Love this video? Check out our new A&P course, with more than 80 videos like this (no watermark, no ads), over 40 PDFs and hundreds of images: For student: www.alilaacademy.com/courses/anatomy-and-physiology-for-students For teachers: www.alilaacademy.com/courses/anatomy-and-physiology-for-teachers NEW: Now you can also get access to our courses with our RUclips channel membership (Academy Access levels)
It should be mentioned too, that LDL is not a cholesterol at all, but a cholesterol "transporter". We just call it LDL "cholesterol" for convenience but, it's not really correct.
it is said in the beggining of the video, that cholesterol is transported in lipoprotein particles and she talks about “low density lipoprotein - LDL” and not LDL cholesterol
@@michaell132 Yeah, I've always hated that term "bad" cholesterol. No such thing as bad cholesterol, just two different kinds of cholesterol. LDL is not necessarily "bad". I much prefer the more descriptive term of "small dense particles" and large. The large ones are harmless and just bounce around in the bloodstrream. Those small ones though, are the bad ones that lodge on artery walls, Atherosclerosis.
The BEST explanation. All you gotta do is brush up on some notes if you haven't already and you're good. Or can also serve as a wonderful review to put everything together. Amazing!
Learning this a while back is what made me want to limit/stop my intake of animal products. Over time, i have now been vegan for a good few years. No bad cholesterol in my diet 🙏
Hi, just wondering what your thoughts are on the different types of LDL - pattern A and pattern B which are increased in different diets? Also, thank you simplifying all these processes. Very helpful.
@MrBilld75 Agreed. I'm glad to see more people are catching up on that distinction. It is important to note that unbiased evidence indicates that LDL is "associative" in atherosclerotic plaque formation as opposed to being "causative". There's a huge difference between the two particularly with regard to prevention and treatment. We are still looking into this but the current evidence indicates that LDL can get damaged by glycation, oxidation and inflammation as a result of too much sugar/refined carbs intake, plant sterols (yes..in spite of the fact that it's ironically used to lower supposedly "bad" cholesterol) and a state of systemic inflammation (from the progression of insulin resistance for e.g.). I'm on the train right now so I can't type much...I'll try and elaborate on this another time. Damaged LDL are mostly of type B (dense). For example, one mechanism causing issues is the fact that the apoprotein B100 on LDL get damaged enough so that they can't be recognised and reabsorbed by the liver receptors for recycling. So they end up pooling in the circulation hence promoting adhesion to the vascular endothelium. Inflammation also makes the endothelium prone to that phenomenon. LDL is also a repair molecule so it will also migrate (by transcytosis using ATP) to sites of inflammation in an attempt to repair thus further exacerbating plaque formation over time as this process is repeated. Macrophages also try to engulf those inflammatory LDL complex resulting in foam cells and this also triggers more cytokines release (pro inflammatory). So you can see how this cascade can result in more plaque formation over time. Too long to elaborate on but hope that quick summary helps.
@@junemercado Cholesterol does not just float around freely in your bloodstream. Cholesterol is like a fat and your blood is like water. And we know fat and water don't mix. Therefore, the cholesterol we typically learn about in our blood work (i.e. LDL-C, HDL) is carried within LDL particles that transport cholesterol throughout your body. In simple terms, there are two types of particles, small dense particles and large buoyant particles. Many experts now believe it is the nature of the particles, not the cholesterol they are carrying, that really matters when it comes to things like heart disease. The particles themselves can be measured with advanced lipoprotein testing, typically NMR (nuclear magnetic resonance) testing. It sounds intimidating but can be done via a routine blood test that is sent to labs to do this sort of testing (which are becoming more commonplace as time goes on). Most often the particle numbers are reported in nmol/L (nanomoles per liter). Optimally, you want results showing a total LDL particle number of about 1000 nmol/L or less. And you want your small (dense) particle number to be 200 nmol/L or less (optimally). The large buoyant portion, which your NMR result will also provide, is not the number to focus on according to some experts, as they are not atherogenic. But the small dense particles (so the theory goes) can get into the endothelium of your coronary arteries and contribute to the heart disease process. Why is that? Well, large LDL particles have a relatively short time duration, say 24 hours, and are "dispensed" with fairly quickly, but small LDL particles are not easily recognized by the liver and hence float around in your circulation much longer (e.g. a week or so) giving them more time to do their damage. You can appreciate therefore why standard cholesterol measurements (like LDL-C) never seem to correlate well to the occurrence of heart disease. Cardiologist Dr. Stephen Sinatra, who operated on thousands of patients and actually saw their arteries with his own eyes, used to say many patients with very high LDL-C would have beautiful, pristine arteries, yet many with low LDL-C had prolific heart disease. We now know the nature of LDL particles can be very much in our control by lifestyle and diet. Diets high in carbohydrates, wheat, grains, sugar etc. provoke the occurrence of abundant, dangerous small LDL particles. But low-carb diets (even if high in fat), support metabolic health and most often will result in a healthy small LDL particle sub-fraction (along with increased HDL by the way), thereby lowering your cardiovascular disease risk. To sum up, heart disease is a metabolic disease. Cholesterol is not the problem. And the sooner less attention is paid to cholesterol and the focus gets changed to metabolic health, the sooner we will see some progress in reducing heart disease. C'mon, we've been doing it wrong for 50 years. Let's change the paradigm now so we can start making strides.
