Fantastic summaries of these pathways at a level of granularity that avoids the trees to let us see the woods and the beauty of how our biochemistry works.
Thanks Anthony. I don't think I have ever had anyone articulate their appreciation in the way you have for one of my videos. It was almost poetic. No, let me re-phrase that. It was poetic :-)
@@wondersofchemistry thanks, you’re most welcome! Changing the subject, what software tools do you use to put your video content together? It’s very good, something I could use myself.
Amazing explanation. You really understand this well and have the capability of sumarising and structruing things in a way that it is easy to understand. Many thanks for sharing.
Yes that is correct, however, i believe plants may have the ability to over come this is issue throught the glyoxylate cycle. You might like to look this up? Regards, MG
Please sir, is metabolic water formed during lipolysis or lipogenesis? And how do dessert animals survive staying without external water and solely by metabolic water
Jemima, to answer your question metabolic water is produced from mainly fatty acid and glucose oxidation. With fats this begins with lipolysis, then beta oxidation. The products of beta oxidation enter into the common metabolic pathway to generate most of the metabolic water. Theoretically, 1 mole of stearic acid will yield 18 moles of metabolic water. With dessert animals the production of metabolic water for survival is crucial. Equally, important are the special adaptions that reduce metabolic water from being lost (e.g., extremely concentrated urine, low moisture content of faeces, condensation of water vapour in the breath within the oral cavity (i.e., re-cycling), reduced panting and increase tolerance to homeostatic temperature regulation and using the bladder as storage container for water (when external water becomes available) all help :-)
Electron transport chain and oxidative phosphorylation are the same! Oxidative phosphorylation refers to the events in the ETC as well as the synthesis of ATP by ATP synthase. Good overview, but be sure to let the people know the accurate truth, since there are students.
In the brain, when 50 molecules of β-hydroxybutyrate are oxidized, 20% of acetoacetate is converted to acetone. Calculate how many ATP molecules will be synthesized if all the acetyl-CoA and NADHH + molecules formed in this process are included in the Citric cycle and ETC.
@@Praveenbhupathi22 Hi Praveen. Lets begin by breaking down the question into steps. Step 1: How many molecules of Acetoacetate and NADH are produced from the oxidation of one molecule of beta-hydroxybutyrate? Answer = 1 Acetoacetate + 1 NADH. Step 2: Assuming 100% of all the acetoacetate is converted into acetyl coA, how many acetyl coA will one molecule of acetoacetate give? Answer = 2. Step 3. However, the question implies only 80% of acetoacetate (100% - 20% = 80%) is converted into acetyl coA molecules, therefore giving (0.8 x 2) = 1.6 molecules acetyl coA per acetoacetate. Step 4. Assuming each acetyl coA that enters into the citric acid cycle generates 10 ATP (recall that one turn of the cycle produces 3NADH => 3 x 2.5ATP="7.5ATP", 1GTP = "1ATP" and 1FADH2 = "1.5ATP" giving a total of "10ATP" per acetyl coA)., then 1.6 acetyl coA will give 16ATP. Step 5. Calculate the number of ATPs produced from the one NADH generated when one molecule of beta hydroxybutyrate that was converted into one molecule of acetoacetate from step 1. Answer 1NADH = 2.5ATP when connected to the ETC. So in total one beta hydroxybutrate molecule will generate 2.5ATP (from its oxidation to acetoacetate and production of 1NADH) and 16ATP (based on 80% conversion rate) from the 1.6 acetyl coA molecules that enter into the citric acd cycle giving a total of 2.5ATP + 16ATP = 18.5ATP per betahydroxybutyrate. Finally multiply this by 50 to get the answer to the question => 50 x 18.5 = 925ATP. Note the assumptions made to arrive at this answer are as follows: 1NADH = 2.5ATP, 1FADH2 = 1.5ATP, 1GTP = 1ATP. Note if the rounded up figures where used (for both the high energy electron carriers) i.e., 1NADH = 3ATP, 1FADH2 = 2ATP then the answer would have been 22.2ATP per betahydroxybutyrate => 22.2 x 50 = 1110ATP for 50 molecules of betahydroxybutyrate. Oh there is one more assumption that acetatone cannot be metabolised to produce ATP in the brain. Hope this is useful. Regards, Wonders of Chemistry
Dear Ibrahim and all your fellow students from your CHG 22 Class thank you for taking the time to comment on my video. I hope you all found it usefu;l and feel free to share it with others that might also find it useful. Regards, Wonder of Chemistry in Australia :-)
Are the fed and fasted states the only two? One is normally presented as being in the presence of glucose and insulin and the other is normally presented as being in the absence of all calories, but there's also what happens if you are fed without glucose. Does that fall into one of those two states?
Hi Tristan, that is a very good question. Are you pointing towards very low carbohydrate type diets? If so, then you are 100% correct :-) You would clearly be in a fed state as you are still consuming food, however, the very low intake of carbohydrate (and therefore lack of oxaloacetate availability to the citric acid cycle) would favour ketogenesis. Maybe I should have pointed this out in the presentation? I could always do it again and include this. What do you think? PS. I have to apologise for not getting back to with your previous comments regarding some of other videos.
