Visceral fat: A key mediator of steatohepatitis in metabolic liver disease

David van der Poorten, Kerry‐Lee Milner, Jason Hui, Alexander Hodge, Michael I. Trenell, James G. Kench, Roslyn London, Tony Peduto, Donald J. Chisholm, Jacob George – 11 April 2008 – Visceral obesity is intimately associated with metabolic disease and adverse health outcomes. However, a direct association between increasing amounts of visceral fat and end‐organ inflammation and scarring has not been demonstrated.

Proprotein convertase subtilisin/kexin type 9 (PCSK9): Hepatocyte‐specific low‐density lipoprotein receptor degradation and critical role in mouse liver regeneration

Ahmed Zaid, Anna Roubtsova, Rachid Essalmani, Jadwiga Marcinkiewicz, Ann Chamberland, Josée Hamelin, Michel Tremblay, Hélène Jacques, Weijun Jin, Jean Davignon, Nabil G. Seidah, Annik Prat – 11 April 2008 – The gene encoding the proprotein convertase subtilisin/kexin type 9 (PCSK9) is linked to familial hypercholesterolemia, as are those of the low‐density lipoprotein receptor (LDLR) and apolipoprotein B. PCSK9 enhances LDLR degradation, resulting in low‐density lipoprotein accumulation in plasma.

Improved survival in patients receiving medical therapy as compared with banding ligation for the prevention of esophageal variceal rebleeding

Gin‐Ho Lo, Wen‐Chi Chen, Chiun‐Ku Lin, Wei‐Lun Tsai, Hoi‐Hung Chan, Tai‐An Chen, Hsien‐Chung Yu, Ping‐I Hsu, Kwok‐Hung Lai – 11 April 2008 – Both medical therapy and endoscopic variceal ligation (EVL) have proven to be comparable in the prevention of variceal rebleeding. However, the long‐term results are still lacking. Our previous study enrolled 121 patients with history of esophageal variceal bleeding and randomized to receive EVL (EVL group, 60 patients) or drug therapy, nadolol plus isosorbide‐5‐mononitrate (N+I) (N+I group, 61 patients) to prevent variceal rebleeding.

Sinusoidal endothelial cells prevent rat stellate cell activation and promote reversion to quiescence

Laurie D. DeLeve, Xiangdong Wang, Yumei Guo – 11 April 2008 – Capillarization precedes hepatic fibrosis. We hypothesize that capillarization of sinusoidal endothelial cells (SEC) is permissive for hepatic stellate cell (HSC) activation and therefore permissive for fibrosis. We examined whether freshly isolated SECs prevent activation of HSCs and promote reversion to quiescence, and whether this effect was lost in capillarization. HSCs were cultured alone or co‐cultured with differentiated or capillarized SECs.

Autophagy in the liver

Xiao‐Ming Yin, Wen‐Xing Ding, Wentao Gao – 7 April 2008 – A great part of our current understanding of mammalian macroautophagy is derived from studies of the liver. The term “autophagy” was introduced by Christian de Duve in part based on ultrastructural changes in rat liver following glucagon injection. Subsequent morphological, biochemical, and kinetics studies of autophagy in the liver defined the basic process of autophagosome formation, maturation, and degradation and the regulation of autophagy by hormones, phosphoinositide 3‐kinases, and mammalian target of rapamycin.

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