Fat Metabolism Explained

While you may not feel the need to read this chapter, because it could be too complicated, I will make it simple to understand in laymen’s terms by using an analogy. The analogy will be the entire cycle of a car from it’s start at the manufacturing plant to it’s end at the recycling yard.

In a fat cell we have two pools of fat. In one of the pools more fat (TAG) is being manufactured and in the other it is being broken down for parts. When TAG is broken down the components are FFA’s and glycerol. . The FFA’s can be recycled back into TAG or they can be eliminated from the cell. When the FFA’s are eliminated from the cell, that is the process called lipolysis. The glycerol is always expelled from the cell because it cannot be used by the fat cell. In the kidney and liver glycerol can be turned back into glucose.

TAG is the main component of the fat cell and is broken down and recycled continuously. When it is broken down the components are FFA’s and glycerol. Glycerol is always eliminated from the cell. FFA’s can be recycled back into TAG. This manufacturing and recycling takes place regardless of the presence of insulin. Lack of insulin allows for the release of FFA’s into the plasma which is lipolysis.

Let’s look at the manucturing and recycling analogy now. Let TAG be a ‘completed car’ direct from the manufacturing plant. The TAG cannot, however, be driven because it has a small add on, namely that white plastic you see on the hood and roof of a new car. The white plastic is equal to glycerol. Now that the car is ‘ready to drive’ will we call it an FFA. A road ready car is an FFA. If there is nowhere for the car (FFA) to be driven it is sent to the recycling plant. There it is reformed into a ‘completed car’ (TAG) by putting new white plastic (glycerol) back on until road ready cars are needed.

If the cell is not engaged by insulin, FFA’s will leave the cell which is the process of lipolysis. Let the cell membrane be the intersection where cars flow out into the rest of the world. The insulin receptor is the traffic light. The red light is insulin. The process of lipolysis is equal to cars leaving the lot.

Now let’s look at the process in the absence of insulin which is lipolysis. The manufacturing plant sends out completed cars (TAG). These completed cars (TAG) are broken down into cars (FFA’s) and white plastic (glycerol). The white plastic (glycerol) is discarded. There is no insulin (red light) on at the traffic light (receptor) at the intersection (cell membrane). With no insulin (red light) the process of lipolysis (flow of cars (FFA’s) leaving the lot) continues. So, you can see that in the absence of insulin the process is rather simple. TAG is broken down into FFA’s and glycerol. Glycerol always leaves the cell and FFA’s leave the cell when insulin is not present on the insulin receptor at the cell membrane. That entire process of FFA’s leaving the cell is lipolysis.


Inhibition does not equal activation.


Lipolysis continues until insulin makes itself present on the surface of the cell. But is the presence of insulin an inhibitor or an activator? Again, this may seem to be a technical discussion that maybe you can skip over, but it is key you understand this concept so you will be able to see why all your previous diets have failed and even why eating 5-6 small meals a day which is recommended by nearly everyone is making you fat.

When I started to look at this whole lipolytic process and the research behind it. something struck me as strange and seemed to be missing from the explanations offered by the medical and sports communities alike. The term ‘inhibition’ kept coming up as in, ‘Insulin is an inhibitor of lipolysis.’ In hormones that act on fat cells for lipolysis, the word antagonist kept coming up as in, ‘Insulin is an antagonist of glucagon.’ The researchers used these terms over and over again and always in this manner to describe the actions of insulin. In the reall real world, however, I have yet to see an author use it correctly in explanation of the process of lipolysis and how it pertains to diet.. I don’t think they know what it means! Does anyone know what inhibitor means as it pertains to biological functions?

The medical and sports communities describe the lipolytic process (release of FFA’s from the fat cells) in as if inhibition is just the opposite as activation. IT IS NOT! Activation means that a stimuli is required to begin a process. Activation means that a process is not going to happen no matter what until that stimuli is present. Nothing will happen until the activator comes along. Example, pinching my skin activates a pain receptor which causes a pain response. If the pinch is not there, the pain is not there. You have to have an activator to get the response. Again, nothing will happen until the activator is present.

