ArticleThe Biochemical journal1992
Ethanol increases receptor-dependent cyclic AMP production in cultured hepatocytes by decreasing G(i)-mediated inhibition.
Article in The Biochemical journal, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 47 citations in OpenAlex.
- Hepatic Aquaporin 8 Promotes Alcohol Consumption and Ameliorates Alcohol-Induced Liver Injury by Facilitating Acetaldehyde Excretion.International journal of biological sciences · 2026Article
- Dysregulated Cyclic Nucleotide Metabolism in Alcohol-Associated Steatohepatitis: Implications for Novel Targeted Therapies.Biology · 2023Article
- Ethanol interaction with α3β4 nicotinic acetylcholine receptors in neurons of the laterodorsal tegmentum.Alcoholism, clinical and experimental research · 2021Article
- cAMP Signaling in Pathobiology of Alcohol Associated Liver Disease.Biomolecules · 2020Review
- Cytochrome P450s and Alcoholic Liver Disease.Current pharmaceutical design · 2018Review
- Chronic alcohol feeding potentiates hormone-induced calcium signalling in hepatocytes.The Journal of physiology · 2017Article
- Alcoholic Liver Disease: from CYP2E1 to CYP2A5.Current molecular pharmacology · 2017Review
- Dysregulation of hepatic cAMP levels via altered Pde4b expression plays a critical role in alcohol-induced steatosis.The Journal of pathology · 2016Article
- Ethanol-Induced Motor Impairment Mediated by Inhibition of α7 Nicotinic Receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Effects of the lifestyle habits in breast cancer transcriptional regulation.Cancer cell international · 2016Review
- Behavioral Neuroadaptation to Alcohol: From Glucocorticoids to Histone Acetylation.Frontiers in psychiatry · 2016Review
- Ecklonia cava Polyphenol Has a Protective Effect against Ethanol-Induced Liver Injury in a Cyclic AMP-Dependent Manner.Marine drugs · 2015Article
- Activation of carbohydrate response element-binding protein by ethanol.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2013Article
- Early signalling events implicated in leukotriene B4-induced activation of the NADPH oxidase in eosinophils: role of Ca2+, protein kinase C and phospholipases C and D.The Biochemical journal · 1995Article
- Effects of acute and chronic ethanol on cyclic AMP accumulation in NG108-15 cells: differential dependence of changes on extracellular adenosine.British journal of pharmacology · 1995Article
- Adenosine A1 receptors mediate chronic ethanol-induced increases in receptor-stimulated cyclic AMP in cultured hepatocytes.The Biochemical journal · 1994Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence suggests that ethanol-induced changes in cyclic AMP (cAMP) signal transduction play a critical role in the acute and chronic effects of ethanol. Here we have investigated the effects of ethanol on cAMP signal transduction in primary cultures of rat hepatocytes. Acute exposure to ethanol had a biphasic effect on glucagon-receptor-dependent cAMP production in intact cells: 25-50 mM-ethanol decreased cAMP, whereas treatment with 100-200 mM-ethanol increased cAMP. After chronic exposure to 50-200 mM-ethanol for 48 h in culture, glucagon-receptor-dependent cAMP levels were increased, but no change in glucagon receptor number was observed. These effects of ethanol were independent of ethanol oxidation. Chronic ethanol treatment also increased adenosine-receptor- and forskolin-stimulated cAMP production. Increased cAMP production was also observed upon stimulation of adenylate cyclase with glucagon, forskolin and F- in membranes isolated from cells cultured with 100 mM-ethanol for 48 h. However, no differences were observed in basal and MnCl2-stimulated adenylate cyclase activity. The quantity of alpha i protein was decreased by 35% after chronic ethanol treatment, but no change in the quantity of alpha s protein was detected. Decreased alpha i protein was associated with a decrease in G(i) function, as assessed by the ability of 0.1 nM-guanosine 5'-[beta gamma-imido]triphosphate and 1 microM-somatostatin to inhibit forskolin-stimulated adenylate cyclase activity. Taken together, these results suggest that chronic exposure to ethanol increases receptor-dependent cAMP production in hepatocytes by decreasing the quantity of alpha i protein at the plasma membrane and thereby decreasing the inhibitory effects of G(i) on adenylate cyclase activity.
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Registered trials
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