Lipid (Fat) Metabolism Overview, Animation
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- Опубликовано: 28 июл 2020
- (USMLE topics) Lipid digestion and absorption; exogenous and endogenous pathways; lipolysis and lipogenesis.
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Voice by: Ashley Fleming
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Although the term “lipid” includes several types of molecules, lipid metabolism usually refers to the breakdown and synthesis of fats. Fats are triglycerides, they are esters of glycerol and three fatty acids. Fats can come from the diet, from stores in adipose tissue, or can be synthesized from excess dietary carbohydrates in the liver.
Dietary fats are digested mainly in the small intestine, by the action of bile salts and pancreatic lipase. Bile salts emulsify fats. They act as a detergent, breaking large globules of fat into smaller micelles, making them more accessible to lipase. Pancreatic lipase then converts triglycerides into monoglycerides, free fatty acids, and glycerol. These products move into the cells of intestinal epithelium - the enterocytes, inside which they re-combine again to form triglycerides. Triglycerides are packaged along with cholesterol into large lipoprotein particles called chylomicrons. Lipoproteins enable transport of water-insoluble fats within aqueous environments. Chylomicrons leave the enterocytes, enter lymphatic capillaries, and eventually pass into the bloodstream, delivering fats to tissues. The walls of blood capillaries have a surface enzyme called lipoprotein lipase. This enzyme hydrolyzes triglycerides into fatty acids and glycerol, enabling them to pass through the capillary wall into tissues, where they are oxidized for energy, or re-esterized for storage.
Fats that are synthesized endogenously in the liver are packed into another type of lipoprotein, the VLDL, to be transported to tissues, where triglycerides are extracted in the same way.
When required, fat stores in adipose tissue are mobilized for energy production, by the action of hormone-sensitive lipase, which responds to hormones such as epinephrine.
Lipid metabolism pathways are closely connected to those of carbohydrate metabolism. Glycerol is converted to a glycolysis intermediate, while fatty acids undergo beta-oxidation to generate acetyl-CoA. Each round of beta-oxidation removes 2 carbons from the fatty acid chain, releasing one acetyl-CoA, which can then be oxidized in the citric acid cycle. Beta-oxidation also produces several high-energy molecules which are fed directly to the electron transport system. Fats yield more energy per unit mass than carbohydrates.
When acetyl-CoA is produced in excess, it is diverted to create ketone bodies. During glucose starvation, ketone bodies are an important source of fuel, especially for the brain. However, ketone bodies are acidic, and when produced in excess, can overwhelm the buffering capacity of blood plasma, resulting in metabolic acidosis, which can lead to coma and death. Ketoacidosis is a serious complication of diabetes, in which cells must oxidize fats for fuel as they cannot utilize glucose. Extreme diets that are excessively low in carbohydrates and high in fat may also result in ketoacidosis.
On the other hand, diets that are high in carbohydrates generate excess acetyl-CoA that can be converted into fatty acids. Synthesis of fatty acids from acetyl-CoA is stimulated by citrate, a marker of energy abundance, and inhibited by excess of fatty acids. Fatty acids can be converted into triglycerides, for storage or synthesis of other lipids, by combining with glycerol derived from a glycolysis intermediate.
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That was the best break down ever. I really needed that explanation because just reading it from the book it was not forming in my head how it all worked. I like the visuals. That really helped me to understand how it works and how to much of something can be bad for you. Great video!!!
You are really the best channel i've found on youtube for medschool. Its comprehensive, short, and extremely rich in information!
Best explanation ever ! .. short and have all the info we need , thank you so much.
💯
This is a very impressive and fact rich outline of lipid metabolism. It's beautifully, clearly and simply presented and I now understand so much more than I did before, in a little over 4 minutes!
Great vid, what an elegantly simple yet highly detailed explanation with great visuals. I knew how it worked already, but wow, this was beautifully done. You could not do any better than this, in explaining fat and lipid metabolism in laymen's terms. Absolutely stellar, well done.
