Ketone Metabolism Explained: Ketogenesis, Ketone Bodies & Energy

Ketone Metabolism: A Complete Guide for Medical Students & Health Professionals

This video provides a detailed, step-by-step breakdown of ketone metabolism, from the triggers for ketogenesis to the clinical complications of excessive ketone production. Ideal for medical students and health professionals looking to solidify their understanding of this critical metabolic pathway.

What Triggers Ketone Body Production?

The body typically prefers glucose as its primary fuel source. However, under specific metabolic stress conditions, it switches to using ketone bodies. The video lists four main triggers for this metabolic shift:

Low Blood Glucose Levels: The primary stimulus.
Prolonged Starvation: Extended fasting depletes glucose stores.
Uncontrolled Diabetes Mellitus (especially Type 1): Lack of insulin prevents glucose uptake, forcing the body to find an alternative fuel.
Very Low-Carbohydrate Diets (e.g., Atkins/Keto Diet): Restricting carbs mimics a starvation-like state.

Where Does Ketogenesis Occur?

Site of Synthesis (Ketogenesis): The liver is the primary site where ketone bodies are formed.
Site of Utilization: The brain and muscles are the main tissues that break down ketone bodies to generate energy (ATP). The brain cannot use fatty acids directly, making ketones a crucial alternative fuel during glucose scarcity.

The Step-by-Step Process of Ketogenesis

This section breaks down the complete biochemical pathway from fatty acid breakdown to the formation of ketone bodies.

Phase 1: The Shift from Carbohydrates to Fatty Acids

Primary Fuel (Carbs): Under normal conditions, glucose is oxidized to pyruvate, then to acetyl-CoA, which enters the Krebs cycle to produce ATP. For a broader perspective, see Understanding Carbohydrate Metabolism and Pathway Integration.
Secondary Fuel (Fatty Acids): When glucose is low, the body increases beta-oxidation of fatty acids. This process generates large amounts of acetyl-CoA. For a detailed walkthrough, visit Fatty Acid Oxidation Explained: Beta Oxidation Steps, Carnitine Shuttle & Energy Yield.
The Problem: Low glucose activates gluconeogenesis. A key intermediate (oxaloacetate) is pulled from the Krebs cycle to make new glucose. This depletes oxaloacetate, preventing acetyl-CoA from entering the cycle efficiently.

Phase 2: Creating Ketone Bodies from Acetyl-CoA

With excess acetyl-CoA and insufficient oxaloacetate, the liver initiates ketogenesis:

Condensation Step: Two molecules of acetyl-CoA are fused together by the enzyme acetoacetyl-CoA transferase to form acetoacetyl-CoA.
Rate-Limiting Step: Acetoacetyl-CoA reacts with another acetyl-CoA, catalyzed by the enzyme HMG-CoA synthase, to form HMG-CoA (3-hydroxy-3-methylglutaryl-CoA) . This is the most important enzyme in the pathway.
Cleavage Step: The enzyme HMG-CoA lyase cleaves HMG-CoA, releasing one free acetyl-CoA and the first ketone body, acetoacetate.
Reduction Step: Acetoacetate can be reduced by the enzyme beta-hydroxybutyrate dehydrogenase to form the second major ketone body, beta-hydroxybutyrate.

Both acetoacetate and beta-hydroxybutyrate are then released into the bloodstream to be used by the brain and muscles. For more on the upstream processes, explore Understanding Lipid Digestion, Absorption, and Metabolism.

Clinical Consequences of Excess Ketone Bodies (Ketoacidosis)

When ketone production exceeds the body's ability to use them (e.g., in uncontrolled Type 1 diabetes), a dangerous condition called ketoacidosis can develop.