@@Malcolm-Achtman Beautifully explained!! A lot of useful information can be gained from videos from Ivor Cummins on this subject. As you explained, LDL in itself is not bad, and high values of measured LDL are not dangerous. The problem arises when these LDL particles become "coated" with "sugary" molecules or oxidized. This changes the appearance of LDL and it is not recognized by special receptors on the liver that control the re-absorption of LDL. It remains floating in the blood for extended periods, causing the discussed health issues. Metabolic disease is caused by sugar- and refined carb loaded products as you explained. Also vegetable or seed oils are abundantly used in the food industry, because very cheap. Think of canola, cottonseed, sunflower, safflouer, soy, peanut and other oils and margerines. These products are highly processed and have nothing in common with the seeds they were taken from. The oils are easily oxidized inside and outside the body (compare this with a sliced apple, parts are browning fast when exposed to air). This oxidized oil leads to chronic low grade inflation in the body and changing the surface of LDL particles, after which they are not recognized by the liver for reuptake. The often demonized natural occurring saturated oils and fats have absolutely no impact on health. They contain no unsaturated (double) carbon-carbon bonds and are more or less inert to oxygen on body temperature. Also in the kitchen their smoke point is high. Unsaturated fatty acids like the omega varieties (e.g. in fatty fish) are heart healthy. It is best to consume fish, as capsules with oil are more easily oxidized.
@@TheVafa95 If you obtain a routine lipid panel it will include your triglyceride and HDL values. A crude but potentially good way to establish your metabolic health would be to calculate your triglyceride/HDL ratio. Ideally, that ratio should be 1.5 or less. For example, if your trigs were 70 mg/dL and your HDL was 55 mg/dL, the ratio would be 70/55 = 1.27. That's pretty good. Another key blood test to get is fasting insulin. Also get fasting glucose. So, be sure to fast for about 12 hours before getting these tests. You can drink water, but no juice or coffee or food. A very good fasting insulin result would be about 3 uIU/mL. A good fasting glucose result would be 80 - 90 mg/dL. Try to get HbA1c tested as well. An optimal value is 5.0% or close to that.
Right. Here is a Wikipedia article on lacteals that better describes the route taken by chylomicrons: en.m.wikipedia.org/wiki/Lacteal Chylomicrons actually travel through the lymphatic system first before being released into the bloodstream at the thoracic ducts for transit back to the liver. While traveling back to the liver, some triglycerides are removed from the chylomicrons thereby creating a more dense chylomicron remnant that contains a higher concentration of lipoprotein. This remnant is what actually gets reabsorbed into the liver. More triglycerides are then added to this denser structure to form VLDL.
Very good. It would be even more helpful if intracellular processing of LDL cholesterol was included. One point would be to explain how cholesterol is exported from lysosomes. How many pathways are there? One pathway is via the lysosomal membrane protein NPC1 that allows transport of cholesterol to the ER facilitating homeostasis . Defects in this pathwat result in Niemann-Pick type C disease, a severe and fatal condition.
At 1:40 the video states that chylomicrons go from the gut via blood to the liver. They do not. They are secreted by the intestinal cells into the lymphatic system, and drain via the thoracic duct into the venous circulation at the junction of the left subclavian and internal jugular veins, at the commencement of the brachiocephalic vein.
So now they are in the bloodstream and will go to the liver, right? We just skipped the details you mentioned to focus on the MAJOR steps of cholesterol metabolism. Sorry if the video gave the impression that they go directly from the intestine to the liver, they do not, but those steps are not essential for the scope of this video.
