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24 sie 2022 · Alcohol decreases states of respiration in the electron transport chain, and activity and expression of respiratory complexes, with a net effect to decrease ATP content. In addition, alcohol dysregulates major metabolic pathways, including glycolysis, the tricarboxylic acid cycle, and fatty acid oxidation.
21 paź 2020 · According to our previous study, chronic intermittent alcohol (CIA) exposure triggers abnormal impulse and reward-seeking behaviors, which are associated with the mPFC and underlying changes in proteomic profiles (Starski et al., 2019a).
Assessment of a putative indicator of necrosis, the ratio of ADP to ATP, indicated that alcohol exposure accelerates pancreatic necrosis in response to endotoxin.
Adenine nucleotides (ADP and ATP) are released from damaged cells and are dephosphorylated by nucleoside triphosphate phosphohydrolase (CD39) and ecto-5′-nucleotidase (CD73) to adenosine. Adenosine promotes hepatic steatosis through its G-protein-coupled receptors A1 and A2B.
In this new model of alcoholic pancreatitis, LPD-associated pancreatitis was reliably produced by acute ethanol treatment without the need for an additional trigger or chronic alcohol exposure. A hypophosphatemic state predisposed animals to ethanol-induced pancreatitis.
1 mar 2021 · ATP supplementation improves cardiovascular health. Adenosine triphosphate (ATP) is the primary compound that provides energy to drive many processes in living cells, including muscle contraction, neurotransmission, and cardiac function. Initial research used enteric-coated ATP that displayed no apparent efficacy.
We proposed, therefore, that phosphate deficiency might limit adenosine triphosphate synthesis and thereby contribute to alcohol-induced pancreatitis. Methods: Mice were fed a low-phosphate diet (LPD) before orogastric administration of ethanol.
