Glycerophosphate Shuttle: Mitochondrial NADH Transport
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- เผยแพร่เมื่อ 17 มี.ค. 2017
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It was very helpful.. Thank you so much
Hey, you might want to update the thumbnail for this one :)! Love your videos though, they've been helping me a lot recently. This is the third time now that I've stumbled upon a video I thought looked good and it turned out to be one of yours (and they are indeed very good) :D...
easy , simple , clear . thanks :)
Hope you are still here. Very good .. but. It still only shows electron migration and substrate conversion. What is the source of the matrix NAD or FAD. How did it get there if it cannot be transported across mitochondrial membranes? It is vital to the question ... does NAD+ or NADH supplementation augment the ETC? Similarly, does CoQ10 supplementation cross these membranes?
To be honest, I'm not sure about NADH/NAD supplementation, but I have never read that NADH or NAD are able to cross plasma membranes post-supplementation. Rather, I believe any NAD or NADH consumed in the diet is broken down to nicotinamide (~vitamin B3) in the intestines, absorbed, and remade into NAD inside the cell using it through a short biosynthetic pathway. CoQ supplementation does have experimental evidence, especially in cases of low CoQ synthesis (e.g., as with statin drugs). To get NAD back out into the cytoplasm for glycolysis, the malate-aspartate shuttle allows for the net (not direct) translocation of NADH into the matrix. The electrons are simply carried on TCA cycle intermediates.
@@CatalystUniversity Thank you for a kind reply. The shunt is only transferring "energy" in the form of electron flow. It is not actually transporting NAD+ or NADH as you rightly point out. And this was a huge revelation. So the question is what is the derivation or origin of the matrix NAD+? Is it manufactured de novo independent of the TCA? The shunt is only responsible for catalyizng one form into another.