Clear, concise, helpful. Thank you. (The drawings of the two different ketone bodies could be standardized by showing the terminal -CH3 on the beta form and flipping it 90 degrees, so that the -CH3 groups are at the left ends in both figures. The remarkable similarity of the two molecules would then be easy to see, and far easier to remember.)
Short, very concise , the best! I'm very grateful huhu. Hope for more video lectures in the future. May God bless you, In Jesus' Name, Amen! Thank youuuuu
The liver has acetyl-CoA (from fatty acids, for example) which is its energy source and also what it uses to make ketone bodies. (In periphery, the ketone bodies are turned back into acetyl-CoA for energy). In essence, ketone bodies are a way of transporting acetyl-CoA from the liver to other cells. Since the liver has its own acetyl-CoA it doesn’t need ketone bodies and doesn’t express SCOT enzyme. Because the entry of acetyl-CoA into the TCA cycle is down-hill energetically, that’s what drives hydroxybutyrate -> acetoacetate.
Sir, if they starting material & end product of ketogenesis & ketolysis is “Acetyl CoA” then why we need this for! Can’t cells use that pre “Acetyl CoA” I wonder.
During a period of glucose depletion, Ketogenesis will take place in liver cells and majority of the ketone bodies that is produced from it are transported out and through the bloodstream to the brain....thats when it will go through ketolysis...the Acetyl CoA produced in ketolysis is used by the mitochondria of the brain cells to eventually produce ATP.
It seems some cells (like, and maybe only the brain) cannot accept fatty acids so they cannot simply break down fatty acids into acetyl CoA. The liver is also the only organ that can synthesize glucose from proteins and lactic acid. So the brain relies mostly entirely on glucose (blood sugar) supplied by the liver into the blood. Or in the case of low glucose levels, ketone bodies. But anyways... Acetyl CoA cannot be transported in the blood, period. Not just to the brain. So Acetyl CoA must first be converted to ketone bodies in the liver. (ketogenesis) Then cells accept this ketone body from tthe blood and break it down for energy (ketolysis). From my understanding, all cells seem to enjoy themselves on both blood sugar and ketone bodies even though the nervous system is the only body part that exclusively needs them. Edit: Also (and this is mainly my conjecture) LDLs are what transport fatty acids to cells. And in high amounts are known to cause heart diseases like heart attacks, I imagine ketogenesis is a evolutionarily safer way to transport fatty acids in mass to the blood. Maybe its how carnivores can survive high fat levels in their diet. hmmm.
I loved your video. I have one question though? How acetylCoA going to produce energy through TCA cycle when there is not enough OAA. Isn't that the reason why ketone bodies formed in the first place? Does anyone has an answer for this?
@@merinphilips5060do u mean that while during Beta oxidation the more amount of Acetyl CoA is not handled by TCA cycle bcoz in TCA cycle there are limited enzymes which occurs in mitochondria cell of liver ...so in that case the body adapted this mechanism for survival....while ketone bodies r made and is ultimately converted into acetyl COA during utlization(ketolysis) but in this case it goes to blood cell where the enzymes r in sufficient amount while it goes too peripheral tissues.......is this right?????
@@jakebarnett8837 So levels went from .13 to .29 (not significant) and the participants were likely fasted. Start = 0.131±0.177 30mins = 0.124±0.149 60mins = 0.296±0.375
@@jakebarnett8837 The abstract doesn't say that production increased _because_ of the exercise (ie, doesn't report a difference vs each subjects fasting increase and justify the specific difference measure used). How can you report to the public a finding like that without such a thing?
Hey man, great vids So i'm on the ketogenic diet, and was wondering whether you could try and explain why my ketone readings are getting lower as i progress in the diet. Is my body getting more efficient at burning ketones, or more adept at burning free fats for energy?
Burning free fatty acids for energy is a common cause of decreasing ketone levels in ketosis (many tissues, particularly skeletal muscle, adapt to utilizing to free fatty acids instead of ketone bodies after a few weeks of being in ketosis). Also, ketone levels can drop when there is not much gluconeogenesis going on. Yes, gluconeogenesis does increase blood ketone levels despite the fact that in increases blood glucose levels. When there is a lot of gluconeogenesis going on, oxaloacetate levels decrease (because it gets converted to phosphoenolpyruvate, which then enters the gluconeogenesis pathway), and when oxaloacetate levels are low, there ends up being a high acetyl-coa:oxaloacetate ratio. The excess acetyl-coa that does not need to enter the krebs cycle would then enter the ketogenesis pathway, and increase blood ketone levels. So from a nutritional standpoint, carbs obviously can decrease blood ketone levels (because when there is plenty of glucose in the blood from the carbs you eat, there is not a lot of gluconeogenesis going on, and therefore not a high acetyl coa:oxaloacetate ratio which is needed to produce ketone bodies). Also, too much protein also generally decreases blood ketone levels because dietary protein is insulinogenic, which obviously stimulates the secretion of insulin from the pancreas. Insulin inhibits gluconeogenesis (which then leads to a low acetyl-coa:oxaloacetate ratio) and beta-oxidation, (which inhibits fatty acids from being oxidized to yield acetyl-coa), so insulin inhibits ketogenesis.