Now, let’s look at an inhibitor. Definition: A substance that decreases or stops the rate of a reaction..This may seem to be picky technical definition, but stick with me and you will soon understand An inhibitor stops or slows down something that was already happening. Insulin is an inhibitor of lipolysis. Insulin STOPS a reaction that would normally take place! The reaction, lipolysis, is running until interrupted by insulin . Notice that the description researchers use does not say, ‘Insulin activates lipogenesis.’ because that is WRONG! Well, how can that be wrong if it is true?. Yes it is true, but it is not CORRECT. To explain the action of insulin as an activator hides the fact that reactions were taking place before the insulin got there! This is why the scientific community DOES NOT describe it as such. Lipolysis would run until all the fat is gone UNLESS insulin comes along to STOP it.

In real life, what can we use as an example of a true inhibitor? Rust is one. On steel, rust is always there on the surface . You can spray paint it with a rust inhibitor, but notice that the paint is not called a rust stopper or steel activator. Why is that? Because rust can NEVER be stopped. It can only by inhibited. Even though you can’t see the rust happening it is still there. One day it bursts through the paint on you car and you have confirmation of its presence. The rust was not activated at the time you saw it, but it was always there.


The same holds true for lipolysis. And brings us back to the car and traffic light example. As illustrated earlier, we have the following: The manufacturing plant sends out completed cars (TAG). These completed cars (TAG) are broken down into cars (FFA’s) and white plastic (glycerol). The white plastic (glycerol) is discarded. There is no insulin (red light) on at the traffic light (receptor) at the intersection (cell membrane). With no insulin (red light) the process of lipolysis (flow of cars (FFA’s) leaving the lot) continues. But remember, that was in the absence or insulin. Also be aware that I did not say, ‘In the presence of glucagon’, because glucagon is not needed for lipolysis. Only lack of insulin is required.


Now we add insulin (red light) to the receptor (traffic light) at the cell membrane (intersection). Manufacturing and recycling at our two plants continues! There is no stopping of the process just because insulin (red light) is present at the cell membrane (intersection) In other words, what is happening at the cell membrane (intersection) has no bearing on manufacturing and recycling, but does stop FFA’s (cars) from leaving the lot because the intersection (cell membrane) is blocked. To make it even simpler, think of it like this: a manufacturing plant is running and products and supplies are going in and out at the front intersection. If the flow of traffic is halted at the intersection for a time by a red light does all or any process inside the plant stop? Certainly not and the same holds true for our fat cell.

But what does happen? The rate of TAG manufacturing to FFA release increasess. Let’s go back to our plant and the cars. The building of completed cars (TAG) increases in relation to the cars (FFA’s) that are released. The completed car (TAG) breakdown and recycling continues as normal. At the cell membrane (intersection) the light (receptor) is red (insulin) and the flow of cars (FFA’s) is inhibited from leaving the lot. Cars (FFA’s) CONTINUE TO MOVE AND BUILD UP BEHIND THE LIGHT!!!!! Since they cannot leave the lot (lipolysis) as we said earlier, the cars (FFA’s) are sent back to be recycled. Leaving the lot (lipolysis) has now been inhibited by the red light (insulin). A red light appears (insulin) appears at the traffic light (receptor) and leaving the lot ( lipolysis is) is inhibited.

That is all there is to it and insulin does nothing more than change the ratio of TAG made to the FFA’s released. The process of lipolysis continues to build up and recycle inside the cell just as cars continues to build up behind a red light at an intersection. We can now see that lipolysis is inhibited by the presence of insulin. Insulin inhibits the FFA’s from leaving.

When the insulin is gone the breakdown of TAG to FFA’s ratio changes and the FFA’s begin to flow out of the cell (lipolysis) again and will continue to do so until insulin is again present. Insulin is used up and lipolysis begins again. When insulin is gone the lipolysis can continue once again.

