Label-free multiphoton imaging to detect hepatic steatosis in chronic liver disease

2021 ◽  
Author(s):  
Xingxin Huang ◽  
JiaJia He ◽  
XunBin Yu ◽  
Liqin Zheng ◽  
Jianxin Chen ◽  
...  
Keyword(s):  
Liver Disease ◽  
Chronic Liver Disease ◽  
Hepatic Steatosis ◽  
Chronic Liver ◽  
Label Free ◽  
Multiphoton Imaging

Prevalence and Predictors of Hepatic Steatosis in Adults With Newly Diagnosed Chronic Liver Disease due to Hepatitis C

Medicine ◽  
2009 ◽  
Vol 88 (5) ◽  
pp. 302-306 ◽  
Author(s):  
Amanda V. Hayman ◽  
Andre N. Sofair ◽  
M. Michele Manos ◽  
Ann Thomas ◽  
Norah Terrault ◽  
...  
Keyword(s):  
Liver Disease ◽  
Hepatitis C ◽  
Chronic Liver Disease ◽  
Hepatic Steatosis ◽  
Chronic Liver ◽  
Newly Diagnosed

scholarly journals Diagnostic accuracy of B-Mode ultrasound and Hepatorenal Index for graduation of hepatic steatosis in patients with chronic liver disease

PLoS ONE ◽  
2020 ◽  
Vol 15 (5) ◽  
pp. e0231044 ◽  
Author(s):  
Golo Petzold ◽  
Julian Lasser ◽  
Janina Rühl ◽  
Sebastian C. B. Bremer ◽  
Richard F. Knoop ◽  
...  
Keyword(s):  
Liver Disease ◽  
Diagnostic Accuracy ◽  
Chronic Liver Disease ◽  
Hepatic Steatosis ◽  
Chronic Liver

scholarly journals Deficiency of gluconeogenic enzyme PCK1 promotes non-alcoholic steatohepatitis progression by activation of PI3K/AKT/PDGF axis

2021 ◽  
Author(s):  
Qian Ye ◽  
Yi Liu ◽  
Guiji Zhang ◽  
Haijun Deng ◽  
Chang Chen ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Liver Disease ◽  
Chronic Liver Disease ◽  
Hepatic Steatosis ◽  
Chronic Liver ◽  
List Type ◽  
High Fat ◽  
Hepatic Lipid ◽  
Alcoholic Steatohepatitis ◽  
Gluconeogenic Enzyme

AbstractBackground and AimsNonalcoholic steatohepatitis (NASH) is a chronic liver disease characterized by hepatic lipid accumulation, inflammation, and progressive fibrosis. However, the pathomechanisms underlying NASH are incompletely explored. Phosphoenolpyruvate carboxykinase 1 (PCK1) catalyzes the first rate-limiting step of gluconeogenesis in the cytoplasm. This study was designed to determine the role of PCK1 in regulating NASH progression.MethodsLiver metabolism, hepatic steatosis, and fibrosis were evaluated at 24 weeks in liver-specific Pck1-knockout (L-KO) mice fed with NASH diet (high fat diet with ad libitum consumption of water containing glucose and fructose). AKT and RhoA inhibitors were evaluated for disease treatment in L-KO mice fed NASH diet.ResultsPCK1 is downregulated in patients with NASH and mouse models of NASH. L-KO mice displayed hepatic lipid disorder and liver injury fed with normal diet, while fibrosis and inflammation were aggravated when fed NASH diet. Mechanistically, transcriptome analysis revealed PCK1 deficiency upregulated genes involved in fatty acid transport and lipid droplet formation. Moreover, untargeted metabolomics analysis showed the accumulation of glycerol 3-phosphate, the substrate of triglyceride synthesis. Furthermore, the loss of PCK1 could activate the RhoA/PI3K/AKT pathway, which leads to increased secretion of PDGF-AA and promotes the activation of hepatic stellate cells. RhoA and AKT inhibitors alleviated NASH progression in L-KO mice fed NASH diet.ConclusionsPCK1 deficiency plays a key role in the development of hepatic steatosis and fibrosis by facilitating the RhoA/PI3K/AKT/PDGF-AA axis. These findings provide a novel insight into therapeutic approaches for the treatment of NASH.Lay summaryNon-alcoholic steatohepatitis (NASH) is currently the most common chronic liver disease, which is correlated with progressing chronic disorder of lipid metabolism and a persistent inflammatory response. In the present study, decreased PCK1 is observed in patients with NASH and mouse NASH models, and its loss aggravates steatohepatitis in NASH mice fed high-fat, high-fructose diet by stimulating expression of lipogenic genes and lipid synthesis. Inhibitors of proteins involved in the underlying molecular process alleviated the liver disease, highlighting a new therapeutic strategy for NASH.Graphical abstractHighlightsGluconeogenic enzyme PCK1 is downregulated in both human patients and NASH mice.PCK1 depletion promotes hepatic steatosis by dysregulating lipid metabolism and synthesis.PCK1 loss promotes hepatic fibrosis by activating RhoA/PI3K/AKT/PDGF-AA axis.Targeting RhoA/AKT alleviates NASH progression in liver-specific Pck1-knockout mice.

Exacerbation of Insulin Resistance and Hepatic Steatosis Deriving from Zinc Deficiency in Patients with HCV-Related Chronic Liver Disease

2014 ◽  
Vol 163 (1-2) ◽  
pp. 81-88 ◽  
Author(s):  
Takashi Himoto ◽  
Takako Nomura ◽  
Joji Tani ◽  
Hisaaki Miyoshi ◽  
Asahiro Morishita ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Chronic Liver Disease ◽  
Hepatic Steatosis ◽  
Zinc Deficiency ◽  
Chronic Liver
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