Great video! thanks a lot. This is helping me so much on my explanation about the pathways.
Thanks very much for your videos. They've made me understand medicine more than any of my teachers could.
This 4 minute videos explained better than my 2 hours lecture
same thing happened to me
I read a book for 1/2hr and I didn't get it clearly, then i came here to understand and got it!! 😊
This video is really good. I summarizes it so neatly and the pictures complement it well.
That's fantastic explanation I have ever heard. Thanks ❤️
Thank you.
I really appreciate your work.
I've been doing animal based keto + 16-8 IF for 2 years, better blood glucose ( 60-100) and blood pressured lowered (125/90), feeling energetic all day long, no brain fog, no ketoacidosis... Without medication. What a great video.
Excellent overview of lipids, help us see the big picture! Thanks a lot for sharing!
Beautifully done ! Thanks
Very clear and well explained!
This gave me a good overview of the process - thank you so much!
When blood glucose is high, insulin tells cells to turn excessive carbs into triglycerides for fat storage. When blood sugar is low (during fasting) IGH1 tells the liver to make ketones, an alternative fuel the brain can use. Fat is robed from storage. The ketoacidosis situation happens under extreme cases.
fantastic.you should do USMLE content.your channel will boom.the way you combined three cycles ...OMG
Thank you for providing this information, it is very useful for my studies
Amazing video, very illustrative!
Very useful ,many thanks
Good explanation thanks 😉👍✌
Better explanations and diagrams done than my prof.
Lovely, distinction level
Embora o termo "lipídio" inclua vários tipos de moléculas, o metabolismo lipídico geralmente se refere à degradação e síntese de gorduras. As gorduras são triglicerídeos(ésteres de glicerol e de três ácidos graxos). Podem vir da dieta, das reservas no tecido adiposo ou podem ser sintetizadas a partir do excesso de carboidratos dietéticos no fígado.
As gorduras dietéticas são digeridas principalmente no intestino delgado, pela ação dos sais biliares e da lipase pancreática. Os sais biliares emulsificam as gorduras. Eles agem como um detergente, quebrando grandes glóbulos de gordura em micelas menores, tornando-os mais acessíveis à lipase. A lipase pancreática converte então os triglicerídeos em monoglicerídeos, ácidos graxos livres e glicerol. Esses produtos se movem para as células do epitélio intestinal - os enterócitos, dentro dos quais eles se re-combinam para formar triglicerídeos. Os triglicerídeos são embalados junto com o colesterol em grandes partículas de lipoproteínas chamadas quilomícrons. As lipoproteínas permitem o transporte de gorduras insolúveis em água em ambientes aquosos. Os quilomícrons deixam os enterócitos, entram nos capilares linfáticos e, por fim, passam para a corrente sanguínea, levando gorduras aos tecidos. As paredes dos capilares sanguíneos têm uma enzima de superfície chamada lipase lipoproteica. Essa enzima hidrolisa os triglicerídeos em ácidos graxos e glicerol, permitindo que eles passem pela parede capilar para os tecidos, onde são oxidados para obter energia ou reesterizados para armazenamento.
As gorduras sintetizadas endogenamente no fígado são acondicionadas em outro tipo de lipoproteína, a VLDL, para serem transportadas aos tecidos, de onde os triglicerídeos são extraídos da mesma forma.
Quando necessário, os estoques de gordura no tecido adiposo são mobilizados para a produção de energia, pela ação da lipase sensível aos hormônios, que responde a hormônios como a epinefrina.
As vias do metabolismo lipídico estão intimamente ligadas às do metabolismo dos carboidratos. O glicerol é convertido em um intermediário da glicólise, enquanto os ácidos graxos sofrem beta-oxidação para gerar acetil-CoA. Cada rodada de beta-oxidação remove 2 carbonos da cadeia do ácido graxo, liberando um acetil-CoA, que pode então ser oxidado no ciclo do ácido cítrico. A beta-oxidação também produz várias moléculas de alta energia que são alimentadas diretamente ao sistema de transporte de elétrons. As gorduras geram mais energia por unidade de massa do que os carboidratos.
