scholarly journals Cyp1b1 affects external control of mouse hepatocytes, fatty acid homeostasis and signaling involving HNF4α and PPARα

2016 ◽  
Vol 597 ◽  
pp. 30-47 ◽  
Author(s):  
Justin R. Bushkofsky ◽  
Meghan Maguire ◽  
Michele Campaigne Larsen ◽  
Yee Hoon Fong ◽  
Colin R. Jefcoate
Keyword(s):  
Fatty Acid ◽  
External Control ◽  
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 Fatty acid and endotoxin activate inflammasomes in mouse hepatocytes that release danger signals to stimulate immune cells

Hepatology ◽  
2011 ◽  
Vol 54 (1) ◽  
pp. 133-144 ◽  
Author(s):  
Timea Csak ◽  
Michal Ganz ◽  
Justin Pespisa ◽  
Karen Kodys ◽  
Angela Dolganiuc ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Immune Cells ◽  
Danger Signals ◽  
Mouse Hepatocytes

Ursodeoxycholyl Lysophosphatidylethanolamide Inhibits Lipoapoptosis by Shifting Fatty Acid Pools toward Monosaturated and Polyunsaturated Fatty Acids in Mouse Hepatocytes

2013 ◽  
Vol 84 (5) ◽  
pp. 696-709 ◽  
Author(s):  
Walee Chamulitrat ◽  
Gerhard Liebisch ◽  
Weihong Xu ◽  
Hongying Gan-Schreier ◽  
Anita Pathil ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Polyunsaturated Fatty Acids ◽  
Mouse Hepatocytes

Measurement of Fatty Acid β-Oxidation in a Suspension of Freshly Isolated Mouse Hepatocytes

10.3791/62904 ◽  
2021 ◽  
Author(s):  
Schuyler D. Vickers ◽  
Dominique C. Saporito ◽  
Roberta Leonardi
Keyword(s):  
Fatty Acid ◽  
Mouse Hepatocytes

scholarly journals Loss of intracellular lipid binding proteins differentially impacts saturated fatty acid uptake and nuclear targeting in mouse hepatocytes

2012 ◽  
Vol 303 (7) ◽  
pp. G837-G850 ◽  
Author(s):  
Stephen M. Storey ◽  
Avery L. McIntosh ◽  
Huan Huang ◽  
Gregory G. Martin ◽  
Kerstin K. Landrock ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Uptake ◽  
Lipid Binding ◽  
Acid Uptake ◽  
Nuclear Targeting ◽  
Fatty Acid Binding ◽  
Mouse Hepatocytes ◽  
Sterol Carrier Protein 2 ◽  
Lipid Binding Proteins ◽  
Lcfa Uptake

The liver expresses high levels of two proteins with high affinity for long-chain fatty acids (LCFAs): liver fatty acid binding protein (L-FABP) and sterol carrier protein-2 (SCP-2). Real-time confocal microscopy of cultured primary hepatocytes from gene-ablated (L-FABP, SCP-2/SCP-x, and L-FABP/SCP-2/SCP-x null) mice showed that the loss of L-FABP reduced cellular uptake of 12- N-methyl-(7-nitrobenz-2-oxa-1,3-diazo)-aminostearic acid (a fluorescent-saturated LCFA analog) by ∼50%. Importantly, nuclear targeting of the LCFA was enhanced when L-FABP was upregulated (SCP-2/SCP-x null) but was significantly reduced when L-FABP was ablated (L-FABP null), thus impacting LCFA nuclear targeting. These effects were not associated with a net decrease in expression of key membrane proteins involved in LCFA or glucose transport. Since hepatic LCFA uptake and metabolism are closely linked to glucose uptake, the effect of glucose on L-FABP-mediated LCFA uptake and nuclear targeting was examined. Increasing concentrations of glucose decreased cellular LCFA uptake and even more extensively decreased LCFA nuclear targeting. Loss of L-FABP exacerbated the decrease in LCFA nuclear targeting, while loss of SCP-2 reduced the glucose effect, resulting in enhanced LCFA nuclear targeting compared with control. Simply, ablation of L-FABP decreases LCFA uptake and even more extensively decreases its nuclear targeting.

