We show that adenoviral-mediated silencing of hepatic Fsp27 abolishes fasting-induced liver steatosis in the absence of changes in plasma lipids. Finally, we report that anti-Fsp27 shRNA and PPARĪ± agonists synergize to ameliorate hepatosteatosis in mice fed a high fat diet. Together, our data highlight the physiological importance of CIDEC/Fsp27 Selleckchem Erlotinib in triglyceride homeostasis under both physiological and
pathological liver steatosis. Our results also suggest that patients taking fibrates likely have elevated levels of hepatic CIDEC, which may limit the efficient mobilization and catabolism of hepatic triglycerides. This article is protected by copyright. All rights reserved. “
“A 76-year-old man was referred to the hospital because of stomach pain, vomiting, and fever persisting for a few days. On physical examination, there was learn more no abdominal tenderness. CT, computed tomography; MRI, magnetic resonance imaging. Initial blood tests revealed normal white cell count and elevated liver aminotransferases (aspartate aminotransferase = 427 U/L [normal range <32], alanine aminotransferase = 480 U/L [normal range <31]), elevated lactate dehydrogenase (827 U/L, normal range = 240-480), and gamma-glutamyl transferase (1328 U/L, normal range <35). Bilirubin was normal.
At the emergency unit, computed tomography (CT) was performed showing an infiltrating mass with small rather linear calcifications in the right liver
lobe extending through the main bile duct into the pancreatic head. (Fig. 1) Magnetic resonance imaging (MRI) demonstrated a T2 hyperintense to intermediate intense, T1 hypointense, diffusion restrictive, complex solid neoplasm this website with a tubular aspect and slight contrast uptake, extending from the main bile duct into the right intrahepatic bile ducts. There is focal invasion into the cystic duct and the gallbladder. (Fig. 2) The differential diagnosis includes biliary papillomatosis, polypoid cholangiocarcinoma and hepatocellular carcinoma with intraductal growth. Surgery was performed with peroperative histology of frozen samples showing papillary carcinoma. Paraffin embedded samples showed dysplastic epithelium of the bile ducts with diffuse papillary proliferations. There are atypical columnar cells and only slight development of fibrovascular structures. The epithelium shows ulcerations and a high grade of dysplasia with hyperchromatic nuclei and a large number of mitotic figures. There are foci of perineural extension and invasion of the connective tissue. The lumen is filled with mucus, blood remnants and tumoral debris. The diagnosis of biliary papillomatosis of the bile ducts with malignant transformation into an invasive papillary carcinoma was made. (Fig. 3) Caroli first described biliary papillomatosis in 1959.