Quando a acetil-CoA é produzida em excesso, ela é desviada para criar corpos cetônicos. Durante a fome de glicose, os corpos cetônicos são uma importante fonte de combustível, especialmente para o cérebro. No entanto, os corpos cetônicos são ácidos e, quando produzidos em excesso, podem sobrecarregar a capacidade de tamponamento do plasma sanguíneo, resultando em acidose metabólica, que pode levar ao coma e morte. A cetoacidose é uma complicação séria do diabetes, em que as células devem oxidar as gorduras como combustível, pois não podem utilizar a glicose. Dietas extremas que são excessivamente baixas em carboidratos e ricas em gordura também podem resultar em cetoacidose.
Por outro lado, dietas ricas em carboidratos geram excesso de acetil-CoA que pode ser convertido em ácidos graxos. A síntese de ácidos graxos a partir da acetil-CoA é estimulada pelo citrato, marcador de abundância energética, e inibida pelo excesso de ácidos graxos. Os ácidos graxos podem ser convertidos em triglicerídeos, para armazenamento ou síntese de outros lipídeos, por combinação com glicerol derivado de um intermediário da glicólise.
Wow. Amazing explaination
Excellent, perfect, and amazing !!!!!!
This video helped me a lot thank you very much
Best explanation ever thanks
now that was helpful, thank you so much
informative video!
Thank you👏
Animation and all are good and vary helpfull to understand
Good explanation
Excellent!
지방에 대한 폭넓은 이해를 하였습니다
좋은 영상자료에 정말 감사합니다
굿
Supperb explanation!!
An Wonderful overview!!😍😍😍
Hey there, one query about dietary induced ketoacidosis. I have not seen anywhere where a ketogenic diet has the capacity to induce this blood acidity. Can you provide a video and research papers that show this.
There are none. It’s never happened. It’s for all intents and purposes, it’s impossible to induce a state of keto acidosis outside of the context of a very poorly managed type 1 diabetic. She seems to be just kind of repeating some ideology. I don’t think she has an actual understanding of metabolic process.
@@turtledunkknucklebaby8089 I believe also possible with Type II, even though they more commonly go into HHS
Recovering your metabolic health is not for everyone.
Yet...
Looks like it does exist, based on the summary anyway.
www.ncbi.nlm.nih.gov/pmc/articles/PMC7220017/
@@brianboggs8462here is an interesting study about starvation induced ketoacidosis www.ncbi.nlm.nih.gov/pmc/articles/PMC7174867/
Thank you
helpful piece of basic info
Thank you so much 👏👏👏
Outstanding
Really useful!
THE BEST MEDICAL ANIMATION 🤩🤩🤩🤩🤩
this was so elegant
thank you 🙏🏻
thank you!
fantastic
Wow, I'm still in awe! The valid question is...where do all this come from? It's just mindblowing. You have to stop and marvel that it has literally taken _billions_ of years to come to this perfect mechanism!
It is not perfect.
@@life42theuniverse wdym
Only something God himself could design...not billions of years of evolution.
Thanks
Quite interesting!
I want whole video on lipid metabolisom
Hi! Such a great video.
Although I have a question, in min 0:50, shouldn’t pancreatic lipase coverts TAG into MAG and 2 fatty acids, without considering glicerol?
It's a complex mixture, so they are broken down differently: some molecules are partially broken down (to monoglycerides and 2 fatty acids), some are completely broken down (to 3 fatty acids and glycerol).
hi can you help me how TAG convert inti diglycerides and how many fattyacids +glycerol do diglycerides gives? couldnot find the diglycerides part on the vedio
Marvelous ❤️
I have been following a strict ketogenic diet for 9 months already (no carbohydrates and no sugar) and didn't experience any ketoacidosis.
ketoacidosis is a risk only if you are diabetic.