Key Diagnostic Signs & Symptoms

Acetone Breath: A small amount of acetoacetate is spontaneously decarboxylated into acetone. This is a volatile compound that is exhaled, giving the breath a characteristic "fruity" or sweet odor.
Metabolic Acidosis: Acetoacetate and beta-hydroxybutyrate are relatively strong acids. Their accumulation in the blood donates protons, leading to a drop in blood pH (acidosis).
Elevated Anion Gap: An increased anion gap (>11 mEq/L) is a key laboratory finding in ketoacidosis.
Kussmaul Breathing: The body attempts to compensate for the acidosis by breathing rapidly and deeply, in an effort to expel more CO2.
Vomiting & Hypovolemia: High ketone levels can stimulate the chemoreceptor trigger zone in the brainstem, leading to vomiting. This can cause severe fluid loss (hypovolemia).
Ketonuria: Elevated ketones will be present in the urine as the kidneys try to excrete the excess.

How the Brain and Muscles Use Ketone Bodies for Energy

This is the reverse process of ketogenesis, occurring in the target tissues.

Reactivate Ketone Bodies: Inside the muscle or brain cell, beta-hydroxybutyrate is first converted back to acetoacetate.
Add a CoA Group: An enzyme called succinyl-CoA transferase (or thiophorase) transfers a Coenzyme A group to acetoacetate, reforming acetoacetyl-CoA.
Cleave for Energy: The enzyme acetoacetyl-CoA thiolase cleaves acetoacetyl-CoA into two molecules of acetyl-CoA.
Fuel the Krebs Cycle: These two acetyl-CoA molecules enter the Krebs cycle (citric acid cycle).
Generate ATP: The Krebs cycle produces NADH and FADH2, which feed into the electron transport chain to generate large quantities of ATP, the cell's energy currency. For a foundational overview of these intersecting pathways, see Comprehensive Biochemistry Overview: Metabolism, Enzymes, and Amino Acids Explained.

Key Takeaways

Ketone bodies (acetoacetate, beta-hydroxybutyrate) are primarily produced in the liver during periods of low glucose.
The rate-limiting enzyme for ketogenesis is HMG-CoA synthase.
Glucose must be conserved via gluconeogenesis, which depletes oxaloacetate and pushes acetyl-CoA toward ketogenesis.
While a normal adaptive response to starvation, uncontrolled overproduction (as in Type 1 diabetes) leads to life-threatening diabetic ketoacidosis (DKA).
The brain and muscles can use ketone bodies to generate ATP, which is critical for survival during prolonged fasting. For more on the cellular structures involved in lipid metabolism, check Understanding the Structure and Function of Peroxisomes: Key Organelles in Cellular Metabolism.

all right engineers in this video we're going to talk about Ketone metabolism okay so when does the body actually you

know utilize ketones it's not usually a preferable source of energy it is usually usually utilized whenever we're

in certain conditions so let's say that you have low blood glucose levels let's say

that's one reason all right so let's say that you have extreme low blood glucose

levels another reason this pathway could occur this Ketone metabolism could be if you actually have prolonged starvation

so another reason could be prolonged starvation so prolonged

starvation another reason this pathway could occur is because of diabetic condition so in other words you

have diabetes malius and it's not being well regulated so you're not taking your insulin properly so it could be due to

uncontrolled diabetes malius specifically though type one it's less common in type two but it can happen in

type two and the last thing is it could be due to a uh some type of diet where you're restricting carbohydrates for

example the Atkins diet okay so these could be certain conditions or reasons upon why you're

exhibiting this Ketone metabolism now why are these things stimuli for that okay if you're actually

having low blood glucose levels your body is going to have to utilize some form of energy now the brain this is the

brain's primary source of energy so the brain's primary source of energy is going to be that of glucose but in any

condition in which there is extremely low blood glucose levels whether it be due to prolonged starvation uncontrolled

