Alcohol metabolism (L34)

Question 1

What receptor in the CNS is activated by alcohol?

Answer 1

GABAa receptor

Question 2

What is the biochemical effect of GABAa receptor activation?

Answer 2

Opens so conducts Cl- into cell

Question 3

Describe what the GABAa receptor is

Answer 3

Membrane bound, ligand gated chloride channel

Question 4

What is the effect of GABAa receptor activation?

Answer 4

Dampens down responses to other stimuli

Question 5

What is the reaction that converts ethanol to acetaldehyde?

Answer 5

Oxidation of ethanol with NAD being reduced

Question 6

What is the reaction that converts acetaldehyde to acetate?

Answer 6

Oxidation acetaldehyde with NAD being reduced

Question 7

What are the 2 enzymes involved in ethanol metabolism?

Answer 7

Alcohol dehydrogenase, acetaldehyde dehydrogenase

Question 8

What is the rate determining step in ethanol metabolism?

Answer 8

Alcohol dehydrogenase converting to acetaldehyde

Question 9

Where in the cell is acetate converted to ATP?

Answer 9

Mitochondria

Question 10

How is acetate further metabolised to make ATP energy?

Answer 10

Converted to Acetyl-CoA by to either be stored or enter CAC, ETC and oxidative phosphorylation

Question 11

What enzyme breaks down acetate for it to be further metabolised by the cell?

Answer 11

acetyl CoA synthetase converts acetate to acetyl-CoA

Question 12

In what organ of the body does ethanol metabolism primarily take place in?

Answer 12

liver

Question 13

What is the relationship between absorption and elimination of alcohol with BAC?

Answer 13

Can process 10g.hr, 5 drinks takes at least 5 hours to be absorbed by body
ADH is maxed out after a few drinks

Question 14

If large amounts of ethanol are being oxidised, what is the consequence on other metabolic pathways? (4)

Answer 14

Increased NADH and increased ATP
= Slows CAC and ETC, pyruvate dehydrogenase, glycolysis, fatty acid oxidation as less NAD to activate
= Fatty acids esterified to TAGS -> fatty liver
= Causes pyruvate -> lactate which decreases pH
= Inhibits gluconeogenesis - can cause low blood glucose -> sometimes coma

Question 15

How does oxidation of ethanol as a fuel differ to oxidation of glucose and fatty acids?

Answer 15

The enzymes have no regulation so acetyl CoA (and .: lactate) keeps increasing conc.

Question 16

What happens to the alcohol if there is enough/excess ATP?

Answer 16

Excess acetyl CoA shunted into pathway to make fatty acids/triacyl glycerides, which is taken away by VLDLs and stored in adipose tissue

Question 17

Is ethanol oxidation subject to feedback regulation?

Answer 17

Nope

Question 18

T or F - regular drinkers metabolise alcohol faster

Answer 18

True! Ethanol up regulates gene for microsomal ethanol oxidising system so regular drinkers have more of the oxidase enzyme

Question 19

What is the alternative pathway for ethanol metabolism? Dangers?

Answer 19

Microsomal ethanol oxidising system in ER: alcohol oxidised to acetaldehyde by oxidase enzyme, with reduction of NADPH + O2.
Can lead to reactive oxygen species (O2-)

Question 20

What toxic effects can chronic alcohol consumption have on the body?

Answer 20

Toxic aldehyde, reactive oxygen species
-> fatty liver, inflammation
-> alcoholic hepatitis
-> necrosis
-> cirrhosis
-> coma and death