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Chapter 18: Ethanol Metabolism

Induction of CYP2E1 would be expected to result in which of the following?

A. decreased rate of ethanol clearance from the blood

B. decreased rate of acetaldehyde production

C. increased level of alcohol tolerance

D. protection from alcohol-induced hepatic necrosis

E. reduced likelihood of free radical production

Answer C: The primary pathway of ethanol metabolism is that initiated by ADH. The second major pathway for ethanol metabolism is the microsomal ethanol-oxidizing system (MEOS), which involves the cytochrome P450 enzyme CYP2E1. The MEOS pathway is induced in individuals who chronically consume alcohol, resulting in higher rates of metabolism leading to increased tolerance to alcohol ingestion.

Which of the following chronic effects of alcohol consumption is irreversible?

A. activation of triglyceride synthesis

B. inhibition of fatty acid oxidation

C. ketoacidosis

D. lactic acidosis

E. liver cirrhosis

Answer E: Chronic ethanol consumption and alcohol metabolism contributes to the spectrum of metabolic disorders frequently found in alcoholics. These disorders include fatty liver syndromes such as NAFLD and NASH, hyperlipidemia, lactic acidosis, ketoacidosis, and hyperuricemia. The first stage of liver damage following chronic alcohol consumption is the appearance of fatty liver, which is followed by inflammation, apoptosis, fibrosis, and finally cirrhosis. These negative and toxic changes within the liver are irreversible even when alcohol consumption is terminated.

Acetate, derived from the oxidation of ethanol, has which of the following fate?

A. due to its toxicity it leads to necrosis of the liver

B. it directly enters the TCA cycle and is oxidized

C. it is converted into NADH via the action of ADH

D. it is excreted in the bile

E. it is taken up by nonhepatic tissues and converted to acetyl-CoA

Answer E: Acetate, from whatever source, is converted to acetyl-CoA by ATP-dependent acetyl-CoA synthetases (AceCS). Following the consumption of ethanol, acetate levels can be elevated by as much as 20-fold. The primary causes of fatty liver syndrome (hepatic steatosis), induced by excess alcohol consumption, are the altered NADH/NAD+ levels that in turn inhibits gluconeogenesis, inhibits fatty acid oxidation, and inhibits the activity of the TCA cycle. Each of these inhibited pathways results in ...

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