Diabetes metis Type 1 or some type of specialized diet where you're avoiding carbohydrates more of a ketogenic diet

like the Atkins diet this can cause the brain to have to switch from its primary choice of fuel to a secondary choice of

fuel which is that of Ketone bodies also the muscles our muscle tissues can also utilize these Ketone bodies so our

muscles they also prefer to use fatty acids and glucose as their source of energy but

whenever there is a situation which the blood glucose levels are extremely low and there's excessive fatty acid

oxidation they can utilize Ketone bodies so again we know why it's occurring it's occurring because of low blood glucose

levels whether that be du do prolonged starvation uncontrolled type 1 diabetes militis or the Atkins diet or some type

of diet which is restricting carbohydrates now we know that the uh organs that can utilize that as sources

of fuel is going to be the brain and the muscles now the next question is where is this ketogenesis actually occurring

it's mainly occurring in the liver so this is mainly occurring in the liver this is where the the Genesis of

these Ketone bodies are being formed but the Lis the breaking down of those Ketone bodies to generate energy is

occurring within the muscles and the Brain okay now let's go over how this process is occurring and why it's

occurring in a little bit more detail so you know uh inside of our liver cell it's utilizing glucose it can utilize

glucose and you guys remember that glucose uh under goes oxidation to produce

pyruvate and then if you remember pyate can get converted into what eventually it can get converted into acetyl COA and

then what does acetyl COA combine with you know aceto COA combines with oxaloacetate I'm going to denote that as

OAA and what happen happens if you guys remember oxaloacetate and aceto COA actually do what they fuse together

right to form what molecule what is this next molecule that it forms it forms a molecule called

citrate and then the kreb cycle will continue right it'll go from citrate to isocitrate to alphaet toluate to soxo to

soate to fate to malate to OA okay you know there's another path that can occur if the glucose levels on

our body body is low we have low blood glucose levels wouldn't that mean that we have very little pyruvate if we have

very little pyruvate we have very little acetyl COA and there's going to be less kreb cycle activity and now what that

means is is you know your body has to take this to a specific point in the body you know it takes it to the

electron transport chain you know the nadhs that you get from this the nadh's and the

fadh2s they'll take those hydrides to the electron transport chain and what will come out of the electron transport

chain ATP you'll generate ATP so you'll produce ATP now in a

situation in which our body has what low blood glucose levels this pathway is not going to be utilized as much our body

switches gears so now this is our primary I told you guys again let's write it above it glucose are

carbohydrates in general so let's write it above like this this is our carbs this this is our first

source of fuel it's our primary source of fuel this is the one that we would actually go to first we want to go to

carbs first but in a situation in which these are not available or they're very Li limited amounts our body will switch

to a second source of fuel and that second source of fuel is going to be fatty

acids okay so again let's write it up here this is our second source of of

fuel now what happens with these fatty acids you know these fatty acids they undergo specific process that you guys

have we've already talked about remember beta oxidation beta oxidation was that four-step process that was literally

generating acetylcoa now if we're having excessive breakdown of fatty acids because our

glucose levels are low and our ATP levels what was going on with our ATP levels because there was low glucose

there was low at ATP our cells are going to require that ATP for many many different activities transport pumps

contraction even uh generating DNA and transcription translation tons of processes so our body switches gears it

goes to the second source of energy Fuel and starts breaking down lots of fatty acids and again what is this process

called when you're breaking down these fatty acids this is called beta

oxidation so beta oxidation is the process in which there is actually going to be the breakdown of fat acids into

acetyl COA and we already talked about in an individual video now what happens as a result of making

lots of breaking down these fatty acids what do you make a lot of a lot of acetyl COA so as I start making a lot of

acetyl COA I'm going to have a lot of crab cycle activity and produce a lot of ATP so again what's going to happen as a

result I'm going to have a lot of acetyl COA and then as as a result I'm going to have a lot of

nadh's a lot of fadh2s I'll go to the electron trans transport chain and what will happen to my ATP levels it'll go

up problem is though when our blood glucose levels are low you remember that that mechanism our body does it's called

gluconeogenesis where the oxaloacetate can be utilized for what remember the oxaloacetate can actually get converted

into a molecule called malate and it can get pushed out of the mitochondria when it gets pushed let's

say that for example this is the mitochondria Mito there malet can get pushed out can get converted back into

