scholarly journals Cyclophilin Inhibitor NV556 Reduces Fibrosis and Hepatocellular Carcinoma Development in Mice With Non-Alcoholic Steatohepatitis

2019 ◽  
Vol 10 ◽  
Author(s):  
Joseph Kuo ◽  
Sonia Simón Serrano ◽  
Alvar Grönberg ◽  
Ramin Massoumi ◽  
Magnus Joakim Hansson ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Alcoholic Steatohepatitis ◽  
Cyclophilin Inhibitor

scholarly journals Dual-specificity phosphatase 3 deletion promotes obesity, non-alcoholic steatohepatitis and hepatocellular carcinoma

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sophie Jacques ◽  
Arash Arjomand ◽  
Hélène Perée ◽  
Patrick Collins ◽  
Alice Mayer ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Liver Damage ◽  
Chow Diet ◽  
Serum Triglycerides ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Steatohepatitis ◽  
Dual Specificity ◽  
Dual Specificity Protein Phosphatase

AbstractNon-alcoholic fatty liver disease (NAFLD) is the most common chronic hepatic pathology in Western countries. It encompasses a spectrum of conditions ranging from simple steatosis to more severe and progressive non-alcoholic steatohepatitis (NASH) that can lead to hepatocellular carcinoma (HCC). Obesity and related metabolic syndrome are important risk factors for the development of NAFLD, NASH and HCC. DUSP3 is a small dual-specificity protein phosphatase with a poorly known physiological function. We investigated its role in metabolic syndrome manifestations and in HCC using a mouse knockout (KO) model. While aging, DUSP3-KO mice became obese, exhibited insulin resistance, NAFLD and associated liver damage. These phenotypes were exacerbated under high fat diet (HFD). In addition, DEN administration combined to HFD led to rapid HCC development in DUSP3-KO compared to wild type (WT) mice. DUSP3-KO mice had more serum triglycerides, cholesterol, AST and ALT compared to control WT mice under both regular chow diet (CD) and HFD. The level of fasting insulin was higher compared to WT mice, though, fasting glucose as well as glucose tolerance were normal. At the molecular level, HFD led to decreased expression of DUSP3 in WT mice. DUSP3 deletion was associated with increased and consistent phosphorylation of the insulin receptor (IR) and with higher activation of the downstream signaling pathway. In conclusion, our results support a new role for DUSP3 in obesity, insulin resistance, NAFLD and liver damage.

Molecular characterization of hepatocellular carcinoma in patients with non-alcoholic steatohepatitis

2021 ◽  
Author(s):  
Roser Pinyol ◽  
Sara Torrecilla ◽  
Huan Wang ◽  
Carla Montironi ◽  
Marta Piqué-Gili ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Molecular Characterization ◽  
Alcoholic Steatohepatitis

scholarly journals Natural Progression of Non-Alcoholic Steatohepatitis to Hepatocellular Carcinoma

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 184
Author(s):  
Daryl Ramai ◽  
Waqqas Tai ◽  
Michelle Rivera ◽  
Antonio Facciorusso ◽  
Nicola Tartaglia ◽  
...  
Keyword(s):  
Public Health ◽  
Hepatocellular Carcinoma ◽  
Lipid Peroxidation ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Steatohepatitis ◽  
Natural Progression ◽  
Public Health Threat ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic steatohepatitis (NASH) is a chronic and progressive form of non-alcoholic fatty liver disease (NAFLD). Its global incidence is increasing which makes NASH an epidemic and a public health threat. Due to repeated insults to the liver, patients are at risk for developing hepatocellular carcinoma (HCC). The progression of NASH to HCC was initially defined according to a two-hit model which involved the development of steatosis, followed by lipid peroxidation and inflammation. However, current research defines a “multi-hit” or “multi-parallel hit” model which synthesizes several contributing pathways involved in progressive fibrosis and oncogenesis. This perspective considers the effects of cellular, genetic, immunologic, metabolic, and endocrine pathways leading up to HCC which underscores the complexity of this condition. This article will provide an updated review of the pathogenic mechanisms leading from NASH to HCC as well as an exploration of the role of biomarkers and screening.

scholarly journals A case of double cholangiolocellular carcinoma and hepatocellular carcinoma complicated with non-alcoholic steatohepatitis

Kanzo ◽  
2012 ◽  
Vol 53 (10) ◽  
pp. 615-623 ◽  
Author(s):  
Yutaka Kawano ◽  
Shohei Kikuchi ◽  
Koji Miyanishi ◽  
Hiroyuki Nagashima ◽  
Masahiro Hirakawa ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cholangiolocellular Carcinoma ◽  
Alcoholic Steatohepatitis

A murine model for non-alcoholic steatohepatitis showing evidence of association between diabetes and hepatocellular carcinoma

2013 ◽  
Vol 46 (3) ◽  
pp. 141-152 ◽  
Author(s):  
Masato Fujii ◽  
Yuichiro Shibazaki ◽  
Kyoko Wakamatsu ◽  
Yutaka Honda ◽  
Yusuke Kawauchi ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Murine Model ◽  
Alcoholic Steatohepatitis

Hepatocellular Carcinoma Arising from Non-Cirrhotic Non-Alcoholic Steatohepatitis

2014 ◽  
Vol 37 (Suppl) ◽  
pp. S33
Author(s):  
Min Roh ◽  
Tae Yeob Kim ◽  
Joo Hyun Sohn ◽  
Jae Keun Park ◽  
Seung Lee ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Alcoholic Steatohepatitis

THU-461-A diet-induced lean non-alcoholic steatohepatitis-associated hepatocellular carcinoma mouse model

2019 ◽  
Vol 70 (1) ◽  
pp. e362-e363
Author(s):  
Paraskevi Farazi ◽  
Shilpa Karanjit ◽  
Elizabeth Keuter ◽  
Dong Liu ◽  
Geoffrey Talmon
Keyword(s):  
Hepatocellular Carcinoma ◽  
Mouse Model ◽  
Alcoholic Steatohepatitis

Association of non-alcoholic steatohepatitis without significant fibrosis with hepatocellular carcinoma

2004 ◽  
Vol 41 (4) ◽  
pp. 685-686 ◽  
Author(s):  
Rachel E. Bullock ◽  
Abed M. Zaitoun ◽  
Guruprasad P. Aithal ◽  
Stephen D. Ryder ◽  
Ian J. Beckingham ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Significant Fibrosis ◽  
Alcoholic Steatohepatitis
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