scholarly journals Δ9-Tetrahydrocannabinol induces endocannabinoid accumulation in mouse hepatocytes: antagonism by Fabp1 gene ablation

2018 ◽  
Vol 59 (4) ◽  
pp. 646-657 ◽  
Author(s):  
Avery L. McIntosh ◽  
Gregory G. Martin ◽  
Huan Huang ◽  
Danilo Landrock ◽  
Ann B. Kier ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Amide Hydrolase ◽  
Acid Amide ◽  
Fatty Acid Binding ◽  
Gene Ablation ◽  
Primary Mouse ◽  
Degradative Enzymes ◽  
Mouse Hepatocytes ◽  
Amide Hydrolase ◽  
The Impact

Phytocannabinoids, such as Δ9-tetrahydrocannabinol (THC), bind and activate cannabinoid (CB) receptors, thereby “piggy-backing” on the same pathway’s endogenous endocannabinoids (ECs). The recent discovery that liver fatty acid binding protein-1 (FABP1) is the major cytosolic “chaperone” protein with high affinity for both Δ9-THC and ECs suggests that Δ9-THC may alter hepatic EC levels. Therefore, the impact of Δ9-THC or EC treatment on the levels of endogenous ECs, such as N-arachidonoylethanolamide (AEA) and 2-arachidonoylglycerol (2-AG), was examined in cultured primary mouse hepatocytes from WT and Fabp1 gene-ablated (LKO) mice. Δ9-THC alone or 2-AG alone significantly increased AEA and especially 2-AG levels in WT hepatocytes. LKO alone markedly increased AEA and 2-AG levels. However, LKO blocked/diminished the ability of Δ9-THC to further increase both AEA and 2-AG. In contrast, LKO potentiated the ability of exogenous 2-AG to increase the hepatocyte level of AEA and 2-AG. These and other data suggest that Δ9-THC increases hepatocyte EC levels, at least in part, by upregulating endogenous AEA and 2-AG levels. This may arise from Δ9-THC competing with AEA and 2-AG binding to FABP1, thereby decreasing targeting of bound AEA and 2-AG to the degradative enzymes, fatty acid amide hydrolase and monoacylglyceride lipase, to decrease hydrolysis within hepatocytes.

Hyperpolarization of the cell membrane of mouse hepatocytes by fatty acid oxidation

1995 ◽  
Vol 57 (3) ◽  
pp. 509-514 ◽  
Author(s):  
R. Rusk ◽  
M. Geronimi ◽  
P. Gloor ◽  
M.C. Seebacher ◽  
E. Scharrer
Keyword(s):  
Fatty Acid ◽  
Cell Membrane ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Mouse Hepatocytes

Temperature Dependence of the Critical Electron Dose for Fatty Acid Monolayers

1982 ◽  
Vol 40 ◽  
pp. 78-79
Author(s):  
Kenneth H. Downing ◽  
Robert M. Glaeser
Keyword(s):  
Electron Beam ◽  
Fatty Acid ◽  
Inelastic Scattering ◽  
Temperature Dependence ◽  
Structural Damage ◽  
Direct Result ◽  
Second Step ◽  
Strong Temperature Dependence ◽  
Electron Dose ◽  
Covalent Bonds

The structural damage of molecules irradiated by electrons is generally considered to occur in two steps. The direct result of inelastic scattering events is the disruption of covalent bonds. Following changes in bond structure, movement of the constituent atoms produces permanent distortions of the molecules. Since at least the second step should show a strong temperature dependence, it was to be expected that cooling a specimen should extend its lifetime in the electron beam. This result has been found in a large number of experiments, but the degree to which cooling the specimen enhances its resistance to radiation damage has been found to vary widely with specimen types.

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