LDL transports cholesterol which all cells if the body need, without it you would die. Therefore why is it “bad”. If it’s “bad” why did we evolve to have it in the first place? Also she said it’s associated with strokes and heart attacks. Is association causation or is there another mechanism at work and LDL gets the blame?
I'm experienced now high cholesterol is problem exist more than 20 from normal range, i am taking drug for this, as well as drugs for my hyperthyroidism, and high blood. And even my doctor tell me i have a liver problem too. I'm 38 yrs old heavy drunker before i diagnosed this problem, i completely stop drinking alcohol 6 months ago, i started exercise work today and diet, my next laboratory will be in February, hope there will be a good result. Thanks for the video.
It might be a bit late to ask, but Im curious whether dietary cholesterol generally is processed more into LDL, since there was a lot of controversy regarding dietary cholesterols.
One addition/correction: Chylomikrones are not transported via the (portal) blood to the liver, but through the lypmh fluid in the ductus thorcicus, then into blood circulation, first reaching the periphery then the liver (remenants). Its important for pharmacokinetics.
The term "blood circulation" is never meant to be the "portal vein". Although we skipped the "lymph" part here, for simplicity, the main point was made: chylomicrons go to blood circulation first before reaching the liver.
@@Alilamedicalmedia @Alilamedicalmedia Sure Sure. However, i think if you talk about digestion people assume entering blood is Portal vein. Our Professor recommended us this Video, thats just why it was funny to spot an issue ^^
Our bad, we could not foresee that some people may "assume" something then make an "issue" about their own assumption. Thankfully, from the overall reaction to this video, most people know that "blood circulation" should never be confused with (or assumed to be) the "portal vein".
Love this video? Check out our new A&P course, with more than 80 videos like this (no watermark, no ads), over 40 PDFs and hundreds of images:
For student: www.alilaacademy.com/courses/anatomy-and-physiology-for-students
For teachers: www.alilaacademy.com/courses/anatomy-and-physiology-for-teachers
NEW: Now you can also get access to our courses with our RUclips channel membership (Academy Access levels)
Explained to me in 4 minutes what my lecturers couldn't explain me to in 1 hour. Thank you
Danny Williams
It’s very limitedly informative but good for premed beginners tho (not even enough for premed)
@@xufenghuang1634 yeah ! But for example, i will be working on lipid metabolism disorders and I am here to get some info before that
In harper it is given nicely....and after that you can see Lippincott for revision too
Very true
Seems like someone is a bit stupid
Best video in 4 mins. Let's show some love here.
What an incredible, clear and concise run through of lipid transport. The best I've seen. Thank you
It should be mentioned too, that LDL is not a cholesterol at all, but a cholesterol "transporter". We just call it LDL "cholesterol" for convenience but, it's not really correct.
Absolutely.....
it is said in the beggining of the video, that cholesterol is transported in lipoprotein particles and she talks about “low density lipoprotein - LDL” and not LDL cholesterol
@@nikoletavassova3927 Hmmm, I must have missed that part. Thank's for pointing that out.
Also listen at 3:05 where it’s stated that LDL is known as bad cholesterol
@@michaell132 Yeah, I've always hated that term "bad" cholesterol. No such thing as bad cholesterol, just two different kinds of cholesterol. LDL is not necessarily "bad". I much prefer the more descriptive term of "small dense particles" and large. The large ones are harmless and just bounce around in the bloodstrream. Those small ones though, are the bad ones that lodge on artery walls, Atherosclerosis.
Hands down the best explanation with best visuals I've seen yet! Thank you so much for sharing!
The BEST explanation. All you gotta do is brush up on some notes if you haven't already and you're good. Or can also serve as a wonderful review to put everything together. Amazing!
you're the real MVP! short & simple way to review! THANKS!
Oh my god. This video just packed together an entire day of gibberish so it made sense. Its SO FUCKING GOOD.
Learned something new about the difference between HDL and LDL. Thanks!
thank you for explaining this biochemistry and pharmacology stuff in such simple way!
content that is compact and easy to understand. I Stan
5 hours lectures in 3min you saved my semester!!
Such explanations are useful to all medical professionals& I expect more such useful information
Learning this a while back is what made me want to limit/stop my intake of animal products. Over time, i have now been vegan for a good few years. No bad cholesterol in my diet 🙏
Great VDO! Highly knowledgable was that stuff! 🤩
crazy how much you can learn in 4 minutes, while ive been reading for hours not getting it
because school is meant to enslave and confuse you.
