Undoubtedly, significant challenges remain; however, the remarkable progress in iPS technology through the effort of a large number of innovative investigators

will impact our ability to understand liver diseases and to develop novel therapeutic interventions for years to come. 1 “
“Post liver transplantation care begins with immunosuppression induction and maintenance and continues with close monitoring of graft function as well as renal, metabolic selleck chemical and infectious diseases complications. A number of recipient, donor and operative factors influence post-operative complications. Neurogenic, cardiovascular, renal, gastrointestinal and metabolic side effects may manifest early or later in the post-transplant period, while primary disease recurrence and malignancy issues most often manifest later in the course. With improvement Selleckchem NVP-BGJ398 in survival rates after liver transplantation, due to advances in surgical techniques and immunosuppression

drugs, non-transplant related causes like cardiovascular disease and de novo malignancies are becoming responsible for most late deaths in the recipients. Liver transplant recipients hence require a multi-disciplinary team approach from day one after the transplant followed by a tailored screening and health maintenance regimen. “
“Lipin-1 regulates lipid metabolism by way of its function as an enzyme in the triglyceride synthesis pathway and as a transcriptional coregulatory protein and is highly up-regulated in alcoholic fatty liver disease. In the present study, using a liver-specific lipin-1-deficient (lipin-1LKO) mouse model, we aimed find more to investigate the functional role of lipin-1 in the development of alcoholic steatohepatitis and explore the underlying

mechanisms. Alcoholic liver injury was achieved by pair feeding wild-type and lipin-1LKO mice with modified Lieber-DeCarli ethanol-containing low-fat diets for 4 weeks. Surprisingly, chronically ethanol-fed lipin-1LKO mice showed markedly greater hepatic triglyceride and cholesterol accumulation, and augmented elevation of serum liver enzymes accompanied by increased hepatic proinflammatory cytokine expression. Our studies further revealed that hepatic removal of lipin-1 in mice augmented ethanol-induced impairment of hepatic fatty acid oxidation and lipoprotein production, likely by way of deactivation of peroxisome proliferator-activated receptor γ coactivator-1alpha, a prominent transcriptional regulator of lipid metabolism. Conclusions: Liver-specific lipin-1 deficiency in mice exacerbates the development and progression of experimental alcohol-induced steatohepatitis. Pharmacological or nutritional modulation of hepatic lipin-1 may be beneficial for the prevention or treatment of human alcoholic fatty liver disease.