Made my life easy
Nice!
3:33 - Why is the information about ketoacidosis on very low carbohydrate diets incomplete? There is no risk of acidosis in dietary interventions since the levels of ketones on i.e. a ketogenic diet rarely reach 2 mol in combination with very low blood glucose. Acidosis is a metabolic problem of people with Diabetes, often they show super high ketones way beyond 10 mmol in combination with severely elevated blood glucose. This issue is specifically tied to diabetics with insulin dependent therapy or - less frequently - blood sugar lowering drugs. It's so sad because the general way of explaining in this video is exceptionally good and easy to understand. It would be great if you could add some information about the difference between ketosis as physiological metabolic state due to carbohydrate or energy deprivation compared to a life threatening metabolic derailment of chronic disease.
Has anyone actually gotten ketoacidosis from ketogenic diets (aka very low to zero carbs and higher fats) or is it just people still mixing up ketosis and ketoacidosis?
Yep, there are cases of people who can't regulate insulin like those with undiagnosed T1D that have gotten ketoacidosis from doing keto. I don't think she means for healthy individuals.
Bile salt helps in breaking globules into droplets & formation of micelle..✍
Coo, coo
Acetyl-coa can turn into ketone bodies or fatty acids. But what makes the choice?
THANKYOU.. THANK YOU... THANK YOU... 💓🤧
More please
What if have malabsorbtion issues and genetic defects where cells have issues doing process and lack of production of energy. Is this going to cause issues with lipds in MRmA vac?
Good
Why triglyceride breaks and than again for chylomicron and again hydrolysed in the form of fatty acid and glycerol,
What is the reason, why triglyceride is not directly enters into the blood vessels
So eating carbs uses up the vitamin c the kerb cycle makes? While burning fats produce excess vitamin c? This correct.
Excellent video. Question: I was not clear on what makes the difference in excess acetyl co A going the route of becoming fatty acids and TGs vs ketones. Can anyone help?
Glucose absorption stimulates glycolysis which generates pyruvate then acetyl-coA. Acetyl-coA has multiple purposes including feeding into the TCA cycle to further go into oxidative phosphorylation and ETC to generate ATP, and fatty acid synthesis (TAG), or form cholesterol. You need glucose to form pyruvate which also forms oxaloacetate by pyruvate carboxylase. Inadequate glucose absorption like in people with diabetes results in a decrease of oxaloacetate formation thus it is depleted and cannot form citrate anymore by combining with acetyl-coA and thus cannot enter the TCA cycle. There is an accumulation or excess acetyl-coA due to lipolysis. Acetyl-coA will then go on to form ketone bodies which can be utilized in periods of starvation especially. Lipogenesis (forming TAGS) is energetically expensive and requires ATP consumption, but since TCA cycle is rendered (due to oxaloacetate depletion) the body cannot afford to stimulate gluconeogenesis later on because it also requires high ATP. Thats why ketone bodies are produced and can be utilized by the brain and other tissues in extreme starvation. Hope that answers your question!
@@fahadalmulla9504 that’s a great answer thank you 😊. I’m wondering something else ... in a non diabetic that is fasting any idea why ketones might be overproduced to the point of trending to keto acidosis? Day 5 of zero calorie fasting ketone levels were 7.6
@@part-timephilosopherLol Just to clarify, short term fasting will not cause ketoacidosis. In non-diabetics, ketoacidosis will only occur in periods of extreme starvation (weeks). During this period, there is severe hypoglycemia due to lack of glucose intake, therefore, as explained before, not enough oyruvate will be made so lack of oxaloacete, leading to disruption of the TCA cycle and accumulation of acetyl coA. In the fed state, glucose is the primary source of energy for the body and especially the brain. Since glucose is not present, the next best alternative is ketone bodies. Ketone bodies are produced by acetyl coA. Since we established that there is an accumulation of acetyl coA, then ketone bodies formation will be favored.
