system
Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, RESULTS. Meshes: Animals, Cluster Analysis, Disease Models, Animal, Fatty Liver, Gene Expression Profiling, Gene Expression Regulation, Gene Regulatory Networks, Hepatic Stellate Cells, Hepatitis, Lipid Metabolism, Liver Cirrhosis, Metformin, Mice, Mice, Inbred NOD, Non-alcoholic Fatty Liver Disease, Plasminogen Activator Inhibitor 1, Signal Transduction.
user
Does metformin prevent and reverses inflammation in a non-diabetic mouse model of nonalcoholic steatohepatitis? Context: Optimal treatment for nonalcoholic steatohepatitis (NASH) has not yet been established, particularly for individuals without diabetes. We examined the effects of metformin, commonly used to treat patients with type 2 diabetes, on liver pathology in a non-diabetic NASH mouse model. Eight-week-old C57BL/6 mice were fed a methionine- and choline-deficient plus high fat (MCD+HF) diet with or without 0.1% metformin for 8 weeks. Co-administration of metformin significantly decreased fasting plasma glucose levels, but did not affect glucose tolerance or peripheral insulin sensitivity. Metformin ameliorated MCD+HF diet-induced hepatic steatosis, inflammation, and fibrosis. Furthermore, metformin significantly reversed hepatic steatosis and inflammation when administered after the development of experimental NASH.
assistant
These histological changes were accompanied by reduced hepatic triglyceride content, suppressed hepatic stellate cell activation, and the downregulation of genes involved in fatty acid metabolism, inflammation, and fibrogenesis. Metformin prevented and reversed steatosis and inflammation of NASH in an experimental non-diabetic model without affecting peripheral insulin resistance. Final Decision: yes