No the reasoning is faulty. Nadh gets regenerated into NAD + in the electron transport chain without the kreb cycle being necessary. Nadh goes directly from glycolysis 2 the electron transport chain, dumps off it's electrons and hydrogen's and becomes NAD + again. The electrons and hydrogen's bind to oxygen at the end of the electron transport chain. At no point is the conversion of pyruvate to acetyl-coa necessary. Now, you will have a massive excess of pyruvate which could cause all sorts of problems including overloading the lactic acid fermentation pathway. Leading to lactic acidosis, but the reason isn't because the NAD needs to be regenerated
michalchik Nice catch dude! Except I wouldn't say NADH goes directly into the mitochondria because NADH is impermeable to the inner mitochondrial membrane. For this reason, there's shuttle mechanisms involved like the malate-aspartate and glycerol-3-phosphate shuttles but yeah you are right about Krebs not being involved.
Hi, thanks for the easy-to-understand explanation. I would to ask you what are the treatments in this case? Q1: Some internet sites propose IV potassium/sodium bicarbonate to alkalize the blood. But there are some controversial opinion on this treatment. Q2: And in some other sites, biotin, thiamine, lipoic acid, dichloroacetate, aspartic acid, and citrate can sometimes help to reduce the levels of pyruvate and lactate. Wht do you think? Q3: If someone were to take pyruvate supplements and suffer from excessive fatigue, does that prove that the person has pyruvate dehydrogenase deficiency? I would really appreciate it is you could spare me your opinion?
Thanks! This was great for my RD exam. I had to understand the role of thiamin.
Thank you! Saw a pt with this in clinic today
Great video! Keep it up
No the reasoning is faulty. Nadh gets regenerated into NAD + in the electron transport chain without the kreb cycle being necessary. Nadh goes directly from glycolysis 2 the electron transport chain, dumps off it's electrons and hydrogen's and becomes NAD + again. The electrons and hydrogen's bind to oxygen at the end of the electron transport chain. At no point is the conversion of pyruvate to acetyl-coa necessary.
Now, you will have a massive excess of pyruvate which could cause all sorts of problems including overloading the lactic acid fermentation pathway. Leading to lactic acidosis, but the reason isn't because the NAD needs to be regenerated
michalchik Nice catch dude! Except I wouldn't say NADH goes directly into the mitochondria because NADH is impermeable to the inner mitochondrial membrane. For this reason, there's shuttle mechanisms involved like the malate-aspartate and glycerol-3-phosphate shuttles but yeah you are right about Krebs not being involved.
thanks doc
Hi, thanks for the easy-to-understand explanation. I would to ask you what are the treatments in this case?
Q1: Some internet sites propose IV potassium/sodium bicarbonate to alkalize the blood. But there are some controversial opinion on this treatment.
Q2: And in some other sites, biotin, thiamine, lipoic acid, dichloroacetate, aspartic acid, and citrate can sometimes help to reduce the levels of pyruvate and lactate. Wht do you think?
Q3: If someone were to take pyruvate supplements and suffer from excessive fatigue, does that prove that the person has pyruvate dehydrogenase deficiency?
I would really appreciate it is you could spare me your opinion?