Free fatty acids repress small heterodimer partner (SHP) activation and adiponectin counteracts bile acid‐induced liver injury in superobese patients with nonalcoholic steatohepatitis

Lars P. Bechmann, Peri Kocabayoglu, Jan‐Peter Sowa, Svenja Sydor, Jan Best, Martin Schlattjan, Anja Beilfuss, Johannes Schmitt, Rebekka A. Hannivoort, Alpaslan Kilicarslan, Christian Rust, Frieder Berr, Oliver Tschopp, Guido Gerken, Scott L. Friedman, Andreas Geier, Ali Canbay – 8 January 2013 – Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease in industrialized countries and may proceed to steatohepatitis (NASH). Apoptosis and free fatty acid (FFA)‐induced lipotoxicity are important features of NASH pathogenesis.

Immunoglobulin G4+ clones identified by next‐generation sequencing dominate the B cell receptor repertoire in immunoglobulin G4 associated cholangitis

Lucas J. Maillette de Buy Wenniger, Marieke E. Doorenspleet, Paul L. Klarenbeek, Joanne Verheij, Frank Baas, Ronald P. Oude Elferink, Paul P. Tak, Niek de Vries, Ulrich Beuers – 8 January 2013 – Immunoglobulin G4 (IgG4)‐associated cholangitis (IAC) is a manifestation of the recently discovered idiopathic IgG4‐related disease. The majority of patients have elevated serum IgG4 levels and/or IgG4‐positive B‐cell and plasma cell infiltrates in the affected tissue.

p53 regulates a mitotic transcription program and determines ploidy in normal mouse liver

Svitlana Kurinna, Sabrina A. Stratton, Zeynep Coban, Jill M. Schumacher, Markus Grompe, Andrew W. Duncan, Michelle Craig Barton – 8 January 2013 – Functions of p53 during mitosis reportedly include prevention of polyploidy and transmission of aberrant chromosomes. However, whether p53 plays these roles during genomic surveillance in vivo and, if so, whether this is done via direct or indirect means remain unknown. The ability of normal, mature hepatocytes to respond to stimuli, reenter the cell cycle, and regenerate liver mass offers an ideal setting to assess mitosis in vivo.

Health care costs associated with hepatocellular carcinoma: A population‐based study

Hla‐Hla Thein, Wanrudee Isaranuwatchai, Michael A. Campitelli, Jordan J. Feld, Eric Yoshida, Morris Sherman, Jeffrey S. Hoch, Stuart Peacock, Murray D. Krahn, Craig C. Earle – 8 January 2013 – Although the burden of hepatocellular carcinoma (HCC) is an escalating public health problem, it has not been rigorously estimated within a Canadian context. We conducted a population‐based study using Ontario Cancer Registry linked administrative data. The mean net costs of care due to HCC were estimated using a phase of care approach and generalized estimating equations.

Retinol binding protein 4 stimulates hepatic sterol regulatory element‐binding protein 1 and increases lipogenesis through the peroxisome proliferator‐activated receptor‐γ coactivator 1β‐dependent pathway

Min Xia, Yan Liu, Honghui Guo, Duan Wang, Yun Wang, Wenhua Ling – 8 January 2013 – Recent studies have revealed the essential role of retinol binding protein 4 (RBP4) in insulin resistance. However, the impact of RBP4 on aberrant lipogenesis, the common hepatic manifestation in insulin resistance states, and the underlying mechanism remain elusive. The present study was designed to examine the effect of RBP4 on sterol regulatory element‐binding protein (SREBP‐1) and hepatic lipogenesis.

Toll‐like receptor 4 activity protects against hepatocellular tumorigenesis and progression by regulating expression of DNA repair protein Ku70 in mice

Ziyan Wang, Jun Yan, Heng Lin, Fang Hua, Xiaoxing Wang, Hanzhi Liu, Xiaoxi Lv, Jiaojiao Yu, Su Mi, Jiaping Wang, Zhuo‐Wei Hu – 8 January 2013 – Hepatocellular carcinoma (HCC) is a devastating consequence of chronic inflammatory liver diseases. The goal of this study was to investigate whether Toll‐like receptor 4 (TLR4) activity contributes to HCC initiation and progression in mice.

Mitochondrial adaptations and dysfunctions in nonalcoholic fatty liver disease

Karima Begriche, Julie Massart, Marie‐Anne Robin, Fabrice Bonnet, Bernard Fromenty – 8 January 2013 – The worldwide epidemic of obesity and insulin resistance favors nonalcoholic fatty liver disease (NAFLD). Insulin resistance (IR) in the adipose tissue increases lipolysis and the entry of nonesterified fatty acids (NEFAs) in the liver, whereas IR‐associated hyperinsulinemia promotes hepatic de novo lipogenesis. However, several hormonal and metabolic adaptations are set up in order to restrain hepatic fat accumulation, such as increased mitochondrial fatty acid oxidation (mtFAO).

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