The role of glycerol-3-phosphate dehydrogenase 1 in the progression of fatty liver after acute ethanol administration in mice

2014 ◽  
Vol 444 (4) ◽  
pp. 525-530 ◽  
Author(s):  
Tomoki Sato ◽  
Akihito Morita ◽  
Nobuko Mori ◽  
Shinji Miura
Keyword(s):  
Fatty Liver ◽  
Ethanol Administration ◽  
Acute Ethanol ◽  
Glycerol 3 Phosphate Dehydrogenase

Fish oil fed prior to ethanol administration prevents acute ethanol-induced fatty liver in mice

2008 ◽  
Vol 49 (3) ◽  
pp. 441-450 ◽  
Author(s):  
Satoshi Wada ◽  
Tomomi Yamazaki ◽  
Yukari Kawano ◽  
Shinji Miura ◽  
Osamu Ezaki
Keyword(s):  
Fatty Liver ◽  
Fish Oil ◽  
Ethanol Administration ◽  
Acute Ethanol

scholarly journals The role of free serum tryptophan in the biphasic effect of acute ethanol administration on the concentrations of rat brain tryptophan, 5-hydroxytryptamine and 5-hydroxyindol-3-ylacetic acid

1976 ◽  
Vol 160 (2) ◽  
pp. 315-324 ◽  
Author(s):  
A A Badawy ◽  
M Evans
Keyword(s):  
Rat Brain ◽  
Tryptophan Metabolism ◽  
Ethanol Administration ◽  
Acute Administration ◽  
Free Tryptophan ◽  
Biphasic Effect ◽  
Acute Ethanol ◽  
Comparison Of The Results ◽  
Ylacetic Acid

1. Acute administration of ethanol exerts a biphasic effect on the concentrations of rat brain tryptophan, 5-hydroxytryptamine and 5-hydroxyindol-3-ylacetic acid. Both effects are associated with corresponding changes in the availability of circulating free tryptophan. 2. The initial increases in the above concentrations are prevented by ergotamine, are unaltered by allopurinol and are potentiated by theophylline, whereas the later decreases are prevented by both ergotamine and allopurinol. 3. It is suggested that the initial enhancement by ethanol of brain tryptophan metabolism is caused by catecholamine-mediated lipolysis followed by displacement of protein-bound serum tryptophan, whereas the activation of liver tryptophaan pyrrolase, which is produced by the same mechanism, leads to the later decreases in the brain concentrations of tryptophan and its metabolites. 4. The initial effects of ethanol can be reproduced by an equicaloric dose of sucrose, and a comparison of the two treatments alone could therefore be misleading. 5. The effects of ethanol on liver and brain tryptophan metabolism have also been examined in mice, and a comparison of the results with those previously reported suggests that the ethanol effects are strain-dependent.

Effects of Acute Ethanol Administration on Brain Oxidative Status: The Role of Acetaldehyde

2019 ◽  
Vol 43 (8) ◽  
pp. 1672-1681 ◽  
Author(s):  
Pablo Baliño ◽  
Ricard Romero-Cano ◽  
Juan Vicente Sánchez‐Andrés ◽  
Victoria Valls ◽  
Carlos González Aragón ◽  
...  
Keyword(s):  
Oxidative Status ◽  
Ethanol Administration ◽  
Acute Ethanol

Role of endotoxin in the hypermetabolic state after acute ethanol exposure

1998 ◽  
Vol 275 (6) ◽  
pp. G1252-G1258 ◽  
Author(s):  
Chantal A. Rivera ◽  
Blair U. Bradford ◽  
Vitor Seabra ◽  
Ronald G. Thurman
Keyword(s):  
Oxygen Uptake ◽  
Kupffer Cells ◽  
Ethanol Exposure ◽  
Ethanol Administration ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Hypermetabolic State ◽  
Acute Ethanol ◽  
Eicosanoid Release

This study investigated the role of endotoxin in the hypermetabolic state or swift increase in alcohol metabolism (SIAM) due to acute ethanol exposure. Female Sprague-Dawley rats (100–120 g) were given ethanol (5 g/kg) by gavage. Endotoxin measured in plasma from portal blood was not detectable in saline-treated controls; however, 90 min after ethanol, endotoxin was increased to 85 ± 14 pg/ml, and endotoxin clearance was diminished by ∼50%. Oxygen uptake in perfused livers was increased 48% by ethanol, and production of PGE2 by isolated Kupffer cells was increased similarly. These effects were blunted by elimination of gram-negative bacteria and endotoxin with antibiotics before ethanol administration. To reproduce ethanol-induced endotoxemia, endotoxin was infused via the mesenteric vein at a rate of 2 ng ⋅ kg−1 ⋅ h−1. Endotoxin mimicked the effect of ethanol on oxygen uptake. The specific Kupffer cell toxicant GdCl3completely prevented increases in oxygen uptake due to endotoxin. These findings demonstrate that endotoxin plays a pivotal role in SIAM, most likely by stimulating eicosanoid release from Kupffer cells.