@@wondersofchemistry ah, dont worry about my other questions, I'm just an over excited lay person. I always think it's important to be clear with terminology because they can cause a lot of confusion including making it appear that a space is fully covered. Sometimes little things like how everyone except you explains that some process produces 2 ATPs when actually it produces one AMP->ATP conversion, ie two phosphate-phospate bonds which seems innocuous to them but prevents correct quantitative modelling.
@@wondersofchemistry instead of doing it again, why not insert a small comment or an annotation where you introduce the states to explain their names could be misleading, that feeding can involve both states despite their names, although if there are other different major states then it would be important to cover that at least to mention that the exist and are different, I think. Of course it must be more complicated than you can cover fully because there are tissue specific differences and limiting factors but a mention that the story is bigger and the terms might be misleading is important.
@@wondersofchemistry there are other feeding modes too, high protein with little carbs or fat which is now easy for people to get into a habit of now that everything's got low fat variants like lean beef (what's that about?). Feeding on limited protein profiles via supplement or food replacement/enhancement powders is common now and I think I read that dietary malic acid, a common nutrient supplement in some apple flavour sodas, can easily enter the citrate cycle giving another mode that's easy to get to in the modern food landscape maybe keeping the hepatic oxaloacetate supply replete in the otherwise ketogenic states.
What a pitty you didn't mention what happens in the mitochondria and what in the cytosol. Because AcetylCoa in the mitochondria is quite different from AcetylCoa in the cytosol...
![Taurine: The Nutrient of Youth [Science Explained]](http://i.ytimg.com/vi/qH5QumHGrgk/mqdefault.jpg)
Fantastic summaries of these pathways at a level of granularity that avoids the trees to let us see the woods and the beauty of how our biochemistry works.
Thanks Anthony. I don't think I have ever had anyone articulate their appreciation in the way you have for one of my videos. It was almost poetic. No, let me re-phrase that. It was poetic :-)
@@wondersofchemistry thanks, you’re most welcome! Changing the subject, what software tools do you use to put your video content together? It’s very good, something I could use myself.
Hi Anthony, I primarily use apple keynote :-)
Amazing explanation. You really understand this well and have the capability of sumarising and structruing things in a way that it is easy to understand. Many thanks for sharing.
Thank you so much for your kind words :-)
Thank you for this thorough video, I finally understand the whole metabolism with all the pathways.
Glad to be of assistance. Thank you for your comments. Regards, Wonders of Chemistry :-)
Great!
Very good, succinct explanation of the fates of a acetyl coA
No worries, glad you found it useful
Thank you for the good presentation.
Thanks for this crystal clear explanation
All good. Thanks for the feedback :-)
I dnt know how much to thank uuu😔I was very depressed abt this u hve really help meh....thanks
U deserve alot million subscribers 🙄thanks once again
Thank you !
Brilliant! Thank you!!!
Make more video please. Very helpful 👍🏻👍🏻👍🏻
Great video, thnx a lot
I liked your presentation keep going
Hi Yasser, Thank you for your words of encouragement.Regards, Wonders Of Chemistry.
Great video, thank you - am I right in thinking there is no pathway for Acetyl-CoA to be converted back into Pyruvate?
Yes that is correct, however, i believe plants may have the ability to over come this is issue throught the glyoxylate cycle. You might like to look this up? Regards, MG
@@wondersofchemistry Thank you!
Very nice sir
Wow! Just what I was looking for! Thank you!
No worries, glad you found it useful
great video mate
Thanks Abdullah :-)
👏👏👏👏👏👏👏👏mad respect bruh
Please sir, is metabolic water formed during lipolysis or lipogenesis? And how do dessert animals survive staying without external water and solely by metabolic water
Jemima, to answer your question metabolic water is produced from mainly fatty acid and glucose oxidation. With fats this begins with lipolysis, then beta oxidation. The products of beta oxidation enter into the common metabolic pathway to generate most of the metabolic water. Theoretically, 1 mole of stearic acid will yield 18 moles of metabolic water. With dessert animals the production of metabolic water for survival is crucial. Equally, important are the special adaptions that reduce metabolic water from being lost (e.g., extremely concentrated urine, low moisture content of faeces, condensation of water vapour in the breath within the oral cavity (i.e., re-cycling), reduced panting and increase tolerance to homeostatic temperature regulation and using the bladder as storage container for water (when external water becomes available) all help :-)
Electron transport chain and oxidative phosphorylation are the same! Oxidative phosphorylation refers to the events in the ETC as well as the synthesis of ATP by ATP synthase. Good overview, but be sure to let the people know the accurate truth, since there are students.
How is ac ytl coa produced in bets oxidation
In the brain, when 50 molecules of β-hydroxybutyrate are oxidized, 20% of acetoacetate is converted to acetone. Calculate how many ATP molecules will be synthesized if all the acetyl-CoA and NADHH + molecules formed in this process are included in the Citric cycle and ETC.