Good summary of all the processes involved in Lipid transport ...
LDL is not the enemy. It is the inflammation.
what is the enemy then
@@aysumutcan Insulin resistance causes inflammation.
Yes its the inflammation
It gives a fundamental knowledge about lipid metabolism to comman men and students. Thankyou very much with appreciations.
I love that the video that was the easiest and clearst to understand was narrated by a woman :)
Thank you so much Vicky!!
The Video I've been looking for. Great job
je suis en 2e année de médecine en France et je comprenais rien grâce a toi j'ai compris la base de mon cours, MERCII
Amazing video. Thank you so much.
A huge love form India...🙏
Hi, just wondering what your thoughts are on the different types of LDL - pattern A and pattern B which are increased in different diets? Also, thank you simplifying all these processes. Very helpful.
You are missing the transition from VLDL to LDL ( IDL ). Still great job
Jose Cordova, also the difference between liver derived LDL vs LDL derived from VLDL degradation.
Thank you for explaining cholesterol metabolism
Kudos on an awesome informative video. Thanks!!
So helpful 🥺♥️ thank U to make the Arabic translateor
great lecture, thanks.
I have a quesiton:
Cholesterol is an example of what type of lipid?
a) lipid
b) fat oil
c) phospholipid
d) sterol
I have been on Tirzepatide for 8 weeks. I have lost 20lbs. My cholesterol was 400 and is now 168!!!
What you're doing is excellent. Thank you 💕.
@MrBilld75 Agreed. I'm glad to see more people are catching up on that distinction. It is important to note that unbiased evidence indicates that LDL is "associative" in atherosclerotic plaque formation as opposed to being "causative". There's a huge difference between the two particularly with regard to prevention and treatment. We are still looking into this but the current evidence indicates that LDL can get damaged by glycation, oxidation and inflammation as a result of too much sugar/refined carbs intake, plant sterols (yes..in spite of the fact that it's ironically used to lower supposedly "bad" cholesterol) and a state of systemic inflammation (from the progression of insulin resistance for e.g.). I'm on the train right now so I can't type much...I'll try and elaborate on this another time.
Damaged LDL are mostly of type B (dense). For example, one mechanism causing issues is the fact that the apoprotein B100 on LDL get damaged enough so that they can't be recognised and reabsorbed by the liver receptors for recycling. So they end up pooling in the circulation hence promoting adhesion to the vascular endothelium. Inflammation also makes the endothelium prone to that phenomenon. LDL is also a repair molecule so it will also migrate (by transcytosis using ATP) to sites of inflammation in an attempt to repair thus further exacerbating plaque formation over time as this process is repeated. Macrophages also try to engulf those inflammatory LDL complex resulting in foam cells and this also triggers more cytokines release (pro inflammatory). So you can see how this cascade can result in more plaque formation over time. Too long to elaborate on but hope that quick summary helps.
This is amazing and so helpful!!!!
Informative and Straight forward
Hat's off to u champ👏
Great explanation 👍
this is amazing! thank you for this video!!!
I learned in less than 5 minutes about Lipoproteins instead of 5 hours of biochemistry
just wow! soo simplified! thank you :)
Very clearly explained...🥰
Omg thank-you i got confused, this is very helpful
Thanks for the video it's very helpful ^^
best explained........thanks a lottt
Ldl is off two types - small dense ldl and large buoyant ldl
So what does it mean?
