WVSOM ETOH metabolism
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| Carbons from EtOH catabolism are further catabolized by? | citrate synthase
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| What enzyme helps ethanol go to acetaldehyde? | Alcohol dehydrogenase or MEOS system
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| What is produced when ethanol is broken down to acetaldehyde? | NADH + H+
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| What is the enzyme responsible for taking acetaldehyde to acetate? | acetaldehyde dehydrogenase (ALDH)
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| What is produced in the reaction from acetaldehyde to acetate? | NADH + H+
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| Where does ethanol metabolism take place? | liver
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| What is the intermediate product in the conversion of EtOH to acetate? | acetaldehyde
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| Is acetaldehyde toxic? | yes
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| Moderate ethanol consumption uses which enzyme? | ADH
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| What is used to catabolize EtOH in higher and chronic levels of consumption? | microsomal ethanol oxidizing system (MEOS)
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| Where does MEOS take place? | endoplasmic reticulum
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| What enzyme is used to oxidize EtOH to acetaldehyde in the MEOS process? | CYP2E1 (cytochrome P450)
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| What is oxidized besides EtOH in MEOS? | NADPH
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| What is the ultimate oxidizing agent in MEOS? | molecular O2
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| What is O2 reduced to in MEOS? | H2O
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| What has a higher Km? CYP2E1 or ADH? | CYP2E1
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| How is NADH reoxidized in the liver? | oxidative phosphorylation and dehydrogenase reactions
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| What will abnormally high amounts of NADH due in chronic ethanol consumption? May cause hepatic dehydrogenase reactions to occur in the reverse direction and has a negative impact on hepatic metabolism |
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| Acetaldehyde in the bloodstream is a _______________. | pathological occurance
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| Where is acetate used extrahepatically? | heart, kidney and skeletal muscle
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| Why do people have different alcohol metabolism? | There are 5 different classes of isoenzymes of Alcohol Dehydrogenase so the rates vary person to person
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| Which isoenzymes are most specific for metabolism in the liver? | ADH1 and ADH2
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| Which has the higher Km, ADH1 or ADH2? | ADH2
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| Which isoenzyme works in the intestines? | ADH4
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| How many isoenzymes are present for ALDH? | 2
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| Where is ALDH2? | mitochondria
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| Where is ALDH1? | cytosol
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| Which has the higher Km? ALDH1 or ALDH2? | ALDH1
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| What does the genetic variant of ALDH2 do? | has low activity so that toxic levels of acetaldehyde accumulate
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| What causes genes to produce more ADH and ALDH? | ethanol ingestion
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| High levels of NADH would decrease the activity of? | TCA cycle glycolysis and β oxidation
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| What is the cause of excessive EtOH consumption? | high hepatic NADH
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| What happens with too much hepatic NADH? | will exceed the liver’s ability to oxidize NADH
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| How does the body determine how much EtOH is catabalized? | amount of ethanol present
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| High NADH levels would increase the activity of an NADH/NAD+ using dehydrogenase in the direction of? | NADH oxidation/substrate reduction
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| Abnormally high NADH increases? | glycerol 3-p synthesis, pyruvate -> lactate, and oxaloacetate -> malate
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| How does increased EtOH decrease TCA? | inhibits isocitrate dehydrogenase.
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| How does increased EtOH decrease β-oxidation? | Decreased NAD+ substrate / increased NADH product slows this process.
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| How does EtOH decrease glycolysis? | glyceraldehyde 3-P is inhibited due to decreased availability of its NAD+ substrate
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| How does high hepatic NADH levels increase glycerol 3-P production? By glycerol-3P dehydrogenase from the glycolytic pathway intermediate Dihydroxyacetone phosphate |
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| What causes A fatty liver from? | TG and glycerol 3-P increases with a decrease in lipoprotein production resulting in excess fat in the liver
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| Liver damage from excess acetelaldyhyde results in? | decreaed protein synthesis, lipoprotein synthesis and lipoprotein export
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| Why does ketoacidosis occur in chronic EtOH ingestion? | abnormally high NADH decreases TCA cycle and acetyl CoA levels rise due to acetyl CoA entering the TCA cycle being decreased. This results in an increased ketone body production
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| Why is there decreased ketone body utilization occurring? | kidney and heart preferably catabolize acetate rather than ketone bodies.
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| Why does lactic acidosis occur with chronic EtOH? | high NADH levels increase lactate production and decreases its conversion to pyruvate so there is a build up
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| What disease results from lactic acidosis? | gout
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| Why does gout occur with lactate acidosis? | lactate competes with uric acids for excretion
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| Why does hypoglycemia occur with chronic ETOH consumption? | decreased hepatic lactate uptake occurs and pyruvate from tansamination of alanine is converted to lactate instead of glucose to hypoglycemia occurs. BOTTOM LINE – NOT ENOUGH GLUCONEOGENESIS
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| The presence of glutathione ___ free radical levels? | decreases
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| What happens with abnormally high acetealdehyde levels? | binds to glutathione
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| What pathological event occurs with binding of acetealdehyde to glutathione? | increase in free radicals
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| MEOS and CYP21E result in _______ levels of free radicals. | increased
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| What results from acetyladelhyde binding to amino acids? | decreased protein production
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| What happens when the liver tries to heal itself? | fibrosis and thereby cirrosis
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Created by:
tjamrose