Thanks! I know this video is over 5 years old. But based on all the other sources I’ve encountered, it filled in all the gaps, all the missing pieces. Too little importance is placed on knowing where the organs are located and the physical transports between them. Most grateful, Armando Hasudungan.
this is where it all comes down to when it comes to revising for exam times...... I'd honestly prefere to watch all your videos regarding my revision rather than going through some nonsense lecture slides which I didnt even attend for. I appreciate your hard work and your knowledge that you're sharing with us for free.... you couldn't be better..... I hope I'd find some videos to do with my final year as well......... cheeeeeeeers and big thank you.
Insulin-dependent: GLUT 4- adipose tissue, striated muscle Insulin-independent: GLUT1- RBC, brain, cornea GLUT2- liver, beta-cells in the pancreas, kidney, small intestine GLUT3- Brain Ref: FIRST AID FOR THE USMLE STEP 1 2015
@@involuntarytwitch9771 yup sorry typo!. Glut 4 is the only Ins dependant for heart , skmuscle & adipose . Rest tissues Glucose move freely. However it's said that insulin somehow also has a fat sparing effect, don't know how exactly !
This video smartly includes the co-locations of the organs and related transports (vessels, ducts, organs). That made it easier for my brain to understand the processes and biochemical triggers. And lastly at 11:05 This final explanation uses a linear timeline to restate all of it step-by-step. Basically, the same information restated in several ways always helps to answer questions and gaps in my comprehension. Based on the resources I’ve read or listened to, this video seems to be accurate. It uses several teaching aids: concise wording first, visuals (organs, etc), top level general and specifics diagrammed and finally as an action-based timeline. Worth subscribing to.
Hats off the way you present the content man....🙏🙏...I'm medico from India...And I'm glad to have mentor like you sir... Keep uploading.... Lots of love from India🇮🇳...❤️
This video is PERFECT (apart from the dodgy Glut-2 translocation thing which doesn't happen because of insulin since liver tissue is non-insulin dependant) But we know what u mean since it does happen with GLUT 4 in muscle and adipose. Apart from that this is so helpful. I love your videos, thanks for sharing them with us!
me being a very slow learner i would take hours to understand little concepts but after your videos i have gained so much confidence in understanding critical concepts, thank you so much; may God Bless You.
FYI: Insulin upregulates GLUCOkinase, not HEXOkinase. Also, Insulin does not affect GLUT-2 in the liver and pancreas; GLUT-4 (in muscle and fat) is the only GLUT transporter that is insulin dependent.
Glucose uptake by liver is not insulin dependent. It's basically because of stimulation of hexokinase enzyme causing lack of intracytoplasmic glucose leading to facilitated diffusion of glucose via GLUT2 inside hepatocytes. Insulin doesn't play any role in increasing the GLUT2. Though it does increase GLUT 4 in adipose tissues, skeletal muscles and cardiac muscles.
little error: formation of prepro insulin as well as conversion of it to pro insulin by digestion of signal sequence by the help of enzyme endopeptidase ,both occurs in Endoplasmic reticulum only.then only it is budded of in the vesicle from the E.R. to reach golgi -apparatus,where again another endopeptidase separates c peptide from B-A segment(mature insulin)
moshtarakman Insulin binds to tyrosine-kinase receptors in the adipose and skeletal muscle because their glucose is insulin dependent. This stimulates IRS-1, then GLUT 4 release from vesicles into the membrane. You are right. The GLUT 2 receptors are located in the pancreatic beta cells, liver, kidney and small intestine. They are insulin independent. Therefore, binding of Insulin to tyrosine kinase is not necessary. From my understanding. The insulin independent glucose transporters, such as GLUT 2, GLUT 1, and GLUT 3 are always there and are not unregulated or down regulated. Correct me if I'm wrong.
MedEdCYP450 Correct. I wouldn't go as far as saying that the non-insulin dependent GLUT receptors (1,2, and 5) are not regulated - they probably are regulated (depending on pathology) but you are right in that they are not regulated by insulin. Just a recap in case anyone needed it When sugar is high (after a meal), glucose can bind to non-insulin GLUT receptors. When glucose binds to GLUT2 on the B-cells of the pancreas, it induces insulin secretion. Insulin's main role is to prevent hyperglycemia. The big tissues that can really uptake glucose are skeletal tissue and adipose tissue but they can only take up glucose if they have GLUT4 expressed - only insulin can accomplish this upregulation. So what happens? Insulin binds to skeletal and adipose tissue's tyrosine kinase receptor. This causes two things to happen. First, it upregulates GLUT4 onto those tissues to allow glucose enter (and thus prevent hyperglycemia). The second thing it does is within those cells, it increases glycogen, protein, and lipid synthesis - this makes sense because the insulin wants to use up all the glucose to prevent hyperglycemia and so glucose gets used up to drive fat, protein, and glycogen synthesis.
