Ethnic differences in hepatic steatosis: An insulin resistance paradox?

Richard Guerrero, Gloria L. Vega, Scott M. Grundy, Jeffrey D. Browning – 24 February 2009 – Nonalcoholic fatty liver disease is a burgeoning problem. We have previously shown that Hispanics were at greater risk for nonalcoholic fatty liver disease than were African‐Americans despite a similar prevalence of risk factors between these groups.

Ferritin functions as a proinflammatory cytokine via iron‐independent protein kinase C zeta/nuclear factor kappaB–regulated signaling in rat hepatic stellate cells

Richard G. Ruddell, Diem Hoang‐Le, Joanne M. Barwood, Paul S. Rutherford, Terrance J. Piva, Dianne J. Watters, Paolo Santambrogio, Paolo Arosio, Grant A. Ramm – 24 February 2009 – Circulating ferritin levels reflect body iron stores and are elevated with inflammation in chronic liver injury. H‐ferritin exhibits a number of extrahepatic immunomodulatory properties, although its role in hepatic inflammation and fibrogenesis is unknown. Hepatic stellate cells respond to liver injury through production of proinflammatory mediators that drive fibrogenesis.

Sustained virological response reduces incidence of onset of type 2 diabetes in chronic hepatitis C

Yasuji Arase, Fumitaka Suzuki, Yoshiyuki Suzuki, Norio Akuta, Masahiro Kobayashi, Yusuke Kawamura, Hiromi Yatsuji, Hitomi Sezaki, Tetsuya Hosaka, Miharu Hirakawa, Kenji Ikeda, Hiromitsu Kumada – 24 February 2009 – Diabetes is present in patients with chronic hepatitis C virus infection. The aim of this retrospective cohort study was to assess the cumulative development incidence and predictive factors for type 2 diabetes after the termination of interferon therapy in Japanese patients positive for hepatitis C virus (HCV).

Multiple division cycles and long‐term survival of hepatocytes are distinctly regulated by extracellular signal‐regulated kinases ERK1 and ERK2

Christophe Frémin, Anne Bessard, Frédéric Ezan, Luc Gailhouste, Morgane Régeard, Jacques Le Seyec, David Gilot, Gilles Pagès, Jacques Pouysségur, Sophie Langouët, Georges Baffet – 24 February 2009 – We investigated the specific role of the mitogen‐activated protein kinase (MAPK) extracellular signal‐regulated kinase 1 (ERK1)/ERK2 pathway in the regulation of multiple cell cycles and long‐term survival of normal hepatocytes. An early and sustained epidermal growth factor (EGF)‐dependent MAPK activation greatly improved the potential of cell proliferation.

CD56+ T cells inhibit hepatitis C virus replication in human hepatocytes

Li Ye, Xu Wang, Shihong Wang, Yanjian Wang, Li Song, Wei Hou, Lin Zhou, He Li, Wenzhe Ho – 24 February 2009 – CD56+ T cells are abundant in liver and play an important role in defense against viral infections. However, the role of CD56+ T cells in control of hepatitis C virus (HCV) infection remains to be determined. We investigated the noncytolytic anti‐HCV activity of primary CD56+ T cells in human hepatocytes.

Deficiency of nicotinamide adenine dinucleotide phosphate, reduced form oxidase enhances hepatocellular injury but attenuates fibrosis after chronic carbon tetrachloride administration

Ghazaleh Aram, James J. Potter, Xiaopu Liu, Lan Wang, Michael S. Torbenson, Esteban Mezey – 24 February 2009 – Reactive oxygen species (ROS) activate hepatic stellate cells and enhance fibrogenesis. This study determined the role of nicotinamide adenine dinucleotide phosphate, reduced form (NADPH) oxidase deficiency in the development of hepatocellular necrosis, inflammation, and apoptosis in relation to fibrosis produced by chronic carbon tetrachloride (CCl4) administration.

Unique phenotype of hepatocellular cancers with exon‐3 mutations in beta‐catenin gene

Benjamin Cieply, Gang Zeng, Tracy Proverbs‐Singh, David A. Geller, Satdarshan P. S. Monga – 24 February 2009 – Wnt/β‐catenin signaling plays an important role in liver development and regeneration. Its aberrant activation, however, is observed in a subset of primary hepatocellular cancers (HCCs). In the current study, we compare and contrast the tumor characteristics of HCC in the presence or absence of mutations in the β‐catenin gene (CTNNB1).

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