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Alcohol Metabolism

Alcohol metabolism involves three enzyme systems: alcohol dehydrogenase, microsomal ethanol oxidizing system (MEOS), and aldehyde dehydrogenase, with MEOS being the primary pathway in chronic consumption. Chronic alcohol intake leads to fatty liver due to increased fatty acid synthesis and decreased oxidation, as well as complications like hypoglycemia and lactic acidosis. Additionally, alcohol consumption can exacerbate conditions such as gout and contribute to alcoholic ketoacidosis.

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37 views10 pages

Alcohol Metabolism

Alcohol metabolism involves three enzyme systems: alcohol dehydrogenase, microsomal ethanol oxidizing system (MEOS), and aldehyde dehydrogenase, with MEOS being the primary pathway in chronic consumption. Chronic alcohol intake leads to fatty liver due to increased fatty acid synthesis and decreased oxidation, as well as complications like hypoglycemia and lactic acidosis. Additionally, alcohol consumption can exacerbate conditions such as gout and contribute to alcoholic ketoacidosis.

Uploaded by

Asta
Copyright
© © All Rights Reserved
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3 enzyme systems take part in the alcohol metabolism

 Alcohol dehydrogenase (utilizing NAD+)


 Microsomal ethanol oxidising system (MEOS)
 Aldehyde dehydrogenase
MEOS

Aldehyde Dehydrogenase

Acetate

Acetyl CoA Enters into TCA cycle


• Ethanol consumption leads to accumulation of
fattyacids in the liver due to endogenous synthesis

• Major pathways for oxidation of alcohol is by


microsomal ethanol oxidising system (MEOS) in the
smooth endoplasmic reticulum.

• This is highly inducible enzyme system and persistent


ethanol consumption leads to marked proliferation of
SER in liver
• Alcohol is metabolized in the liver by two oxidation
reactions

Aldehyde Dehydrogenase
Disulfiram

Acetate

• Aldehyde dehydrogenase enzyme is inhibited by disulfiram, a drug


that has found some use in patients desiring to stop alcohol
ingestion.
• It causes the accumulation of acetaldehyde in the blood, which
results in flushing, tachycardia, hyperventilation, and nausea. In
each reaction, electrons are transferred to NAD+, resulting in a
massive increase in the concentration of cytosolic NADH.
 Deficiency of pyruvate affects formation of
Oxaloacetate (intermediate in gluconeogenesis) – leads
to hypoglycemia

 Deficiency of NAD+ and non availability of OAA


hamper the TCA cycle. As a result Acetyl coA
accumlates and diverted to fattyacid, cholesterol and
ketone bodies synthesis
 Elevated levels of fat accumulates in liver causing fatty

liver
Alcoholism leads to fatty liver
 Oxidation of Alcohol  produces acetate  converted

to acetyl CoA  synthesis of fattyacid and TAG


accumulates  results in fattyliver

Alcoholism aggravates gout


 Increased NADH/NAD ratio  Increased blood lactate

(lacticacidosis)  Decreases the capacity of the kidney


to excrete uric acid.
• The rise in lactate can result in lactic acidosis and,
because lactate competes with urate for excretion by the
kidney, can also result in hyperuricemia.

• Thus, the ethanol-mediated increase in NADH causes


the intermediates of gluconeogenesis to be diverted into
alternate reaction pathways, resulting in the decreased
synthesis of glucose (Hypoglycemia)
 Decreased availability of OAA allows acetyl CoA to be
diverted to ketone body synthesis in liver and can result
in alcoholic ketoacidosis.
 Alcohol consumption can produce hypoglycemia that

may contribute to the behavioral effects of alcohol


like agitation, impaired judgement, and combativeness.
(who are Prolonged fasting, strenuous exercise)
 Alcohol consumption can also increase the risk for

hypoglycemia in patients using insulin (risk of


hypoglycemia that generally occurs many hours after
the alcohol has been consumed)
Chronic alcohol consumption can also result in alcoholic fatty liver
due to increased synthesis of triacylglycerols.
•Decreased NAD+/NADH ratio  Decreased fatty acid oxidation  increased
lipogenesis
•With continued alcohol consumption  alcoholic fatty liver  alcoholic
hepatitis  alcoholic cirrhosis

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