@@junemercado Cholesterol does not just float around freely in your bloodstream. Cholesterol is like a fat and your blood is like water. And we know fat and water don't mix. Therefore, the cholesterol we typically learn about in our blood work (i.e. LDL-C, HDL) is carried within LDL particles that transport cholesterol throughout your body. In simple terms, there are two types of particles, small dense particles and large buoyant particles. Many experts now believe it is the nature of the particles, not the cholesterol they are carrying, that really matters when it comes to things like heart disease. The particles themselves can be measured with advanced lipoprotein testing, typically NMR (nuclear magnetic resonance) testing. It sounds intimidating but can be done via a routine blood test that is sent to labs to do this sort of testing (which are becoming more commonplace as time goes on). Most often the particle numbers are reported in nmol/L (nanomoles per liter). Optimally, you want results showing a total LDL particle number of about 1000 nmol/L or less. And you want your small (dense) particle number to be 200 nmol/L or less (optimally). The large buoyant portion, which your NMR result will also provide, is not the number to focus on according to some experts, as they are not atherogenic. But the small dense particles (so the theory goes) can get into the endothelium of your coronary arteries and contribute to the heart disease process. Why is that? Well, large LDL particles have a relatively short time duration, say 24 hours, and are "dispensed" with fairly quickly, but small LDL particles are not easily recognized by the liver and hence float around in your circulation much longer (e.g. a week or so) giving them more time to do their damage. You can appreciate therefore why standard cholesterol measurements (like LDL-C) never seem to correlate well to the occurrence of heart disease. Cardiologist Dr. Stephen Sinatra, who operated on thousands of patients and actually saw their arteries with his own eyes, used to say many patients with very high LDL-C would have beautiful, pristine arteries, yet many with low LDL-C had prolific heart disease. We now know the nature of LDL particles can be very much in our control by lifestyle and diet. Diets high in carbohydrates, wheat, grains, sugar etc. provoke the occurrence of abundant, dangerous small LDL particles. But low-carb diets (even if high in fat), support metabolic health and most often will result in a healthy small LDL particle sub-fraction (along with increased HDL by the way), thereby lowering your cardiovascular disease risk. To sum up, heart disease is a metabolic disease. Cholesterol is not the problem. And the sooner less attention is paid to cholesterol and the focus gets changed to metabolic health, the sooner we will see some progress in reducing heart disease. C'mon, we've been doing it wrong for 50 years. Let's change the paradigm now so we can start making strides.
@@Malcolm-Achtman Beautifully explained!!
A lot of useful information can be gained from videos from Ivor Cummins on this subject.
As you explained, LDL in itself is not bad, and high values of measured LDL are not dangerous.
The problem arises when these LDL particles become "coated" with "sugary" molecules or oxidized. This changes the appearance of LDL and it is not recognized by special receptors on the liver that control the re-absorption of LDL. It remains floating in the blood for extended periods, causing the discussed health issues.
Metabolic disease is caused by sugar- and refined carb loaded products as you explained. Also vegetable or seed oils are abundantly used in the food industry, because very cheap. Think of canola, cottonseed, sunflower, safflouer, soy, peanut and other oils and margerines. These products are highly processed and have nothing in common with the seeds they were taken from. The oils are easily oxidized inside and outside the body (compare this with a sliced apple, parts are browning fast when exposed to air). This oxidized oil leads to chronic low grade inflation in the body and changing the surface of LDL particles, after which they are not recognized by the liver for reuptake.
The often demonized natural occurring saturated oils and fats have absolutely no impact on health. They contain no unsaturated (double) carbon-carbon bonds and are more or less inert to oxygen on body temperature. Also in the kitchen their smoke point is high.
Unsaturated fatty acids like the omega varieties (e.g. in fatty fish) are heart healthy. It is best to consume fish, as capsules with oil are more easily oxidized.
@@Malcolm-Achtmanthanks for your explanation. How would you measure metabolic health at low cost?
@@TheVafa95 If you obtain a routine lipid panel it will include your triglyceride and HDL values. A crude but potentially good way to establish your metabolic health would be to calculate your triglyceride/HDL ratio. Ideally, that ratio should be 1.5 or less. For example, if your trigs were 70 mg/dL and your HDL was 55 mg/dL, the ratio would be 70/55 = 1.27. That's pretty good. Another key blood test to get is fasting insulin. Also get fasting glucose. So, be sure to fast for about 12 hours before getting these tests. You can drink water, but no juice or coffee or food. A very good fasting insulin result would be about 3 uIU/mL. A good fasting glucose result would be 80 - 90 mg/dL. Try to get HbA1c tested as well. An optimal value is 5.0% or close to that.
to the point, simple, clear. G-d sent! tysm!
really good explanation, thanks
Great explanation👍👍👍
Wow! Thank you! Was so well explained ,thank you
You're very welcome!
wow, for me am highly educated by this info thanks
Glad to hear!
Awesome Video! Had a much clearer concept about LDL & HDL now. Thank you!
Short and excellent explanation... thanks for the video 😊
Chylomicron is not always transported to the liver , some times the chylomicrons move from small intestine to peripheral tissues
Right. Here is a Wikipedia article on lacteals that better describes the route taken by chylomicrons:
en.m.wikipedia.org/wiki/Lacteal
Chylomicrons actually travel through the lymphatic system first before being released into the bloodstream at the thoracic ducts for transit back to the liver.
