Maam, If insulin n thyroxine increase the synthesis of cholesterol then how come in hypothyroidism sr. cholesterol level Increases and similarly in case of diabetes Sr. Cholesterol increases
Thyroid hormone has both actions 1. Increases activity of HMG CoA reductase..leads to increase cholesterol synthesis 2.Increases LDL receptors' activity resulting in increased catabolism of LDL and IDL... leading to decrease cholesterol Both actions are opposite to each other.Second action outweighs first one. Hence, in hypothyroidism due to decreased LDL receptors'activity... decreased clearance of LDL and IDL leads to hypercholesterolemia.(Second action dominates)
Mam in case of starvation or diabetes when insulin is either not produced (typeI) or receptors are non functional (type II)---(hence glucose uptake by cell is prevented in both),so glucagon is released for getting energy from non carbohydrate source like lipolysis where fatty acids are fed into Beta oxidation to produce energy (also help in supressing malonyl CoA to dilute its effect on carnitune shuttle's carnitine transferase I) ...this increase acetyl coA which through kreb cycle produce ATP.... But in this way we can say glucagon cause increase in Acetyl CoA pool,which will cause ketogenesis (as gluconeogenesis as side rxn decrease oxaloacetate level via malate shuttle ). But if cholesterol is low ,this will cause release of SREBP-SCAP release from SER as insig protein will no further be a hindrance--> then proteolytic cleavage in golgi finally in nucleus where interaction with Sterol regulatory element cause transcription of mRNA and translation of HMG -CoA reductase..which is rate limiting enzyme of cholesterol synthesis...so we can say increase glucagon is stimulating cholesterol synthesis....*but on the other hand in the topic of sterol independent covalent modification and hormonal regulation,glucagon is causing phosphorylation of HMG-CoA reducatse (causing its inactivation) which means decrease cholesterol synthesis*... Isn't in contradictory! What actually glucagon want to do... In diabetes cholesterol should be increase by the effect of glucagon as described earlier or should be inhibited as describe later.. Mam bht confusion ho rhi is me... And if in case of diabetes mellitus II insulin is produced but cells are insulin resistant then this released amount lf insulin should increase malonyl CoA,thereby blocking carnitine shuttle as its inhibitory effect.so from where did body get energy in this case as neither beta oxidation will take place to yield 131 ATP nor the ketogenic products will yield their respective 21 ATP in case of beta hydroxybutyrate or 19 ATP in case of acetoacetate ,🚨🚨🚨🚨
@@NJOYBiochemistry so,mam,the patient need not be diabetic to have high cholesterol level as hyperinsulinemia occurs due to Insulin Resistance much before clinical Diabetes takes place.
Cholesterol has important roles and it is formed mainly endogenously.Statins blocks endogenous cholesterol formation by inhibition of HMG CoA Reductase,a rate limiting enzymes.Then how these important and useful functions will be performed during Statin therapy especially when exogenous cholesterol intake is also curtailed (which is done usually)?
Gooday ma Thanks for the video Pls how many ATL is been generated in a roll of glucose metabolism???? What are the important event of the glycolytic pathway??? Thank you so much Am waiting for answers
Mam in Rafi textbook of biochemistry it is given that '36 moles of ATP for synthesis of a mole ofcholesterol' how it is needed? Would you please explain.
Detailed explanation for energy cost of 36 ATP is not given in any standard textbook. 1.Formation of 6 Isoprenoid units require 18 ATP 2.Formation of squalene from Six Isoprenoid units is complex reaction involving many steps.During the formation of squalene, pyrophosphate molecules (PPi) are released which are further cleaved to two phosphates each. Pyrophosphate cleavage ensures irreversibility of these complex reactions. Release of energy by pyrophosphate cleavage drives reaction further. This process is energy requiring. Remaining 18 ATP might be required for this.( This is logical explaination.Its not mentioned in any textbook) If anyone has exact explaination for the use of 36 ATP, Please comment.
Ma'am you're amazing😩... Your biochemistry series r engaging and mind-blowing.... We love you so very much♥️..
Thank you so much🙂
mam please mam please it's a request please increase the frequency of lecture.because we r really dpnd upon u mam for biochem
Thank you for your love and appreciation. I shall do my best to provide good content ❤
Mam , need a class on AMPK_Master metabolic regulator...
Maam plz do more videos.. Ur videos are nice
Thank you ❤️
Maam, If insulin n thyroxine increase the synthesis of cholesterol then how come in hypothyroidism sr. cholesterol level Increases and similarly in case of diabetes Sr. Cholesterol increases
Thyroid hormone has both actions
1. Increases activity of HMG CoA reductase..leads to increase cholesterol synthesis
2.Increases LDL receptors' activity resulting in increased catabolism of LDL and IDL... leading to decrease cholesterol
Both actions are opposite to each other.Second action outweighs first one.