moshtarakman I would like to add to this conversation that GLUT2 has a low affinity for glucose, which means it will only be "stimulated" or rather "accept" glucose in high levels. This makes perfect sense when it comes to the pancreas. The GLUT2 will only be stimulated after a meal (when you have high glucose levels) and thus release insulin, but as soon as the glucose levels diminish it won't be stimulated anymore due to it's low affinity. This is (probably) the reason why insulin is not released at normal P-glucose levels. EDIT: To clarify, GLUT1 and GLUT3 does NOT have a low affinity for glucose, they work just as well as GLUT4 but are insulin independent. Correct me if I'm wrong.
Insulin stimulates glucokinase (not hexokinase) to create glucose-6-phosphate in the liver. Hexokinase is found in most tissues other than the liver and pancreatic beta cells. Correct?
Glucokinase is in the liver which phosphorylates glucose to G6P. In other tissues, such as adipose and muscles, it's hexokinase which phosphorylates glucose to G6P. So essentially yeah, you got it :)
No words for your excellence You are making a topic very interesting and informative. I think I can pass my exams without reading whole the year but only watching ur videos on last night before exams 😁😀 Thank uhhhhh😘
A small point, but i believe the tyrosine kinase autophosphorylation occurs when the receptor is activated by insulin. It just seems like you suggest that they are always phosphorylated rather than when activated. Otherwise great video :D
I may be wrong but I think GLUT2, whilst mainly being expressed in the liver, is not insulin responsive in the way you described. GLUT2 channels have a high Km and so work with glucokinase in the liver to "sense" glucose levels (I think :P), but I don't think they respond to insulin...
Hi Armando. i really appreciate your videos. You are doing a fantastic job. Maybe you should explain the difference between GLUT2 transporters (insulin independant) and GLUT4 (insulin dependant).
You can use Ambrosia Blucon with Libre sensor and check your glucose values on your watch without even your phone in every 5 minutes. I check glucose values on my watch when my phone is not with me.
yeah ur right, liver uses GLUT 2 which is non-insulin dependant. but insulin does everything in this guys explanation in the liver but the translocation bit. The translocation thing happens in adipose and muscle though as they use GLUT 4 :)
Isn't it glucokinase that is activated by insulin?Also was going to comment on GLUT4 being the transporter that is insulin dependent in muscle and adipose tissue. GLUT 2 is in the liver but not insulin dependent for anyone watching currently.
I did not know that insulin stimulated the uptake of glucose to liver? I thought that insulin just stimulated the uptake of glucose via GLUT 4, and not GLUT 2 (in liver) :)
GLUT4 is in the muscle and adipose tissues, so a low insulin level would trigger the translocation of GLUT4 from vesicles intracellularly, to the cell membrane. The GLUT4 then fuse to the membrane and allow a rapid increase of glucose uptake into the cell. GLUT2 is associated with the liver
Super video thanks.What happened if stomack produce massive acidity? How is effective to pancreas the cells and insulin in for example as protein? s-s connection? ph in this area? Thanks
Very informative. Thanks for sharing this and now I will share with people that don't think type 1 diabetes is a very serious disease. I'm hoping there is a cure someday even if it's not in my lifetime but just so so many people don't have to suffer anymore. Also hoping for a cure for type 2 diabetes both diseases are so terrible and lead to all kind of other diseases.
Hi, nice video.. But I learned, that the GLUT2 is insulin INDEPENDENT, and that just the GLUT4 is put in the membran of muscles by an insulin signal...
There is some complex mechanism involving internalization and regeneration of insulin receptor. I thought you have explained that too, but you have not explained it. :(
QUESTION: In the absence of blood glucose while in a state of ketosis (where glycogen stores in the liver and skeletal muscles are depleted), will the insulin increase caused by PROTEIN result in protein being shuttled into cells as fat, in which case what is the process by which this protein would be converted into fat?
Thanks! I know this video is over 5 years old. But based on all the other sources I’ve encountered, it filled in all the gaps, all the missing pieces. Too little importance is placed on knowing where the organs are located and the physical transports between them. Most grateful, Armando Hasudungan.
this is where it all comes down to when it comes to revising for exam times...... I'd honestly prefere to watch all your videos regarding my revision rather than going through some nonsense lecture slides which I didnt even attend for. I appreciate your hard work and your knowledge that you're sharing with us for free.... you couldn't be better..... I hope I'd find some videos to do with my final year as well......... cheeeeeeeers and big thank you.