OAA and then OAA can get converted into a special molecule which was called what what was that molecule called phospho

enol pyruvate and then that could get converted into glucose and if you remember what was the enzyme was

regulating this step from OA to pep it was called pep c k this enzyme was stimulating this step so whenever there

is low blood glucose levels our body deals with that with trying to make gluc glucose through this process of

gluconeogenesis so what is this process here called this process is called gluco

neo genesis okay well as a result then what happens to your oxyacetate levels if you're utilizing that oxyacetate to

make glucose won't his concentration start going down yes and look what happens when his concentration starts

going down as his concentration starts going down this acetyl COA can't react with this oxaloacetate anymore because

there's very little of them so very little acyoa is going to react with the OA and you're going to make less

citrate now what happens in response to this very little citrate our body decides to shuttle or shift this acetyl

COA production into a different molecule so now look what happens this acetyl COA is going to go

into a special pathway I'm going to have a lot of acetal coas here what I'm going to do

is I'm going to take an acetyl COA here and another acetyl COA and I'm going to fuse them together

okay so I'm going to take these two acetyl coas and I'm going to fuse these two

acetyl coas together and as I fuse them one of the coas is going to have to come off and so out of this reaction will

come off a CO enzyme a so I lose a CO enzyme a in this process another thing that's happening is what enzyme is

triggering this pathway because this enzyme isn't just occurring like automatically there has to be an enzyme

that's triggering this pathway this enzyme is called acetal acetal

COA AAL transferase okay so this aceto COA acal

transferase enzyme is doing what it's taking the the aceto COA and the other aceto COA and fusing them together and

as a result what is the molecule that you're forming as a result you're going to form a molecule

called aceto aceto COA so what's this new molecule here formed this called molecule is called

aceto actil COA so I went from two acetyl coas reacting with the presence of acoa

AAL transferase and I'm going to get rid of co-enzyme a and I'm going to form aceto

aceto coate it's just these two guys fused together without a COA then I'm going to take this aceto aceto

COA and I'm going to do another special reaction with it I'm going to add in another COA okay so I'm gonna add in

another COA another acetyl COA so look what I'm going to do here I'm going to take this acetyl

COA and I'm G to add in another acetyl COA so what I'm going to do is I'm going to take acetyl COA here

and I'm going to add this puppy in right there and I'm going to get rid of another COA so I'm going to lose another

COA as a result of this so what am I going to do I'm going to lose a COA as a result of this Co enzyme

a then when I have this aceto acoa combined with another aceto COA I'm

going to get a new molecule and this new molecule that I'm going to form as a result of this

reaction is going to be specifically called they abbreviated I'm going to write down

the abbreviation but I'll write down the name also just for the heck of it it's called HMG COA so HMG COA stands for

three hydroxy three methyl

glutaral COA so now you guys see why people refer to this as HMG COA because it's it's a heck of a name okay so HMG

COA is going to be formed by what taking aceto aceto COA reacting with another aceto because you have tons of those

aceto why not use them up so now when we do that when we take this aceto aceto COA put in another aceto COA we form HMG

COA which is also referred to as three hydroxy three methyl gluto COA some literatures because the three carbon is

usually also the beta carbon you might hear it written as beta hydroxy beta methyl gluto COA but we can just refer

to it as HMG COA now what enzyme is catalyzing this step the enzyme catalyzing this step is specifically

called HMG COA synthes HMG COA

synthes if you don't remember any of these enzymes please remember this one because this enzyme is the rate limiting

enzyme so this step right here that we're going to right now this is called the rate limiting step so the

rate limiting step okay so it's one of the most

important steps within this process now this HMG COA what's going to happen with him this HMG COA is going to

do something really cool he's going to get acted on by another

enzyme okay and this enzyme that's going to work on this HMG COA okay we already know the name of this molecule okay but

again you can refer to it as HMG COA or three hydroxy three methyl glutaral COA but look what enzymes coming into this

area this enzyme is going to stimulate this step now you're probably going to be

like I don't get why we keep doing this Zach but it's all part of our body's amazing way to deal with this see how we

put in a COA in this step we're going to get rid of it we're going to get rid of an acetal COA so what we're going to do

