TRAIL deletion prevents liver inflammation but not adipose tissue inflammation during murine diet‐induced obesity

Petra Hirsova, Peggy Weng, Warda Salim, Steven F. Bronk, Thomas S. Griffith, Samar H. Ibrahim, Gregory J. Gores – 20 July 2017 – Tumor necrosis factor‐related apoptosis‐inducing ligand (TRAIL) and its cognate receptor(s) are up‐regulated in human and murine nonalcoholic steatohepatitis (NASH); however, the consequence of this enhanced expression on NASH pathogenesis remains unclear. TRAIL may either accentuate liver injury by promoting hepatic steatosis and inflammation or it may mitigate the disease process by improving systemic insulin resistance and averting hepatic fibrosis.

Hepatocytes contribute to residual glucose production in a mouse model for glycogen storage disease type Ia

Brenda S. Hijmans, Andreas Boss, Theo H. van Dijk, Maud Soty, Henk Wolters, Elodie Mutel, Albert K. Groen, Terry G.J. Derks, Gilles Mithieux, Arend Heerschap, Dirk‐Jan Reijngoud, Fabienne Rajas, Maaike H. Oosterveer – 20 July 2017 – It is a long‐standing enigma how glycogen storage disease (GSD) type I patients retain a limited capacity for endogenous glucose production despite the loss of glucose‐6‐phosphatase activity.

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