Suppression of Hepatic Cyp1a2 by Total Ginsenosides in Lipopolysaccharide-Treated Mice and Primary Mouse Hepatocytes

2016 ◽  
Vol 64 (11) ◽  
pp. 2386-2393 ◽  
Author(s):  
Haiyan Sun ◽  
Yijing Yan ◽  
Chenshu Xu ◽  
Hongxia Wan ◽  
Dong Liu
Keyword(s):  
Primary Mouse Hepatocytes ◽  
Primary Mouse ◽  
Mouse Hepatocytes

Characterization of the TGF-β antagonistic properties of Ski, SnoN and Smad7 in primary mouse hepatocytes

2006 ◽  
Vol 44 (08) ◽  
Author(s):  
L Ciuclan ◽  
P Godoy ◽  
VM Singer ◽  
S Dooley ◽  
K Breitkopf
Keyword(s):  
Primary Mouse Hepatocytes ◽  
Primary Mouse ◽  
Mouse Hepatocytes

Proteome analysis of 3,5-T2-treated primary mouse hepatocytes

2018 ◽  
Author(s):  
Janine Golchert ◽  
Julika Lietzow ◽  
Uwe Volker ◽  
Georg Homuth ◽  
Josef Kohrle
Keyword(s):  
Proteome Analysis ◽  
Primary Mouse Hepatocytes ◽  
Primary Mouse ◽  
Mouse Hepatocytes

Glucose Production Assay in Primary Mouse Hepatocytes

BIO-PROTOCOL ◽  
2012 ◽  
Vol 2 (21) ◽  
Author(s):  
Michihiro Matsumoto ◽  
Mashito Sakai
Keyword(s):  
Glucose Production ◽  
Primary Mouse Hepatocytes ◽  
Primary Mouse ◽  
Mouse Hepatocytes

scholarly journals Lipid and glucose metabolism in hepatocyte cell lines and primary mouse hepatocytes: a comprehensive resource for in vitro studies of hepatic metabolism

2019 ◽  
Vol 316 (4) ◽  
pp. E578-E589 ◽  
Author(s):  
Shilpa R. Nagarajan ◽  
Moumita Paul-Heng ◽  
James R. Krycer ◽  
Daniel J. Fazakerley ◽  
Alexandra F. Sharland ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Glucose Metabolism ◽  
Cell Lines ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Primary Hepatocytes ◽  
Primary Mouse Hepatocytes ◽  
Primary Mouse ◽  
Mouse Hepatocytes

The liver is a critical tissue for maintaining glucose, fatty acid, and cholesterol homeostasis. Primary hepatocytes represent the gold standard for studying the mechanisms controlling hepatic glucose, lipid, and cholesterol metabolism in vitro. However, access to primary hepatocytes can be limiting, and therefore, other immortalized hepatocyte models are commonly used. Here, we describe substrate metabolism of cultured AML12, IHH, and PH5CH8 cells, hepatocellular carcinoma-derived HepG2s, and primary mouse hepatocytes (PMH) to identify which of these cell lines most accurately phenocopy PMH basal and insulin-stimulated metabolism. Insulin-stimulated glucose metabolism in PH5CH8 cells, and to a lesser extent AML12 cells, responded most similarly to PMH. Notably, glucose incorporation in HepG2 cells were 14-fold greater than PMH. The differences in glucose metabolic activity were not explained by differential protein expression of key regulators of these pathways, for example glycogen synthase and glycogen content. In contrast, fatty acid metabolism in IHH cells was the closest to PMHs, yet insulin-responsive fatty acid metabolism in AML12 and HepG2 cells was most similar to PMH. Finally, incorporation of acetate into intracellular-free cholesterol was comparable for all cells to PMH; however, insulin-stimulated glucose conversion into lipids and the incorporation of acetate into intracellular cholesterol esters were strikingly different between PMHs and all tested cell lines. In general, AML12 cells most closely phenocopied PMH in vitro energy metabolism. However, the cell line most representative of PMHs differed depending on the mode of metabolism being investigated, and so careful consideration is needed in model selection.

scholarly journals Cholesterol Enhances the Toxic Effect of Ethanol and Acetaldehyde in Primary Mouse Hepatocytes

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Anayelly López-Islas ◽  
Victoria Chagoya-Hazas ◽  
Benjamin Pérez-Aguilar ◽  
Mayrel Palestino-Domínguez ◽  
Verónica Souza ◽  
...  
Keyword(s):  
Er Stress ◽  
Toxic Effect ◽  
Nuclear Translocation ◽  
Cholesterol Content ◽  
Primary Hepatocytes ◽  
Transmission Electron ◽  
Primary Mouse Hepatocytes ◽  
Primary Mouse ◽  
Mouse Hepatocytes ◽  
Stress Oxidative

Obesity and alcohol consumption are risk factors for hepatic steatosis, and both commonly coexist. Our objective was to evaluate the effect of ethanol and acetaldehyde on primary hepatocytes obtained from mice fed for two days with a high cholesterol (HC) diet. HC hepatocytes increased lipid and cholesterol content. HC diet sensitized hepatocytes to the toxic effect of ethanol and acetaldehyde. Cyp2E1 content increased with HC diet, as well as in those treated with ethanol or acetaldehyde, while the activity of this enzyme determined in microsomes increased in the HC and in all ethanol treated hepatocytes, HC and CW. Oxidized proteins were increased in the HC cultures treated or not with the toxins. Transmission electron microscopy showed endoplasmic reticulum (ER) stress and megamitochondria in hepatocytes treated with ethanol as in HC and the ethanol HC treated hepatocytes. ER stress determined by PERK content was increased in ethanol treated hepatocytes from HC mice and CW. Nuclear translocation of ATF6 was observed in HC hepatocytes treated with ethanol, results that indicate that lipids overload and ethanol treatment favor ER stress. Oxidative stress, ER stress, and mitochondrial damage underlie potential mechanisms for increased damage in steatotic hepatocyte treated with ethanol.

scholarly journals Hepatitis B x Protein Inhibits p53-dependent DNA Repair in Primary Mouse Hepatocytes

1998 ◽  
Vol 273 (50) ◽  
pp. 33327-33332 ◽  
Author(s):  
Sandrine Prost ◽  
James M. Ford ◽  
Clare Taylor ◽  
Jennifer Doig ◽  
David J. Harrison
Keyword(s):  
Dna Repair ◽  
Hepatitis B ◽  
X Protein ◽  
Primary Mouse Hepatocytes ◽  
Primary Mouse ◽  
Mouse Hepatocytes

The C-terminal region of the hepatitis B virus X protein is required for its stimulation of HBV replication in primary mouse hepatocytes

2012 ◽  
Vol 165 (2) ◽  
pp. 170-178 ◽  
Author(s):  
Na Luo ◽  
Yuan Cai ◽  
Jun Zhang ◽  
Weixue Tang ◽  
Betty L. Slagle ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Terminal Region ◽  
X Protein ◽  
Hbv Replication ◽  
Primary Mouse Hepatocytes ◽  
Primary Mouse ◽  
B Virus ◽  
Mouse Hepatocytes ◽  
Stimulation Of
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