is we're going to take an enzyme here and we're going to cut this molecule with a molecule called h

mg COA lias so this HMG COA lias is going to be

an enzyme and this enzyme is going to cut the HMG COA or the three hydroxy 3 methyl gluta COA and it's going to pop

out an acetylcoa so it's going to pop out an acetylcoa and as a

result this new molecule that I'm going to get is going to be referred to as aceto

acetate okay so I'm going to get acetoacetate out of that reaction now one more thing can happen as a result of

this the ceto acetate can get put directly into the blood so this aceto acetate can literally get put right into

the blood but some of this acetoacetate is converted into another molecule another type of Ketone body because this

is one of the Ketone bodies let's actually write that this is actually one of the Ketone

bodies so this is the one of the types of Ketone bodies that we're going to call it that's going to be utilized for

energy for the muscles and for the brain right now acetyl acetate has a special mechanism here what it can do is let's

do with a different color here I can take this acetoacetate and I'm going to have this molecule called

nadh come into play this nadh is going to drop some hydrides off into this acetoacetate and convert him

into n a positive right because he's going to drop the hydrides off onto the acetoacetate so this acetoacetate is

going to get reduced it's going to get reduced to a molecule referred to as beta

hydroxy butyrate okay so you're going to get beta hydroxy

butyrate which is going to be one of the Ketone B so this is the other Ketone body that you can develop here this is

the other Ketone body body right and what can happen this beta hydroxy beate can get spit right into

the bloodstream so we can spit this into the bloodstream so what are the two things that we spit into the bloodstream

out here we've put into the bloodstream two types of Ketone bodies and again what are those Ketone bodies that we put

in one is aceto acetate the other one is going to be

beta hydroxy berate these two guys can get taken into this actual muscle cell or again what

other cell it can be taken into the muscle cells or they can be taken into the brain cells right so the our neurons

can utilize that okay none one more thing that I need to point out you know this

acetoacetate okay in order for us this aceto acetate be converted into this beta hydroxy berate you had to have an

enzyme o what did I have here n to n positive you know that whenever you see that there's a dehydrogenase enzyme and

I'm synthesizing beta hydroxy butyrate so this enzyme here must be what do you think this enzyme is called this enzyme

is called beta hydroxy berate dehydrogenase and this enzyme is

stimulating this step okay the beta hydroxy butter dehydrogen is converting acetoacetate

into beta hydroxy beate and then it's getting pushed into blood one thing we need to realize again

these molecules are your Ketone bodies they can get taken up by muscles and by the brain now something happens with

this aceto acetate there's another enzyme for the aceto acetate when it's in the blood so let's show this

acetoacetate here let's say that we spit some acetoacetate right here also from this

process this acetyl acetate can be acted on by another enzyme and this enzyme

is called acetoacetate decarboxylase this enzyme is called

aceto acetate D

carboxylase and what it's going to do is it's going to rip off a carbon off of the acetoacetate now generally aceto

acetate is a four carbon long structure so this is about four carbons but what I'm going to do is I'm

going to rip off a carbon and when I do that I turn it into a very very dangerous molecule inside of our body

and that dangerous molecule that can actually cause certain problems is called

acetone why is that relevant okay in certain um people who have uncontrolled Diabetes metis Type 1

one of the diagnostic tools is to smell their breath you know whenever someone's having uncontrolled diabetes mtis and

they're having a lot of this keto metabolism they're going to be having a lot of acetone that they're going to try

to breathe off now you know why these I'm mentioning that is because the acetyl acetate and beta hydroxy butyrate

are naturally acidic um you might have heard of this term in chemistry these generally have a