You sometimes make me think that I can learn more on youtube than at school. And I don't even pay gas to get to youtube...
you pay internet bills
Obviously... Most of your teachers are bored and often quite dumb...
@@nayomayo603 internet bills! Lol! Who cares about 3$-5$
Also, a teacher can hardly draw a circle nicely, not to mention this kind of graphics!
8 years later your work is still helping all of us so much. You're a gem. God bless you.
Insulin-dependent:
GLUT 4- adipose tissue, striated muscle
Insulin-independent:
GLUT1- RBC, brain, cornea
GLUT2- liver, beta-cells in the pancreas, kidney, small intestine
GLUT3- Brain
Ref: FIRST AID FOR THE USMLE STEP 1 2015
יעל רובה thankyou!
GLuT 4 is the only one which is Independent of Insulin..allows free movement of Glucose.
Isn't this backward? Glut-4 is insulin INDEPENDENT, whilst the others are all dependent?
@@involuntarytwitch9771 yup sorry typo!. Glut 4 is the only Ins dependant for heart , skmuscle & adipose . Rest tissues Glucose move freely. However it's said that insulin somehow also has a fat sparing effect, don't know how exactly !
Beta cells in the pancreas have actually GLUT1. GLUT2 is only in mice and rats and not in humans.
You just saved my 5 hours studying physiology and biochemistry thanks!!!
You are an excellent teacher. Thank you for the class.
you are a hero. thank you so much. i've never thought learning medicine would be easy
This video smartly includes the co-locations of the organs and related transports (vessels, ducts, organs). That made it easier for my brain to understand the processes and biochemical triggers. And lastly at 11:05 This final explanation uses a linear timeline to restate all of it step-by-step. Basically, the same information restated in several ways always helps to answer questions and gaps in my comprehension.
Based on the resources I’ve read or listened to, this video seems to be accurate. It uses several teaching aids: concise wording first, visuals (organs, etc), top level general and specifics diagrammed and finally as an action-based timeline.
Worth subscribing to.
Hats off the way you present the content man....🙏🙏...I'm medico from India...And I'm glad to have mentor like you sir...
Keep uploading....
Lots of love from India🇮🇳...❤️
GREAT work! I've been glued to textbooks and lecture notes trying to sort out everything involved with CHO metabolism, and this video was SO helpful!
This video is PERFECT (apart from the dodgy Glut-2 translocation thing which doesn't happen because of insulin since liver tissue is non-insulin dependant) But we know what u mean since it does happen with GLUT 4 in muscle and adipose. Apart from that this is so helpful. I love your videos, thanks for sharing them with us!
me being a very slow learner i would take hours to understand little concepts but after your videos i have gained so much confidence in understanding critical concepts, thank you so much; may God Bless You.
I used to drop out when it gets too detailed, but these vids are a really helpful quick overview and keep me going (: Thank you!
I just really want to thank you for the clear and informative video. You are making medical school easy for me.
You never stop getting surprised about Armando's pedagogic skills !!!!!!!!!!!
Super
this video is so helpful! finally putting the big picture of all the metabolic pathways/ regulations
FYI: Insulin upregulates GLUCOkinase, not HEXOkinase. Also, Insulin does not affect GLUT-2 in the liver and pancreas; GLUT-4 (in muscle and fat) is the only GLUT transporter that is insulin dependent.
it changes a lot , for better of course , than the woman with no degree teaching endocrinology at my university ! Thanks a lot
I have my exam next month and these videos are surely gonna help me! Thank you for making these topics fun to understand!!!
Thanks so much I am french and for me your video are the best one and the easiest to understand to learn biology in english;
Glucose uptake by liver is not insulin dependent. It's basically because of stimulation of hexokinase enzyme causing lack of intracytoplasmic glucose leading to facilitated diffusion of glucose via GLUT2 inside hepatocytes. Insulin doesn't play any role in increasing the GLUT2. Though it does increase GLUT 4 in adipose tissues, skeletal muscles and cardiac muscles.
Super! you help me understand deeply the mechanism of action which I thought I'd already known
saving me hours of reading books and not understanding Mr. Hasudungan. Cheers!
it really do helps me in understanding more about insulin mechanism of action. thanks a lot!!
little error: formation of prepro insulin as well as conversion of it to pro insulin by digestion of signal sequence by the help of enzyme endopeptidase ,both occurs in Endoplasmic reticulum only.then only it is budded of in the vesicle from the E.R. to reach golgi -apparatus,where again another endopeptidase separates c peptide from B-A segment(mature insulin)
Yupp!