Hence, in hypothyroidism due to decreased LDL receptors'activity... decreased clearance of LDL and IDL leads to hypercholesterolemia.(Second action dominates)
In diabetes mellitus due to insulin resistance, insulin present in circulation activates HMG CoA reductase leading to increased cholesterol level.
Mam in case of starvation or diabetes when insulin is either not produced (typeI) or receptors are non functional (type II)---(hence glucose uptake by cell is prevented in both),so glucagon is released for getting energy from non carbohydrate source like lipolysis where fatty acids are fed into Beta oxidation to produce energy (also help in supressing malonyl CoA to dilute its effect on carnitune shuttle's carnitine transferase I) ...this increase acetyl coA which through kreb cycle produce ATP....
But in this way we can say glucagon cause increase in Acetyl CoA pool,which will cause ketogenesis (as gluconeogenesis as side rxn decrease oxaloacetate level via malate shuttle ).
But if cholesterol is low ,this will cause release of SREBP-SCAP release from SER as insig protein will no further be a hindrance--> then proteolytic cleavage in golgi finally in nucleus where interaction with Sterol regulatory element cause transcription of mRNA and translation of HMG -CoA reductase..which is rate limiting enzyme of cholesterol synthesis...so we can say increase glucagon is stimulating cholesterol synthesis....*but on the other hand in the topic of sterol independent covalent modification and hormonal regulation,glucagon is causing phosphorylation of HMG-CoA reducatse (causing its inactivation) which means decrease cholesterol synthesis*...
Isn't in contradictory!
What actually glucagon want to do...
In diabetes cholesterol should be increase by the effect of glucagon as described earlier or should be inhibited as describe later..
Mam bht confusion ho rhi is me...
And if in case of diabetes mellitus II insulin is produced but cells are insulin resistant then this released amount lf insulin should increase malonyl CoA,thereby blocking carnitine shuttle as its inhibitory effect.so from where did body get energy in this case as neither beta oxidation will take place to yield 131 ATP nor the ketogenic products will yield their respective 21 ATP in case of beta hydroxybutyrate or 19 ATP in case of acetoacetate ,🚨🚨🚨🚨
@@NJOYBiochemistry so,mam,the patient need not be diabetic to have high cholesterol level as hyperinsulinemia occurs due to Insulin Resistance much before clinical Diabetes takes place.
Great video mam a new drug Bempedoic Acid is used to lower cholesterol. It would be nice if you can incorporate it in this lecture.
Thank you
Bilkul b acha nahii parhati app..
Mjha bilkul b samaj nahi i😭😭💔💔
Cholesterol has important roles and it is formed mainly endogenously.Statins blocks endogenous cholesterol formation by inhibition of HMG CoA Reductase,a rate limiting enzymes.Then how these important and useful functions will be performed during Statin therapy especially when exogenous cholesterol intake is also curtailed (which is done usually)?
Mam do you use Lippincott as a reference or satyanarayana ?
For metabolism _ Lippincott
You inspired me with your lecture
Gooday ma
Thanks for the video
Pls how many ATL is been generated in a roll of glucose metabolism????
What are the important event of the glycolytic pathway???
Thank you so much
Am waiting for answers
Video on glycolysis
th-cam.com/video/cQUJSFYE6kI/w-d-xo.html
NYC video
Thank you 😊
thank you so much ma'am , the video is very useful😇🙏
Welcome dear ❤️
exceptional❤
Thank you 😊
❤
God bless you thank you so much all love from ethiopa
Thank you❤
Amazing
Thank you
Mam in Rafi textbook of biochemistry it is given that '36 moles of ATP for synthesis of a mole ofcholesterol' how it is needed? Would you please explain.
Detailed explanation for energy cost of 36 ATP is not given in any standard textbook.
1.Formation of 6 Isoprenoid units require 18 ATP
2.Formation of squalene from Six Isoprenoid units is complex reaction involving many steps.During the formation of squalene, pyrophosphate molecules (PPi) are released which are further cleaved to two phosphates each. Pyrophosphate cleavage ensures irreversibility of these complex reactions. Release of energy by pyrophosphate cleavage drives reaction further.
This process is energy requiring.
Remaining 18 ATP might be required for this.( This is logical explaination.Its not mentioned in any textbook)
If anyone has exact explaination for the use of 36 ATP, Please comment.