The role of cytochrome P-4502E1 in the progression of alcoholic and non-alcoholic fatty liver

2010 ◽  
Vol 48 (08) ◽  
Author(s):  
H Qin ◽  
K Glassen ◽  
G Millonig ◽  
KB Linhart ◽  
H Bartsch ◽  
...  
Keyword(s):  
Fatty Liver ◽  
Alcoholic Fatty Liver

Semi-Quantitative Ultrasonographic Evaluation of NAFLD

2020 ◽  
Vol 26 (32) ◽  
pp. 3915-3927 ◽  
Author(s):  
Stefano Ballestri ◽  
Claudio Tana ◽  
Maria Di Girolamo ◽  
Maria Cristina Fontana ◽  
Mariano Capitelli ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Imaging Techniques ◽  
Metabolic Complications ◽  
Nonalcoholic Fatty Liver ◽  
Non Invasive ◽  
Increased Risk ◽  
Risk Of Progression ◽  
Progressive Liver Disease

: Nonalcoholic fatty liver disease (NAFLD) embraces histopathological entities ranging from the relatively benign simple steatosis to the progressive form nonalcoholic steatohepatitis (NASH), which is associated with fibrosis and an increased risk of progression to cirrhosis and hepatocellular carcinoma. NAFLD is the most common liver disease and is associated with extrahepatic comorbidities including a major cardiovascular disease burden. : The non-invasive diagnosis of NAFLD and the identification of subjects at risk of progressive liver disease and cardio-metabolic complications are key in implementing personalized treatment schedules and follow-up strategies. : In this review, we highlight the potential role of ultrasound semiquantitative scores for detecting and assessing steatosis severity, progression of NAFLD, and cardio-metabolic risk. : Ultrasonographic scores of fatty liver severity act as sensors of cardio-metabolic health and may assist in selecting patients to submit to second-line non-invasive imaging techniques and/or liver biopsy.

scholarly journals The Role of the Transsulfuration Pathway in Non-Alcoholic Fatty Liver Disease

2021 ◽  
Vol 10 (5) ◽  
pp. 1081
Author(s):  
Mikkel Parsberg Werge ◽  
Adrian McCann ◽  
Elisabeth Douglas Galsgaard ◽  
Dorte Holst ◽  
Anne Bugge ◽  
...  
Keyword(s):  
Liver Disease ◽  
Animal Models ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
Precise Control ◽  
Transsulfuration Pathway ◽  
Global Population ◽  
Alcoholic Fatty Liver Disease

The prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing and approximately 25% of the global population may have NAFLD. NAFLD is associated with obesity and metabolic syndrome, but its pathophysiology is complex and only partly understood. The transsulfuration pathway (TSP) is a metabolic pathway regulating homocysteine and cysteine metabolism and is vital in controlling sulfur balance in the organism. Precise control of this pathway is critical for maintenance of optimal cellular function. The TSP is closely linked to other pathways such as the folate and methionine cycles, hydrogen sulfide (H2S) and glutathione (GSH) production. Impaired activity of the TSP will cause an increase in homocysteine and a decrease in cysteine levels. Homocysteine will also be increased due to impairment of the folate and methionine cycles. The key enzymes of the TSP, cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE), are highly expressed in the liver and deficient CBS and CSE expression causes hepatic steatosis, inflammation, and fibrosis in animal models. A causative link between the TSP and NAFLD has not been established. However, dysfunctions in the TSP and related pathways, in terms of enzyme expression and the plasma levels of the metabolites (e.g., homocysteine, cystathionine, and cysteine), have been reported in NAFLD and liver cirrhosis in both animal models and humans. Further investigation of the TSP in relation to NAFLD may reveal mechanisms involved in the development and progression of NAFLD.

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