1 acetoacetate produces 2 Acetyl-CoA molecules that enter the TCA cycle and produce 6 NADH, 2 FADH2 and 2GTP/ATP. NADH produces 3 ATP so 6 x 3 = 18 ATP, while FADH2 produces 2 ATP , so 2 x 2 = 4 ATP. In total we have 18 + 4 + 2 = 24 ATP. But the conversion of Acetoacetate to Acetoacetyl-CoA uses Succinyl-CoA which would normally be converted to Succinate in the TCA cycle with the production of 1 ATP. So the 2 Acetyl-CoA produce 24ATP but the ketogenesis prevent the formation of 1 ATP and 24ATP - 1ATP = 23ATP. Hope this is useful.
Your channel's the best for biochem stuff like this, man.
Clear, concise, helpful. Thank you. (The drawings of the two different ketone bodies could be standardized by showing the terminal -CH3 on the beta form and flipping it 90 degrees, so that the -CH3 groups are at the left ends in both figures. The remarkable similarity of the two molecules would then be easy to see, and far easier to remember.)
Excellent presentation! Thank you for sharing this information. It is invaluable for health.
Thousands time woow really perfect and clear explanations love your lecture
Your videos are extremely organized and detailed. Thank you so much
Excellent explanation - thank you so much!
Short, very concise , the best! I'm very grateful huhu. Hope for more video lectures in the future. May God bless you, In Jesus' Name, Amen! Thank youuuuu
These are amazing
Very helpful 🌸☀️
Hi and thanks for the video
Great course! Since the liver cannot use the ketone body produced by itself, what is the energy source for the liver in a keto diet? thanks!
Basically carbohydrates obtained from Gluconeogenesis pathway, by using glycerol (from triglycerides breakdown) and other hydrocarbon sources.
Yeah cause it lacks thiophorase
@@joselourencoscs Thanks！
The liver has acetyl-CoA (from fatty acids, for example) which is its energy source and also what it uses to make ketone bodies. (In periphery, the ketone bodies are turned back into acetyl-CoA for energy). In essence, ketone bodies are a way of transporting acetyl-CoA from the liver to other cells. Since the liver has its own acetyl-CoA it doesn’t need ketone bodies and doesn’t express SCOT enzyme. Because the entry of acetyl-CoA into the TCA cycle is down-hill energetically, that’s what drives hydroxybutyrate -> acetoacetate.
Your videos are great!
Thanx sir ,very informative video
Subscribed! What an excellent video!
Sir, if they starting material & end product of ketogenesis & ketolysis is “Acetyl CoA” then why we need this for! Can’t cells use that pre “Acetyl CoA” I wonder.
I have the same question
During a period of glucose depletion, Ketogenesis will take place in liver cells and majority of the ketone bodies that is produced from it are transported out and through the bloodstream to the brain....thats when it will go through ketolysis...the Acetyl CoA produced in ketolysis is used by the mitochondria of the brain cells to eventually produce ATP.
It seems some cells (like, and maybe only the brain) cannot accept fatty acids so they cannot simply break down fatty acids into acetyl CoA. The liver is also the only organ that can synthesize glucose from proteins and lactic acid. So the brain relies mostly entirely on glucose (blood sugar) supplied by the liver into the blood. Or in the case of low glucose levels, ketone bodies.
But anyways... Acetyl CoA cannot be transported in the blood, period. Not just to the brain. So Acetyl CoA must first be converted to ketone bodies in the liver. (ketogenesis) Then cells accept this ketone body from tthe blood and break it down for energy (ketolysis). From my understanding, all cells seem to enjoy themselves on both blood sugar and ketone bodies even though the nervous system is the only body part that exclusively needs them.
Edit: Also (and this is mainly my conjecture) LDLs are what transport fatty acids to cells. And in high amounts are known to cause heart diseases like heart attacks, I imagine ketogenesis is a evolutionarily safer way to transport fatty acids in mass to the blood. Maybe its how carnivores can survive high fat levels in their diet. hmmm.