While traveling back to the liver, some triglycerides are removed from the chylomicrons thereby creating a more dense chylomicron remnant that contains a higher concentration of lipoprotein. This remnant is what actually gets reabsorbed into the liver. More triglycerides are then added to this denser structure to form VLDL.
Best Vedio and its very helpful😊😊😊😊
Thank you for the lovely video, very helpful
You are so welcome!
Amazing and easy revision
It's amazing video, thank you so much really
The voice is so soothing!!
Excellent video. It helped me a lot. Thank you. 🙂
Good explanation
Love how you explained this. Thank you
Glad you enjoyed it!
Very good. It would be even more helpful if intracellular processing of LDL cholesterol was included. One point would be to explain how cholesterol is exported from lysosomes. How many pathways are there? One pathway is via the lysosomal membrane protein NPC1 that allows transport of cholesterol to the ER facilitating homeostasis . Defects in this pathwat result in Niemann-Pick type C disease, a severe and fatal condition.
At 1:40 the video states that chylomicrons go from the gut via blood to the liver. They do not. They are secreted by the intestinal cells into the lymphatic system, and drain via the thoracic duct into the venous circulation at the junction of the left subclavian and internal jugular veins, at the commencement of the brachiocephalic vein.
So now they are in the bloodstream and will go to the liver, right? We just skipped the details you mentioned to focus on the MAJOR steps of cholesterol metabolism. Sorry if the video gave the impression that they go directly from the intestine to the liver, they do not, but those steps are not essential for the scope of this video.
@@Alilamedicalmedia First they visit fat cells.
Great explanation.. Keep up the good work.. 👍👍👍👍
Honestly you slayed it. Let me know if you'd like to collab!
Very helpful, thanks.
Absolutely great!
Its is so helpful, thanks!
Fantastic explanations. Thanks!
Glad you enjoyed it!
Thank you so much
thank's from Fac of Medecin of Algeria
Welldone. Good job.Hat off
Good work👍👍👍
G even I can follow this. Great presentation
Nice video, great lecture, understand able.
Best explanation so for.
LDL transports cholesterol which all cells if the body need, without it you would die. Therefore why is it “bad”. If it’s “bad” why did we evolve to have it in the first place? Also she said it’s associated with strokes and heart attacks. Is association causation or is there another mechanism at work and LDL gets the blame?
WOW so good, it was so helpful
You guys are awesome!! Keep it up with the good work.
oh my gosh. Thank youuuuu!
Amazing video thanks very much
Excellent
I'm experienced now high cholesterol is problem exist more than 20 from normal range, i am taking drug for this, as well as drugs for my hyperthyroidism, and high blood. And even my doctor tell me i have a liver problem too. I'm 38 yrs old heavy drunker before i diagnosed this problem, i completely stop drinking alcohol 6 months ago, i started exercise work today and diet, my next laboratory will be in February, hope there will be a good result. Thanks for the video.
Hi, you may also want to change from a carb loaded menu to low carb. Check out Jason Fung and/or Paul Mason .
Perfect thank you Guys for being here
Great work!
Wonderful. ,,... thx
this is amazing, this vid is SO GOOD
Class khubi sundor vaiya..but camera quality valo hoi nai..lekha bojha jassena sob..
Superb
It might be a bit late to ask, but Im curious whether dietary cholesterol generally is processed more into LDL, since there was a lot of controversy regarding dietary cholesterols.
Awesome 👍 saved me 🙏
So helpful. Thanks!
Good for 0-basis beginners
One addition/correction: Chylomikrones are not transported via the (portal) blood to the liver, but through the lypmh fluid in the ductus thorcicus, then into blood circulation, first reaching the periphery then the liver (remenants). Its important for pharmacokinetics.
The term "blood circulation" is never meant to be the "portal vein". Although we skipped the "lymph" part here, for simplicity, the main point was made: chylomicrons go to blood circulation first before reaching the liver.
@@Alilamedicalmedia @Alilamedicalmedia Sure Sure. However, i think if you talk about digestion people assume entering blood is Portal vein. Our Professor recommended us this Video, thats just why it was funny to spot an issue ^^
Our bad, we could not foresee that some people may "assume" something then make an "issue" about their own assumption. Thankfully, from the overall reaction to this video, most people know that "blood circulation" should never be confused with (or assumed to be) the "portal vein".
thank you ❤
Yes
Thx that was v. Helpful
Why absorbed lipids are carried in blood before they reach to the liver?
Please 🙏🏿🥺
Perfect thank you so much
outstanding
Owo very very nice lecture