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Old 11-16-2015
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Default Alcoholism and Acetyl Coa!

In alcoholism, the acetyl coa which leads to increased lipogenesis and increased ketogenesis. (First Aid 2015 Pg 95).

Isnt this Acetyl Coa from Pyruvate? Wont the increased Nadh inhibit the PDH enzyme inhibiting formation of Acetyl Coa?

Hope someone will reply.

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Old 11-16-2015
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Default Biochemical Alterations of Alcohol

Quote:
Originally Posted by voicesinmyhead View Post
In alcoholism, the acetyl coa which leads to increased lipogenesis and increased ketogenesis. (First Aid 2015 Pg 95).

Isnt this Acetyl Coa from Pyruvate? Wont the increased Nadh inhibit the PDH enzyme inhibiting formation of Acetyl Coa?

Hope someone will reply.

Thanks
Both the oxidation steps of alcohol produces NADH resulting in a high NADH/NAD+ ratio. As a result, several metabolic adaptations occur:
1. In the cytoplasm, the high NADH level favors conversion of pyruvate to lactate, leading to lactic acidosis.
2. Deficiency of pyruvate leads to inadequate formation of oxaloacetate. This results in depression of gluconeogenesis, leading to hypoglycemia
3. Reduced oxaloacetate, decreased pyruvate and high NADH level causes suppression of TCA cycle. So Acetyl CoA is accumulated, which favors ketogenesis.
4. Increased level of Acetyl Co A causes increased fatty acid synthesis, but fatty acid is not oxidized. So fat is accumulated in liver, resulting in fatty liver and steatosis.
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Old 03-07-2017
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Default

In alcoholism, acetyl CoA is not formed from pyruvate (voicesinmyhead's question). It is rather formed from acetate:
Ethanol --> acetaldehyde --> acetate --> acetyl CoA (ethanol metabolism increases NADH)
pyruvate --> lactate (supplies NAD+)

FA 2017 on ethanol metabolism (p. 89):
increased NADH/NAD ratio disfavors TCA production of NADH
--> increased utilization of acetyl CoA for ketogenesis and lipogenesis

In a Kaplan QBank biochemistry question, the explanation states that in alcoholism, the fatty acid oxidation decreases due to relative excess of NADH, leading to decreased ketone body formation because of less acetyl CoA being available.
Kaplan gives another reason for a decreased ketone body synthesis in alcoholism: Long term alcoholism -> alcoholic cirrhosis of the liver
-> any pathway normally conducted by the liver will be impaired, such as gluconeogenesis and ketone body formation.
On the other hand, Kaplan states that there is an increased channeling of acetyl CoA into KB formation because of less oxalacetate being available for the TCA cycle.
("updated on 12/5/16")

In chronic alcoholism, apparently the acetyl CoA is mainly used for fatty acid synthesis (inhibited TCA and respiratory chain).
For ketogenesis, the perfect conditions would be lots of acetyl CoA and NAD+ in the liver. Due to ethanol metabolism, the NADH/NAD ratio is not in favor for ketogenesis as apposed to fatty acid synthesis for which a high NADH is favorable.

I hope this is a useful addition to Dhiegoncx's answer which I find to be a great overview.
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Old 03-19-2017
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Default Acetyl CoA buildup in Alcohol

Although this thread is old, if anyone were to come across it, I wish they'd find it helpful so I want to just add/clarify/re-state some things

The previous two posts are solid in explaining the build-up of Acetyl CoA. Like chaplin states, the build-up of Acetyl CoA can be simply explained from the fact that the acetic acid (acetate) is converted to Acetyl CoA:

Ethanol --(alc DH)--> Acetaldehyde --(aldehyde DH)--> Acetate --(AcCoA synthetase)-> Acetyl CoA

^ this build-up of Acetyl CoA is used for both synthesis of fatty acids and triglycerides (along with glycerol-3-Phosphate (coming from DHAP -> Glycerol-3-P in presence of inc NADH) as well as synthesis of ketone bodies, specifically B-hydroxybutyrate (inc in NADH favors acetoacetate to B-OHB conversion).

(got all dis from Gojlan's RR pg 160)
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