RESUMO
Objective Rats were fed with high-fat diet and were successfully induced the models with non-alcoholic fatty liver disease,and to investigate the effects of liraglutide on the expression of ERp46.Methods Thirty male Sprague-Dawley rats were assigned to normal chow group(NC,n=10)and high-fat diet group(n=20),after 12 weeks,the high-fat diet group rats were divided into high-fat diet group(HF,n=10)and liraglutide group(100L,n=10) and treated with normal saline and liraglutide(100 μg/kg)for 4 weeks respectively. Liver tissues were measured by hematoxylin-eosin(HE),Oil Red O staining,hepatic triglyceride(TG),and hyperinsulinemic-euglycemic clamp test(HECT). Hepatocyte apoptosis rate were evaluated by TdT-mediated dUTP nick-end labeling(TUNEL),and the expressions of ERp46 mRNA and protein were measured.Results Compared with the NC group,the liver tissues in the HF group have steatosis,insulin resistance,and the percentage of apoptosis was significantly increased. ERp46 mRNA and protein expressions were decreased(P<0.05). Compared with the HF group,liraglutide treatment was sufficient to reduce steatosis,insulin resistance,apoptosis,and increase the ERp46 mRNA and protein(P<0.05). Furthermore,the expression of ERp46 protein in the liver was negatively correlated with hepatocyte apoptosis rate,and positive correlated with glucose infusion rate(GIR, P<0. 05). Conclusion Liraglutide may up-regulate the expression of ERp46 to improve IR and hepatocyte apoptosis in NAFLD rats.
RESUMO
Detection of the possible role of ERp46,new endoplasmic reticulum protein,on palmitic acid-inducedendoplasmic reticulum stress-apoptosis pathway in βTC6 cells for the new treatment of type 2 diabetes.Results showed that ERp46 played a protective role in palnutic acid-induced cell apoptosis by decreasing the endoplasmic reticulum stress response through three pathway.