Alcohol Metabolism
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- Опубликовано: 15 авг 2024
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My goal is to reduce educational disparities by making education FREE.
These videos help you score extra points on medical school exams (USMLE, COMLEX, etc.)
For educational purposes only; NOT medical or other advice.
Some videos contain mild profanity and hyperbole solely used to assist with memorization. Viewer discretion advised.
Opinions are entirely my own.
Memory hook for disulfiram: diSUFFERam
the only one there that makes biochemistry (and other topics too) simple and doable! thank you so much for everything
ninja nerd does his thing too. check him out :)
You can't compare him with Dirty med , Dirty med is a bang and a beast
@@DaktuurAmarAKA They just are for different aspects. For in depth, Ninja Nerd is amazing. For quick review for testing, DirtyMed is the Goat.
Mnemonic for Fomepizole: think it as Foam-epizole, which can turn the beer to a lot of foam and less liquid (dehydro).
the way you just broke down the metabolic pathways is just too beneficial to explain !!!!
May you be rewarded ,sir
Superb explaination.. 😍
international mnemonic for NADH:NAD+..
too much *H*eineken leads to too much NAD*H*...
omg the way you explain everything smoothly!!!
Thank you for making biochemistry easier ☺️.
Fatty MiLK:
NADH/NAD+ stimulated pathways increase Fatty Acids, G3P, Triglycerides, and Malate, Lactate acids, and Ketoacids :)
Why can't the body get rid of the NADH via the Electron Transport Chain?
I’m not entirely certain, but I don’t think the liver has an adequate amount of oxygen to use for the etc to work at the level necessary to get rid of the excess nadh
Well to some extent NADH does go to ETC, but it isn't enough in cases of alcohol overdose
Well-done
Thanks very much
Question. In a past video you said Acetyl-CoA cannot be shunted from mitochondria to make ketones, which is why citrate is shuttled out... In this video you say Acetyl-CoA is used directly to make ketones. Can you explain the discrepancy please.
AMAZING!!
Thank u so much for this wonderful explanation 😍
Alse hyperuricemia can occur, uric acid competes with lactate and its elimination may be slowed down
GOAT
Thank you!
So helpful thanks
Is acetaldehyde dehydrogenase similar to Formaldehyde
@slicky villy No need to be a dick about it. Just highlights your intellectual insecurity.
Thank you. Your video is very helpful. :)
I loved it
Ohhh thank you
Love you
If the NADH levels are high wouldn't that favour gluconeogenesis?
yea I'm confused here as well; if TCA is decreased due to low oxaloacetate levels and there is a buildup of acetyl-CoA, wouldn't that promote gluconeogenesis because acetyl-CoA is a positive regulator of pyruvate carboxylase?
@@ASAINsensation Same :') can someone explain ?
@@ASAINsensation Acetyle-CoA is indeed positive regulator of pyruvate carboxylase that coverts pyruvate into oxaloacetate. But here's the catch. In 8:09 minutes into this video he explains that pyruvate is also being used to compensate increased NADH by converting it into lactate. So there is not enough pyruvate left to convert into oxaloacetate so that it can participate in gluconeogenesis.
Thank you!!! Great Help!
THAAAAAAAAANKS
❤️
Alcoholics have small NAD+s
What happens to glycogenolysis ?
Glycogenolysis will be promoted. As vlycogen breakdow:ns it does not necessarily becomes glucose. It can take alternate route and go on to form pyruvate, which as explained in this video at 8:09 can be converted into lactate
witch level of education is this intended for?
This is for medical students studying for board exams, but I’m sure it’s helpful in other medial professions as well.
@@rosyreverie thank you! I was wondering cuz it seemed just slightly above the level I'm on, but I'm also only in my 11th year of education, and half the issue is probably that English isn't my first language. It's very impressive how this is actually understandable to me (a 17 year old) even if it's a bit tough
I'm not sure many 17 year olds would understand it though, I'm very much just a massive nerd
@@alexboyemuller3898 bruh
I understood this in my mom's womb.. I 1 upped you bro.. sorry
Something does not make sense here - if alcohol decreases gluconeogenesis and increases ketosis, would that make it a good thing to have during fasting for the sake of weight/fat loss? Since the whole idea of the keto diet is to deplete glucose and forces your body into a keto state so it burns stored fat. I am talking about pure alcohol here like vodka, not beer or wine.
The fact that it decresease Glucogenesis, it's because you have a high excess of NADH and a low ammount of NAD+.
The high ammount of NADH will lead your body to synthesis all your nutrients into fatty acid... even Fruits, Vegetables and Cereals. So even healthy nutrients will be stored in your fat.
The role of the NAD+ is to be able to increase your gluconeogenesis so you can transform your sugar into glycogene. Glycogene is needed to allow your cells to work. A low ammount of Glycogene means that your cells will go lazy and their membrane will grow larger because of the synthesis of fatty acid.
And voila, you created a situation one can be at risk of gaining weight.
Sorry if it's not 100% clear, english is not my first language.
As gluconeogenesis is not working you’re already at risk of hypoglycaemia, so glycogen here becomes very important. Combine fasting state + alcohol= Severe hypoglycaemia, may even get seizures!
I love you
alcohol being metabolised in first order kinetic, would give the term "Chug chug chug" a whole new level of meaning
I can’t see any health benefits from alcohol but why people like to drink it 🥴
It doesn't go with First aid
It sounds like you're talking to children.
❤