Deficiency of liver adipose triglyceride lipase in mice causes progressive hepatic steatosis

Jiang Wei Wu, Shu Pei Wang, Fernando Alvarez, Stéphanie Casavant, Nicolas Gauthier, Lynda Abed, Krishnakant G. Soni, Gongshe Yang, Grant A. Mitchell – 4 April 2011 – Accumulation of cytoplasmic triacylglycerol (TG) underlies hepatic steatosis, a major cause of cirrhosis. The pathways of cytoplasmic TG metabolism are not well known in hepatocytes, but evidence suggests an important role in lipolysis for adipose triglyceride lipase (ATGL). We created mice with liver‐specific inactivation of Pnpla2, the ATGL gene.

Methodological concerns about a recent meta‐analysis of the influence of the I148M variant of patatin‐like phospholipase domain containing 3 on the susceptibility and histological severity of nonalcoholic fatty liver disease

In vivo consequences of liver‐specific interleukin‐22 expression in mice: Implications for human liver disease progression

Ogyi Park, Hua Wang, Honglei Weng, Lionel Feigenbaum, Hai Li, Shi Yin, Sung Hwan Ki, Seong Ho Yoo, Steven Dooley, Fu‐Sheng Wang, Howard A. Young, Bin Gao – 4 April 2011 – Interleukin‐22 (IL‐22), which acts as either a proinflammatory or anti‐inflammatory cytokine in various disease models, is markedly up‐regulated in chronic liver diseases, including hepatitis B and C. In this report, we demonstrate a strong correlation between IL‐22 expression in the liver with active, inflammatory human liver disease.

Down‐regulation of phosphatase and tensin homolog by hepatitis C virus core 3a in hepatocytes triggers the formation of large lipid droplets

Sophie Clément, Marion Peyrou, Andrea Sanchez‐Pareja, Lucie Bourgoin, Pierluigi Ramadori, David Suter, Manlio Vinciguerra, Kevin Guilloux, Stephanie Pascarella, Laura Rubbia‐Brandt, Francesco Negro, Michelangelo Foti – 4 April 2011 – Hepatitis C virus (HCV) perturbs the host's lipid metabolism and often results in hepatic steatosis. In nonalcoholic fatty liver disease, the intrahepatic down‐regulation of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a critical mechanism leading to steatosis and its progression toward fibrosis and hepatocellular carcinoma.

Hepatitis B virus quasispecies in hepatic and extrahepatic viral reservoirs in liver transplant recipients on prophylactic therapy

Carla S. Coffin, Patricia M. Mulrooney‐Cousins, Guido van Marle, John P. Roberts, Tomasz I. Michalak, Norah A. Terrault – 1 April 2011 – The characterization of hepatitis B virus (HBV) quasispecies in different compartments in liver transplant (LT) recipients may be helpful in optimizing prophylaxis regimens. The aims of this study were to evaluate liver, peripheral blood mononuclear cells (PBMC), and plasma samples for HBV and to compare the quasispecies in hepatic and extrahepatic sites in LT recipients on long‐term prophylaxis.

Should possible recurrence of disease contraindicate liver transplantation in patients with end‐stage alveolar echinococcosis? A 20‐year follow‐up study

Solange Bresson‐Hadni, Oleg Blagosklonov, Jenny Knapp, Frédéric Grenouillet, Yasuhito Sako, Eric Delabrousse, Marie‐Pascale Brientini, Carine Richou, Anne Minello, Anca‐Teodora Antonino, Michel Gillet, Akira Ito, Georges André Mantion, Dominique Angèle Vuitton – 31 March 2011 – Liver transplantation (LT) is currently contraindicated in patients with residual or metastatic alveolar echinococcosis (AE) lesions. We evaluated the long‐term course of such patients who underwent LT and were subsequently treated with benzimidazoles.

Association of hepatic artery stenosis and biliary strictures in liver transplant recipients

Sunil Dacha, Ashis Barad, John Martin, Josh Levitsky – 31 March 2011 – Biliary complications are important causes of morbidity and graft failure in patients after orthotopic liver transplantation. Nonanastomotic biliary strictures (NAS) are frequently the most challenging biliary complications. Hepatic artery stenosis (HAS) as a cause of biliary strictures has not been studied well systematically.

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