Insulin DOES NOT stimulate GLUT2 receptors - only GLUT4.
moshtarakman Insulin binds to tyrosine-kinase receptors in the adipose and skeletal muscle because their glucose is insulin dependent. This stimulates IRS-1, then GLUT 4 release from vesicles into the membrane.
You are right. The GLUT 2 receptors are located in the pancreatic beta cells, liver, kidney and small intestine. They are insulin independent. Therefore, binding of Insulin to tyrosine kinase is not necessary. From my understanding. The insulin independent glucose transporters, such as GLUT 2, GLUT 1, and GLUT 3 are always there and are not unregulated or down regulated. Correct me if I'm wrong.
MedEdCYP450 Correct. I wouldn't go as far as saying that the non-insulin dependent GLUT receptors (1,2, and 5) are not regulated - they probably are regulated (depending on pathology) but you are right in that they are not regulated by insulin. Just a recap in case anyone needed it
When sugar is high (after a meal), glucose can bind to non-insulin GLUT receptors. When glucose binds to GLUT2 on the B-cells of the pancreas, it induces insulin secretion. Insulin's main role is to prevent hyperglycemia. The big tissues that can really uptake glucose are skeletal tissue and adipose tissue but they can only take up glucose if they have GLUT4 expressed - only insulin can accomplish this upregulation. So what happens?
Insulin binds to skeletal and adipose tissue's tyrosine kinase receptor. This causes two things to happen. First, it upregulates GLUT4 onto those tissues to allow glucose enter (and thus prevent hyperglycemia). The second thing it does is within those cells, it increases glycogen, protein, and lipid synthesis - this makes sense because the insulin wants to use up all the glucose to prevent hyperglycemia and so glucose gets used up to drive fat, protein, and glycogen synthesis.
moshtarakman I would like to add to this conversation that GLUT2 has a low affinity for glucose, which means it will only be "stimulated" or rather "accept" glucose in high levels. This makes perfect sense when it comes to the pancreas. The GLUT2 will only be stimulated after a meal (when you have high glucose levels) and thus release insulin, but as soon as the glucose levels diminish it won't be stimulated anymore due to it's low affinity.
This is (probably) the reason why insulin is not released at normal P-glucose levels.
EDIT: To clarify, GLUT1 and GLUT3 does NOT have a low affinity for glucose, they work just as well as GLUT4 but are insulin independent. Correct me if I'm wrong.
+salmjak your comment is Sooooo quite thanks I really enjoyed
moshtarakman yeah u r ri8
Thank you,Your videos are the assets for the medical student as they are excellent and free!
Insulin stimulates glucokinase (not hexokinase) to create glucose-6-phosphate in the liver. Hexokinase is found in most tissues other than the liver and pancreatic beta cells. Correct?
Glucokinase is in the liver which phosphorylates glucose to G6P. In other tissues, such as adipose and muscles, it's hexokinase which phosphorylates glucose to G6P.
So essentially yeah, you got it :)
Its not very complicated.....glucose is a hexose sugar....and thus hexokinase or glucokinase are terms used interchangeably
Well presented and clear, making understanding easy. Excellent.
No words for your excellence
You are making a topic very interesting and informative.
I think I can pass my exams without reading whole the year but only watching ur videos on last night before exams 😁😀
Thank uhhhhh😘
Thank You so very much... You have no Idea how much I appreciate this video
Best explanation so far.. Thankyou So Much
Great way to understand the role of insulin. I have type 1 diabetes so good to know in so much detail.
Thanks alot 👍
Lots of support and love from Pakistan
May God bless you:"(!!! U always save me with ur very very very very useful vedios Thaaaank youuuu
You have helped me alot thank you so much !!! You’re videos are amazing as well as your drawings and your explanation.. thank you from my heart
finally understood the insulin receptor functions... genial artist!!!
A small point, but i believe the tyrosine kinase autophosphorylation occurs when the receptor is activated by insulin. It just seems like you suggest that they are always phosphorylated rather than when activated. Otherwise great video :D
autophosphosphorylation does not means that the tyr kinase is always phosphorylated!
but the rest is great ! ty
i'm just in love with the scientific artist you are.
I may be wrong but I think GLUT2, whilst mainly being expressed in the liver, is not insulin responsive in the way you described. GLUT2 channels have a high Km and so work with glucokinase in the liver to "sense" glucose levels (I think :P), but I don't think they respond to insulin...
I love how i can draw these illustrated diagrams along with the theory explained. Thanks for the help.
