatty liver mouse model which develops fatty liver without alteration of caloric intake. Through transcriptome analysis in the liver, we found that secretory protein lactotransferrin (Ltf) is down-regulated in the model. Expression of Ltf is modulated by GH in hepatocyte and IR-induced fatty liver mouse showed lower serum GH levels. Moreover, it is investigated that GH reduced chylomicron-mediated hepatic lipid accumulation. From these results, we suggest novel fatty liver mouse model for investigation initial development of NALFD andprovided the role of Ltf in regulating hepatic lipid accumulation.