Matthew J. Armstrong, Leon A. Adams, Ali Canbay, Wing‐Kin Syn – 3 September 2013 – Nonalcoholic fatty liver disease (NAFLD) is a leading cause of chronic liver disease, and is strongly associated with the metabolic syndrome. In the last decade, it has become apparent that the clinical burden of NAFLD is not restricted to liver‐related morbidity or mortality, and the majority of deaths in NAFLD patients are related to cardiovascular disease (CVD) and cancer.

Marjon Kerkhof, Pieter Honkoop – 3 September 2013

Véronique Loustaud‐Ratti, Paul Carrier, Chanlina Vong, Marie Essig – 3 September 2013

Matthew J. Armstrong, Leon A. Adams, Ali Canbay, Wing‐Kin Syn – 3 September 2013 – Nonalcoholic fatty liver disease (NAFLD) is a leading cause of chronic liver disease, and is strongly associated with the metabolic syndrome. In the last decade, it has become apparent that the clinical burden of NAFLD is not restricted to liver‐related morbidity or mortality, and the majority of deaths in NAFLD patients are related to cardiovascular disease (CVD) and cancer.

Paul C. Adams – 31 August 2013

Ho Cheol Hong, Soon Young Hwang, Hae Yoon Choi, Hye Jin Yoo, Ji A Seo, Sin Gon Kim, Nan Hee Kim, Sei Hyun Baik, Dong Seop Choi, Kyung Mook Choi – 31 August 2013 – Previous studies have shown that nonalcoholic fatty liver disease (NAFLD) and sarcopenia may share pathophysiological mechanisms, such as insulin resistance, inflammation, vitamin D deficiency, and decreased physical activity. However, their direct relationship has not been investigated.

Michael L. Volk – 31 August 2013

Ling Yang, Yoon Seok Roh, Jingyi Song, Bi Zhang, Cheng Liu, Rohit Loomba, Ekihiro Seki – 30 August 2013 – Transforming growth factor beta (TGF‐β) signaling activates Smad‐ and TGF‐β‐activated kinase 1 (TAK1)‐dependent signaling to regulate cell survival, proliferation, fibrosis, and tumorigenesis. The effects of TGF‐β signaling on metabolic syndrome, including nonalcoholic fatty liver disease, remain elusive. Wild‐type (WT) and hepatocyte‐specific TGF‐β receptor type II‐deficient (Tgfbr2ΔHEP) mice were fed a choline‐deficient amino acid (CDAA)‐defined diet for 22 weeks to induce NASH.

Ling Yang, Yoon Seok Roh, Jingyi Song, Bi Zhang, Cheng Liu, Rohit Loomba, Ekihiro Seki – 30 August 2013 – Transforming growth factor beta (TGF‐β) signaling activates Smad‐ and TGF‐β‐activated kinase 1 (TAK1)‐dependent signaling to regulate cell survival, proliferation, fibrosis, and tumorigenesis. The effects of TGF‐β signaling on metabolic syndrome, including nonalcoholic fatty liver disease, remain elusive. Wild‐type (WT) and hepatocyte‐specific TGF‐β receptor type II‐deficient (Tgfbr2ΔHEP) mice were fed a choline‐deficient amino acid (CDAA)‐defined diet for 22 weeks to induce NASH.

29 August 2013