Hello sir, can you please explain how to calculate the atp?
@@Praveenbhupathi22 Hi Praveen. Lets begin by breaking down the question into steps. Step 1: How many molecules of Acetoacetate and NADH are produced from the oxidation of one molecule of beta-hydroxybutyrate? Answer = 1 Acetoacetate + 1 NADH. Step 2: Assuming 100% of all the acetoacetate is converted into acetyl coA, how many acetyl coA will one molecule of acetoacetate give? Answer = 2. Step 3. However, the question implies only 80% of acetoacetate (100% - 20% = 80%) is converted into acetyl coA molecules, therefore giving (0.8 x 2) = 1.6 molecules acetyl coA per acetoacetate. Step 4. Assuming each acetyl coA that enters into the citric acid cycle generates 10 ATP (recall that one turn of the cycle produces 3NADH => 3 x 2.5ATP="7.5ATP", 1GTP = "1ATP" and 1FADH2 = "1.5ATP" giving a total of "10ATP" per acetyl coA)., then 1.6 acetyl coA will give 16ATP. Step 5. Calculate the number of ATPs produced from the one NADH generated when one molecule of beta hydroxybutyrate that was converted into one molecule of acetoacetate from step 1. Answer 1NADH = 2.5ATP when connected to the ETC. So in total one beta hydroxybutrate molecule will generate 2.5ATP (from its oxidation to acetoacetate and production of 1NADH) and 16ATP (based on 80% conversion rate) from the 1.6 acetyl coA molecules that enter into the citric acd cycle giving a total of 2.5ATP + 16ATP = 18.5ATP per betahydroxybutyrate. Finally multiply this by 50 to get the answer to the question => 50 x 18.5 = 925ATP. Note the assumptions made to arrive at this answer are as follows: 1NADH = 2.5ATP, 1FADH2 = 1.5ATP, 1GTP = 1ATP. Note if the rounded up figures where used (for both the high energy electron carriers) i.e., 1NADH = 3ATP, 1FADH2 = 2ATP then the answer would have been 22.2ATP per betahydroxybutyrate => 22.2 x 50 = 1110ATP for 50 molecules of betahydroxybutyrate. Oh there is one more assumption that acetatone cannot be metabolised to produce ATP in the brain. Hope this is useful. Regards, Wonders of Chemistry
Reductive acetyl coemzyme pathway ?
Sir plz tell me that how we calculate no. Of NADH produced from fatty acids of different no. Of C atoms
CHG 22 class thanks you
Dear Ibrahim and all your fellow students from your CHG 22 Class thank you for taking the time to comment on my video. I hope you all found it usefu;l and feel free to share it with others that might also find it useful. Regards, Wonder of Chemistry in Australia :-)
Are the fed and fasted states the only two? One is normally presented as being in the presence of glucose and insulin and the other is normally presented as being in the absence of all calories, but there's also what happens if you are fed without glucose. Does that fall into one of those two states?
Hi Tristan, that is a very good question. Are you pointing towards very low carbohydrate type diets? If so, then you are 100% correct :-) You would clearly be in a fed state as you are still consuming food, however, the very low intake of carbohydrate (and therefore lack of oxaloacetate availability to the citric acid cycle) would favour ketogenesis. Maybe I should have pointed this out in the presentation? I could always do it again and include this. What do you think? PS. I have to apologise for not getting back to with your previous comments regarding some of other videos.
@@wondersofchemistry ah, dont worry about my other questions, I'm just an over excited lay person. I always think it's important to be clear with terminology because they can cause a lot of confusion including making it appear that a space is fully covered. Sometimes little things like how everyone except you explains that some process produces 2 ATPs when actually it produces one AMP->ATP conversion, ie two phosphate-phospate bonds which seems innocuous to them but prevents correct quantitative modelling.
@@wondersofchemistry instead of doing it again, why not insert a small comment or an annotation where you introduce the states to explain their names could be misleading, that feeding can involve both states despite their names, although if there are other different major states then it would be important to cover that at least to mention that the exist and are different, I think. Of course it must be more complicated than you can cover fully because there are tissue specific differences and limiting factors but a mention that the story is bigger and the terms might be misleading is important.
@@tricky778 I think I'll re-do it, and upload it maybe tomorrow. Thanks once again for your candid feedback.
@@wondersofchemistry there are other feeding modes too, high protein with little carbs or fat which is now easy for people to get into a habit of now that everything's got low fat variants like lean beef (what's that about?). Feeding on limited protein profiles via supplement or food replacement/enhancement powders is common now and I think I read that dietary malic acid, a common nutrient supplement in some apple flavour sodas, can easily enter the citrate cycle giving another mode that's easy to get to in the modern food landscape maybe keeping the hepatic oxaloacetate supply replete in the otherwise ketogenic states.
What a pitty you didn't mention what happens in the mitochondria and what in the cytosol. Because AcetylCoa in the mitochondria is quite different from AcetylCoa in the cytosol...