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Alcohol is also converted into phosphatidylethanol (PEth, an unnatural lipid metabolite) by phospholipase D2. This metabolite competes with PIP 2 agonist sites on lipid-gated ion channels. [28] [29] The result of these direct effects is a wave of further indirect effects involving a variety of other neurotransmitter and neuropeptide systems. [25]
Ethyl glucuronide (EtG) is a metabolite of ethanol which is formed in the body by glucuronidation following exposure to ethanol, usually from drinking alcoholic beverages.It is used as a biomarker to test for ethanol use and to monitor alcohol abstinence in situations where drinking is prohibited, such as by the military, in alcohol treatment programs, in professional monitoring programs ...
Urine drug tests screen the urine for the presence of a parent drug or its metabolites. The level of drug or its metabolites is not predictive of when the drug was taken or how much the patient used. [19] Urine drug testing is an immunoassay based on the principle of competitive binding. Drugs which may be present in the urine specimen compete ...
The Glucuronidated metabolites of various chemicals can be tested for in bodily fluids. [7] Ethyl glucuronide and ethyl sulfate are excreted in urine as metabolites of ethanol and are used to monitor alcohol use. [8] Glucuronic acid and gluconic acid are fermentation products in Kombucha tea. [9]
While urine is commonly used for qualitative analysis, it does not provide indications of impairment since the presence of drugs in urine merely signifies prior exposure. [10] The duration of drug detection in urine varies; for instance, alcohol is detectable for 7–12 hours, cocaine metabolites for 2–4 days, and morphine for 48–74 hours.
Alcoholic ketoacidosis is caused by complex physiology that is the result of prolonged and heavy alcohol intake, usually in the setting of poor nutrition. Chronic alcohol use can cause depleted hepatic glycogen stores and ethanol metabolism further impairs gluconeogenesis.
[5] [6] An increase of alcohol intake by ~20 g ethanol/day will raise the PEth 16:0/18:1 concentration by ~0.10 μmol/L, and vice versa if the alcohol consumption has decreased. However, it has been demonstrated that there can be significant inter-personal variation, leading to potential misclassification between moderate and heavy drinkers. [ 7 ]
N-Acetyltaurine is a direct alcohol biomarker which represents the oxidative pathway of ethanol metabolism. Other direct alcohol biomarkers such as fatty acid ethyl esters (FAEE), ethyl glucuronide, ethyl sulfate, and phosphatidylethanol reflect the non-oxidative pathway of alcohol metabolism, based on conjunction reactions (biotransformation).