Thanks doctor 😊
I loved your video. I have one question though? How acetylCoA going to produce energy through TCA cycle when there is not enough OAA. Isn't that the reason why ketone bodies formed in the first place? Does anyone has an answer for this?
Only in the liver is the oxaloacetate depleted / shunted into gluconeogenesis pathway,hence the TCA cycle can occur in all other cells.
@@merinphilips5060do u mean that while during Beta oxidation the more amount of Acetyl CoA is not handled by TCA cycle bcoz in TCA cycle there are limited enzymes which occurs in mitochondria cell of liver ...so in that case the body adapted this mechanism for survival....while ketone bodies r made and is ultimately converted into acetyl COA during utlization(ketolysis) but in this case it goes to blood cell where the enzymes r in sufficient amount while it goes too peripheral tissues.......is this right?????
EXCELLENT videos!!!
Quite well explained
Why we don't just use Acetyl CoA from the far beginning right after beta-oxidation?
thank you so much
can you cite your source for your statement that 90m of intense exercise increases the level of beta hydroxybuterate? thanks, Mike
Yeah, this is incorrect. Good catch.
www.ncbi.nlm.nih.gov/pubmed/24908238
@@jakebarnett8837
So levels went from .13 to .29 (not significant) and the participants were likely fasted.
Start = 0.131±0.177
30mins = 0.124±0.149
60mins = 0.296±0.375
@@jakebarnett8837 The abstract doesn't say that production increased _because_ of the exercise (ie, doesn't report a difference vs each subjects fasting increase and justify the specific difference measure used). How can you report to the public a finding like that without such a thing?
Could you do a video on reactionary Hypoglycemia?!
Hey man, great vids
So i'm on the ketogenic diet, and was wondering whether you could try and explain why my ketone readings are getting lower as i progress in the diet. Is my body getting more efficient at burning ketones, or more adept at burning free fats for energy?
Burning free fatty acids for energy is a common cause of decreasing ketone levels in ketosis (many tissues, particularly skeletal muscle, adapt to utilizing to free fatty acids instead of ketone bodies after a few weeks of being in ketosis). Also, ketone levels can drop when there is not much gluconeogenesis going on. Yes, gluconeogenesis does increase blood ketone levels despite the fact that in increases blood glucose levels. When there is a lot of gluconeogenesis going on, oxaloacetate levels decrease (because it gets converted to phosphoenolpyruvate, which then enters the gluconeogenesis pathway), and when oxaloacetate levels are low, there ends up being a high acetyl-coa:oxaloacetate ratio. The excess acetyl-coa that does not need to enter the krebs cycle would then enter the ketogenesis pathway, and increase blood ketone levels. So from a nutritional standpoint, carbs obviously can decrease blood ketone levels (because when there is plenty of glucose in the blood from the carbs you eat, there is not a lot of gluconeogenesis going on, and therefore not a high acetyl coa:oxaloacetate ratio which is needed to produce ketone bodies). Also, too much protein also generally decreases blood ketone levels because dietary protein is insulinogenic, which obviously stimulates the secretion of insulin from the pancreas. Insulin inhibits gluconeogenesis (which then leads to a low acetyl-coa:oxaloacetate ratio) and beta-oxidation, (which inhibits fatty acids from being oxidized to yield acetyl-coa), so insulin inhibits ketogenesis.
Thank you man, great answer! :)
Would it also make CO2 also during the TCA cycle?
Do these ketone catabolic processes happen in the cytosol or mitochondria?
Very goooooood
I want to know how much ATP is derived from glucose compared to ketones.
The best
Thanks for posting this. Can anyone answer how 1 acetoacetate makes 22-23 ATP?
1 acetoacetate produces 2 Acetyl-CoA molecules that enter the TCA cycle and produce 6 NADH, 2 FADH2 and 2GTP/ATP. NADH produces 3 ATP so 6 x 3 = 18 ATP, while FADH2 produces 2 ATP , so 2 x 2 = 4 ATP. In total we have 18 + 4 + 2 = 24 ATP. But the conversion of Acetoacetate to Acetoacetyl-CoA uses Succinyl-CoA which would normally be converted to Succinate in the TCA cycle with the production of 1 ATP. So the 2 Acetyl-CoA produce 24ATP but the ketogenesis prevent the formation of 1 ATP and 24ATP - 1ATP = 23ATP.
Hope this is useful.
Vey helpful !!! 👍 Thanks a lot...
So what do ketones do to your body?
from 8:00 onwards you mix up messages about single molecules with moles
Lol diabetes ad damn that TH-cam algorithm is good like scary good
Namste mem my self Roshni tagariya bpt program 1 year
thank you so much
فاتن العراقيه you know about ketones?