Cannot get any better ,, truly magnificent
You are great !! Thank you very much , we even watch your videos from the other side of the world. From saudi arabia ❤️❤️❤️
Excellent work. Very professional and accurate.
very2 contributive, made our revision so much effective and easy, thanks a million sir
that is amazing ... when i do not understand any thing ,u help a lot ... thanks
No. THANK YOU! Subscribed to this AMAZING CHANNEL. I hope you get all the support!
Thanks for your useful video. One remark: GLUT2 (of liver) is insulin-Independent!
Hi Armando. i really appreciate your videos. You are doing a fantastic job. Maybe you should explain the difference between GLUT2 transporters (insulin independant) and GLUT4 (insulin dependant).
Glucose uptake by the liver is actually not insulin-dependent...
Armando u make amazing videos..it has helped me in my entire medicine course. 💙💛💙💛💙💕♥✔
You can use Ambrosia Blucon with Libre sensor and check your glucose values on your watch without even your phone in every 5 minutes. I check glucose values on my watch when my phone is not with me.
Disulphide bonds in A chain too.
Great as always. I passed immunology with your videos and got A this summer. Thank you ❤️
very well explained kindly also make a video on its pharmacolgy
yeah ur right, liver uses GLUT 2 which is non-insulin dependant. but insulin does everything in this guys explanation in the liver but the translocation bit. The translocation thing happens in adipose and muscle though as they use GLUT 4 :)
Isn't it glucokinase that is activated by insulin?Also was going to comment on GLUT4 being the transporter that is insulin dependent in muscle and adipose tissue. GLUT 2 is in the liver but not insulin dependent for anyone watching currently.
well done I like the way you share with us! Can you write clearly the words next time, may be bigger size
Brilliant video, thank you. Question is insulin necessary to synthese protein for muscles?
You are totally amazing
I did not know that insulin stimulated the uptake of glucose to liver? I thought that insulin just stimulated the uptake of glucose via GLUT 4, and not GLUT 2 (in liver) :)
GLUT4 is in the muscle and adipose tissues, so a low insulin level would trigger the translocation of GLUT4 from vesicles intracellularly, to the cell membrane. The GLUT4 then fuse to the membrane and allow a rapid increase of glucose uptake into the cell.
GLUT2 is associated with the liver
You are the best
2022 still your videos are useful
Tnx🇦🇫😍🙏
fantastic! youre helping me with my exam!
Watching this at x2. I have an exam this morning and I'm going to ace it🔥
How do complex carbohydrates with little to no simple carbohydrates affect insulin production and use by cells?
outstanding work
Very helpful , thank you so much
Thank you very much ❤️
You are the best explainer
very good video ,thanks
Very well done explanation. I learn a lot.
The explanation is excellent, greeting from Mexico :)
This is very awesome 👌.
Good stuff, thank you Sir!
Thank you!
amazing map and vids, you rock man
Super video thanks.What happened if stomack produce massive acidity? How is effective to pancreas the cells and insulin in for example as protein? s-s connection? ph in this area? Thanks
Love your videos. Saved my ass in exams time and time again.
And this is how I avoid getting up early in order to attend pointless lectures of 1 hour at the university. 10 min youtube videos is the way to go XD
Very informative. Thanks for sharing this and now I will share with people that don't think type 1 diabetes is a very serious disease. I'm hoping there is a cure someday even if it's not in my lifetime but just so so many people don't have to suffer anymore. Also hoping for a cure for type 2 diabetes both diseases are so terrible and lead to all kind of other diseases.
Thank you so much
You are just love sir❤️
isn't GLUT 2 insulin independent? - idk i maybe wrong but thanks the videos are great overall
great video..but i think insulin has no effect on hexokinase....it is glucokinase that is under the influence of insulin
Amazing videos, thanks a lot!
thank you ..........
love you videos but a little too fast... suggestion slow down just a bit with the fast writing and voice overs
Thanks again for posting
Hi, nice video..
But I learned, that the GLUT2 is insulin INDEPENDENT, and that just the GLUT4 is put in the membran of muscles by an insulin signal...
informative one thanks a lot &great job
There is some complex mechanism involving internalization and regeneration of insulin receptor. I thought you have explained that too, but you have not explained it.
:(
nicely explained. thank you very much for this.
QUESTION: In the absence of blood glucose while in a state of ketosis (where glycogen stores in the liver and skeletal muscles are depleted), will the insulin increase caused by PROTEIN result in protein being shuttled into cells as fat, in which case what is the process by which this protein would be converted into fat?
You are amazing
but liver doesnt hve GLUT4, instead it contains only GLUT2.
you r providing good understanding videos but please do little corrections in this video
Excellent
Thank you some much.. you're a great guy !!
thank you ❤
Kindly share the videos on detailed anatomy.