Literally the best explanation on this topic I've ever come across! You are the best. I'm sitting here in awe at how much clarity I've gained from this one video :o Thank you so much DM!
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@@whitelion124 I would also think that ETC Complex 2 is an enzyme on TCA Cycle (Succinyl DH). So inhibiting TCA cycle directly inhibits ETC. So they can't use it even though there's a high amount of NADH
A 4th way you can form ketone bodies is by following the KETO Diet! haha. But I suppose this can go under starvation because the idea is to deprive your body from Carbs so insulin stays low.
Help me understand the process of alcoholism and TCA cycle shuts down? What happens when that person eats sugar? Where does the sugar go? Stored in the liver and not the cells? Or the sugar doesn’t produce atp energy for the alcoholic? Is seems like the solution would be to take mct oil and exogenous ketones? This is good stuff?? This video has me really curious as to the pathway?
Your DKA argument doesnt make sense to me, how does low insulin=high glucagon, and why would the body make more glucose when its already hyperglycemic?
Ketones get converted back to acetyl-coA when they reach their destination. How are ketones then helping to produce energy if the TCA cycle can't continue because of the lack of oxaloacetat? Why form ketones because of oxaloacetate depletion if you need oxaloacetate to gain energy from ketones?
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To clarify, the body's primary preference is to eliminate glucose as soon as possible. Before the advent of highly processed foods and the introduction of sugar, mankind relied on burning ketones for energy. It is important to remember that the body will make every effort to get rid of glucose due to its potential harm.
Can Someone Please Clear This Doubt For ME.. Why does buildup of acetyl CoA from failure of TCA cycle shunt towards Ketones and not gluconeogenesis? Acetyl CoA stimulates pyruvate carboxylase right
I would be very interested in references on this. It seems not quite right in that 1. OAA scan be supplied from Asp via transamination. 2. Acetyl-CoA is an activator of pyruvate carboxylase which will increase OAA when needed for TCA cycle. No? Also, liver is active in gluconeogenesis but liver doesn’t use ketone bodies. Not a challenge but what about these points?
I'm late to the video but just in case you're still active and replying, I have a question. Is acetylacetyl CoA the same as acetoacetyl CoA? That's what I'm seeing in my textbook
@@sgill4833I don’t think so, cholesterol biosynthesis is a separate pathway from ketone metabolism. It’s just a coincidence that HMG coA is produced in both pathways