Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ethanol and other alcohols stimulate adenylate cyclase activity in various tissues and potentiate its stimulation by some hormones. This effect, however, usually requires a high alcohol concentration. In some cases, an unknown substance, different from cyclic AMP, was formed from ATP in the presence of an alcohol and mimicked stimulation of adenylate cyclase. Ethanol inhibits phosphodiesterase activity in some tissues. In the brain, only the low affinity enzyme of pons-medulla region is inhibited. ATP levels and ATPase activities are affected by ethanol treatment and this can lead to secondary changes of the cyclic AMP levels. Cyclic AMP levels in the brain and liver are decreased by acute ethanol administration while levels in other organs are unchanged. High doses of ethanol inhibit the postdecapitation-induced rise of cyclic AMP level in the brain while low ethanol doses potentiate the postdecapitation rise of cyclic AMP in the lower brain stem. Chronic ethanol administration increases basal adenylate cyclase activity and cyclic AMP levels, and decreases stimulation of adenylate cyclase by norepinephrine in the brain. In contrast, the stimulation of cyclic AMP formation by norepinephrine and other biogenic amines is increased in the brain of ethanol-withdrawn animals. Chronic administration of ethanol affects also cyclic AMP levels and cyclic AMP formation in some peripheral organs. Cyclic AMP might be involved in ethanol-induced fatty liver, since it activates hepatic lipase and might also participate in the fatty acid oxidation.
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PMID:Interactions of ethanol with cyclic AMP. 16 56

A rapidly increasing scientific literature now supports the possibility of an alcohol-prostaglandin interaction. This chapter reviews evidence for both direct and indirect biochemical interactions between ethanol and the metabolism of arachidonic acid and several related compounds. Much of the present data is based on pharmacological manipulation of prostaglandin (PG) levels by potent nonsteroid anti-inflammatory agents such as indomethacin. Indomethacin markedly alters the behavioral response to ethanol, particularly in the mouse model. These data suggest that PGs are involved in the behavioral response to acute ethanol exposure in the mouse. In other animal models, alcohol has been reported to alter blood platelet metabolism of arachidonic acid, to suppress the enzymatic degradation of PGs, and to alter the response of the adenyl cyclase system to several hormones including PGs of the "E" series. In humans, both the stimulation and inhibition of PG synthesis is reported to aid the treatment of various aspects of alcoholism. Further, PGs are reported to protect against alcohol-induced fatty liver, and both PGs and arachidonic acid protect the gastric mucosa against ethanol-induced lesions. Certainly the residual consequences of acute, excessive ethanol consumption are commonly treated with a prostaglandin synthesis inhibitor. The material in this chapter is an attempt to review the data and to discuss the molecular mechanism underlying these observations.
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PMID:Biochemical interactions of ethanol with the arachidonic acid cascade. 298 78

Non alcoholic steatohepatitis (NASH) has gained a lot of attention recently due to the increased prevalence of diabetes, obesity, and hyperlipedemia. The endogenous compounds, endocannabinoids (ECBs), bind to the same receptors as tetrahydrocannabinol, the active component in marijuana and hashish. Recently, two G-proteins coupled, and specific receptors, to cannabinoids, CB1 & CB2, which act via adenylate cyclase and calcium channels, were described. In this brief review, we shed light on the possible relation between NASH and these proteins. It has been hypothesized that ECBs regulate peripheral lipogenesis. Some studies suggest that in CB1-deficient mice there is complete resistance to the development of diet-induced hepatic steatosis, while wild-type mice showed remarkable hepatic steatosis after 3 and 14 weeks of high-fat diet. Based on these results and others, the hepatic ECB system may be a target for the treatment of NASH. The CB1 antagonist, Rimonabant, will shortly be approved for the treatment of obesity and may thus reduce the necessity for bariatric surgery.
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PMID:Endocannabinoids and non-alcoholic steatohepatitis. 1985 84