This doesn’t make sense in non diabetic patients. Even if they are fasting, in the absence of glucose body can generate glucose through gluconeogenesis. So this may not apply.
You are in false @@josephvettoor5780
Pleas explain electrolytes and acid base disorder
We have that, just look in our channel.
@@Alilamedicalmedia ok . Thank you
Glycerol can’t be taken by extrahepatic tissues due to absence glycerol kinase
Tq
honestly, idk if i would survive mediccl school if youtube isn't around.
Plzz some one explain the difference between cholesterol, lipid,fat 😭😭??
I got it, thanks
Wonderful explanation! One issue, though, is that an extremely low carb diet in a non-diabetic person does not cause ketoacidosis.
From other sources, the level of ketone bodies required for ketoacidosis is roughly 10 times that which can be achieved from low-carb dieting. Healthy people can cut carbs to their heart’s content without worrying about turning their blood acid. I’m on an extremely low carb diet now and feel great.
Im curious how did they figure this out?
I will reiterate how good this video is. However, one comment: very low carbohydrate, diets do not Cause keto acidosis. One must be diabetic.
Jajakallah....
Hmm, so is possible that a diabetic actually exclusively relies on fat metabolism to derive energy, because cells won’t accept fast energy from glucose in the blood? Is there ever a case where fat storage stops working? Ok
Diabetes is caused by insulin resistance. Which is caused by too much sugar and carbohydrates in the diet. Humans are evolved to metabolise fat. There's a reason the Inuits never had diabetes and cardiovascular diseases despite having a diet consisting primarily of whale and seal blubber. Sugar and carbohydrate metabolism cause glycation and oxidation of LDL, which damages the lipoprotein. LDL is NOT bad, except when it is damaged. When that is the case it cannot be reabsorbed by the liver and turned back into VLDL. Unabsorbed damaged LDL is scavenged by macrophages that accumulate and form plaques under the intima of arteries, causing atherosclerosis. Plenty of studies now show that putting diabetics on zero sugar/low carb/moderate protein/high fat diets reverses the disease. Patients that stick to the protocol lose weight and come off their meds completely.
im just watching cuz of keto diet
I HAVE A freaking presentation tomorrow..... And I'M SCARED OF STAGE..... Sometimes being an introvert sUcks... 🤧
U missed explaining absorption of fats thro diffusion
interesting
👍👍
Fat is another term called cholesterol. Cholesterol plays a vital important role in cells of liver to work etc. Our cells need fat, but it limited amount too much fat cause diseases. Our liver which is very sensitive organ plays important role in digestion. Good fat contains omega but junk fat is as harmful for other organs especially coronary heart disease.
Nice 🔥 explanation like....prepare maggi in 2 minutes... 😅🔥🤘
Nutritional ketoacidosis is no harmful. infact when your major energy comes from fat(ketones) you feel more energetic. Only pathological acidosis is harmful in case of diabetes
So you're saying that it's not good to be keto???
Whoever is narrating this , sounds cute.
You know...
MY Walter Mitty daydream is to have a fuel cell that burns lipids in multiple steps, perhaps it would need to be in the form of a soap.
Do u want- have u ever- do u- can- have u been-
But then why do keto diets don't cause acidosis??
Keto diets are essentially nutrional ketosis. The ketone production is not severe enough to cause ketoacidosis (such as the one found in Diabetic Ketoacidosis or with starvation).
@@heavythinker16 Thanks
@@mr.greengold8236 I think she was talking about starvation using other words, which is obvious.
Here from risci
Yeah, so what yer sayin’?
hi
So then how can i turn sugar directly into fat in the kitchen? Im out of butter and oil. XD
Excess dietary carbohydrates this is the killer
Hypothyroidism can cause the person to not metabolize lipids