PKA um around four to five which is meaning that they're pretty acidic okay so if it has a pka of around

four to five normally a good buffer is going to be plus or one minus the pH right now if this pka of these Ketone

bodies are excessively you know low it can be very acidic what does that mean that means that these Ketone bodies can

donate protons into the bloodstream and if they donate protons into the bloodstream what does that do

to our blood it makes our blood acidic so if it's donating protons into the actual bloodstream it's making the blood

really really acidic this can lead to acidosis so this can lead to acidosis specifically they refer to it as keto

acidosis and again it's because this acetoacetate and beta hydroxy beate generally have a PKA around four to five

so they're naturally acidic and they can donate protons so one thing you're going to notice with this person who might

have prolong starvation uncontrolled type 1 diabetes metis or a very very prolonged Atkin diet is they'll have

acetone breath a fruity breath because they're trying to breathe it out also they're going to have acidosis their pH

might be a little a little bit low but you can also test this you know uh doctors don't necessarily just go

straight by the pH they also go by another test and a way that they can look for this is what's called an annion

Gap and if they take this person and they see an elevated annion Gap you know usually above approximately 11 Millar

this person could actually have some type of acidosis okay whether that be a keto acidosis or something else

generally whenever is significantly larger than about 11 Millar per liter that can actually say okay this person

has a high an Gap we should evaluate that and we'll talk about this whenever we talk about acid base

balance okay now now that we understand there can be acetone breath there could be acidosis they would have a high

annion Gap what is going to happen with the ceto acetate and the beta hydroxy berate besides that okay you know these

guys here are pretty interesting they can be utilized by certain tissues but when they are caught whenever there is

too much of these Whenever there is excessive excessive excessive amounts of these molecules right here too much of

this beta hydroxy beate and too much of this aceto acetate there's a particular part of our

brain stem and that particular part of our brain stem is called the area

Posta it's where the chemo trigger zone is whenever there is excessive levels of this acetoacetate and beta hydroxy

berate these molecules can stimulate the arop poost streamer within the trio trigger Zone you know what

that's going to do it's going to trigger vomiting and when they're vomiting excessively what happens to these people

then if they're vomiting excessively what are you losing you're losing a lot of fluid so another complication that

can come with these individuals is not just acetone breath not just a high an Gap not just acidosis but also let's add

to the list vomiting and the D with vomiting is that if they're vomiting too much this can

lead to hypo volia which is low blood pressure right and if this gets significant if

hypovolemia becomes so much to where the the person becomes dehydrated significantly it can lead to

Leading the person into a comos state right so they can go into a com state so it's extremely dangerous on top of that

one of the ways that our body tries to be able to deal with this acidosis um is that we try to do three different

mechanisms one is we have a specifically a bicarbonate carbonic acid buffer system but that doesn't last for too

long it usually gets um drawn up within about you know a couple minutes or maybe even seconds but our respiratory system

we're trying to hyperventilate so if we're going to be consistently trying to hyperventilate to get some of that

actual CO2 out decrease in the carbonic acid and decrease in the proton levels that to be able to alleviate the problem

so you're also going to see Within These people what's called a classical sign which is

called cmal breathing so they're going to have cus

small breathing and cus small breathing is basically where and I think there's two s's in this sorry cus small

breathing it's going to be whenever they're having excessive and very very deep and Rapid Inspirations trying to be

able to breathe off some of that acid in the form of CO2 okay and also if they're having

elevated levels of this aceto acetate and this beta hydroxy uate in the blood eventually they're going to spill that

out into the urine and so what's one of the other signs that you can find within this person you can also find what's

called keto Uria which just means they have elevated ketones within the urine and that could

be some diagnostic signs of this okay now what can we do with these molecules now now that we've generated them within

the liver now we have to take it to the organs that are going to utilize it which is the muscles and the Brain how

do they do that exact opposite of what we just did so let's fly through that now first off we have to start up here

with who technically we have to bring this beta hydroxy buttery up here first and then we'll bring this acetoacetate

down here and I'll explain why in just a second aceto acetate okay and then up here

we're going to have beta hydroxy berate okay if you guys remember from

one of the steps there the last steps now we're just going to be working our way backwards if we want to go from beta

hydroxy butyrate to acetoacetate you remember this was a reversible step so going from aeto acetate to a beta

hydroxy beate I had to do what I had to unload nadhs well to go in this way I need to generate nadh's so this would be

the exact opposite reaction I'll be taking NAD positives and generating nadh is okay what else is going to

happen let's get this Arrow out of the way just now that we know that what enzyme was controlling this step you

remember this was a dehydrogenase because anytime you see nadh you know a dehydrogenase so it's called a beta

hydroxy butyrate what dehydrogenase enzyme and this enzyme is

stimulating this Pathway to make acetoacetate now aceto acetate can come straight from the blood into this cell

now now when it's in the cell what's going to happen to the acetoacetate the acetoacetate is

actually going to get converted back into another molecule that next molecule that we're going to make is called

acetoacetyl COA so we're going to make another molecule which is called aceto acoo now in order for this to happen

something really weird is going to happen because if you remember the only thing that was really different whenever

we were going from aceto aceto Co we had to go to an intermediate which which was called HMG COA and then to acetoacetate

we're going to go straight from acetoacetate to aceto acetyl COA so we need a different intermediate in this

case remember from the kreb cycle you generate a specific molecule so let's say here's our kreb cycle with your

acetal COA and then you go through the kreb cycle you know there's a specific

molecule from the Krab cycle that we actually can generate for this pathway it's called

suon COA you see that COA there there's no COA there there guess what he does he comes into this process and drops off

his COA because he's going to come out as soate then when this happens in order

for us to be able to take this acetoacetate into the aceto aceto COA we had to transfer a COA on to this guy so

when we transfer the COA on to this guy then we're going to get the aceto aceto COA then the aceto aceto COA is going to

be broken down broken down into what aetl COA and acetal COA oh man that's awesome so we can take this acetyl COA

this aceto acetyl COA and we can break it down into two different types of molecules now what is the name of the

enzyme controlling this step the enzyme controlling this step is specifically a special enzyme called

tho foras so this soperas enzyme was catalyzing this conversion of aceto

acetate to aceto acetylcoa then the aceto acetylcoa was getting broken down when it was getting broken down it was

getting cleaved into two different structures this aceto COA and this aceto COA so what must have happened here I

must have had to transfer a co-enzyme a in there somewhere so I had to bring a co-enzyme a in there so I must have had

some type of acetylcoa AAL transfer enzyme so must have had some enzyme in here it's called a ACL

COA AAL transferase enzyme who is stimulating this

step then I have these acetyl coas these acetyl Coes we doing what with these acetyl Coes we could actually

bring them down where we could bring them down into the creb cycle out of the crab cycle what do I generate what do I

generate from this I generate nadh's I generate fadh2s I generate ATP wouldn't

it be the same for this guy also yes so this guy's also going to go through the creb

cycle when he goes through the CB cycle what's he going to give up he's going to give away again

nadh's fadh2s as well as some ATP and then what can these nadhs and these

fadh2s do these can come to the electron transport chain and what happens at the electron transport chain

specifically remember these molecules come to the electron transport chain and they're utilized to make what so these

guys over here will come to the electron transport chain and be utilized to make ATP so as a result you'll

produce a TP which was the overall goal ah it's beautiful

okay so now that we've done that we basically took those Ketone bodies that we took from the liver that we

synthesized in the liver brought them over into the muscles skeletal muscles cardiac muscles and brain and then

utilize them for energy and why the question is why is the brain using that when it can't use like fatty acids

because fatty acids have a hard time being able to cross the bloodb brain barrier Ketone bodies can

okay so now that we brought the Ketone bodies in we can make ATP and now the brain is satisfied because it can

produce some ATP from this reaction okay now I hope all of this made sense ninja ners I hope you guys

enjoyed it I know it was a lot of information thanks for sticking in there with me if you guys did like it this

video hit the like button comment down in the comment section and please subscribe all right Ninja nerds until

next time

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This lecture provides a comprehensive overview of lipid digestion, absorption, and metabolism, detailing the processes that occur from the mouth to the small intestine. Key enzymes, the role of bile, and the transformation of triglycerides into absorbable forms are discussed.

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