Can you see the point? Do the cars leaving (lipolysis) need the red light (insulin) to do anything? Does the red light (insulin) activate a manufacturing increase of completed cars (TAG) ? Absolutely not in both cases. Without the presence of the traffic light (insulin receptor) at all, the traffic would still be there. and it would flow continuously and endlessly. Same goes for lipolysis. Without the presence of insulin the lipolysis continues to flow. That is an inhibitor, not an activator. Imagine this, now. We are able, through a great research discovery, to destroy the insulin receptor on the cell membrane on the fat cells. What would happen? Lipolysis (flow of FFA’s out of the cell into the plasma) would continue until all the fat is gone because you have to have insulin for the fat cell to be anabolic with carbohydrates. If no glucose is going into the cell the cells lipolysis cannot be inhibited.


So what does all this mean? Well, for one, you can see that insulin inhibits lipolysis and if insulin is not present we MUST be in lipolysis. Insulin is an activator of lipogenesis or insulin is an inhibitor of lipolysis? What definition have you been led to believe? Either someone doesn’t know their mechanism or you have been intentionally lied to. I

The Next chapter is where we will see how eating multiple meals and complex carbohydrates makes you fat.

Hopefully, by reading the previous chapter you see why we don’t want ANY insulin unless we know it is going to replace glycogen stores. Now, in addition to the fact that carbohydrates are anabolic only to fat cells why would you want an insulin rise throughout the day when the muscles are full and the carbohydrates have nowhere to go. If the carbohydrates don’t go to restoring muscle or liver glycogen they are going to be going towards fat storage.


But isn’t insulin anabolic as we have been told for years?

What is one of the most anabolic hormones we produce. Growth hormone! What is insulin in relation to hGH? It is an antagonist! Insulin is an antagonist to to the most anabolic hormone of the body. So how can insulin then be anabolic? It can’t! Furthermore, hGH and thyroid have a relation as well. If thyroid is low then hGH is low as well. HGH levels of thyroid deficient patients are found to be low, however, oversupplementing or high thyroid causes protein loss. SIf you are antagonizing the effects of insulin all day with your multi-meal regimen you are also going to be reducing your thryroid.

GH is responsible for normal carbohydrate, lipid, nitrogen and mineral metabolism. The growth related effects are primarily mediated by the IGF-1 subfamily. IGF-1 or insulinlike growth factor -1 correlates very similarly with the effects of GH. Does that meant that insulin is anabolic, then?

GH is responsible for protein synthesis and increases the transport of AA’s by a mechanism different from the mechanism of transport. When humans or animals are treated with GH they show a positive nitrogen balance. A positive nitrogen balance means that more muscle is being synthesized than broken down and excreted. The results of positive nitrogen balance show up in decreased plasma amounts of AA’s along with decreased AA’s in the urea.

GH antagonizes the effects of insulin, but GH still increases liver glycogen and lipid metabolism. GH increases the release of FFA’s and causes increased FFA’s in the plasma and increases oxidation of FFA’s (fat burning) in the liver. Are all these benefits something we want to antagonize by loading our bodies with insulin all day.

Glugagon is an antagonist, but it is however, not found in quantity in circulation. When insulin has cleared the pancreas then begins to produce glucagon. The glucagon is dumped into the hepatatic portal vein and the glucagon does not reach general circulation because the liver uses and inactivates it. Glucagon does not have a transport protein and therefore it’s life in circulation is under 5 minutes and glucagon is inactivated by the liver.

Insulin is more anabolic, but IGF-1 and IGF-11 are more potent at stimulating growth.

My one post today. Think about this as I continue to crush the myths!

Anyone ever notice that the ‘anabolic’ hormone insulin is not called ‘growth’ hormone insulin!!!!
Obviously not. This is a bombshell! A prime example of another area in which the medical and sports community has been misleading the public. Anabolism, if you look it up in the dictionary is defined as; synthesis of more complex molecules from simpler ones. Amazing, because that is ALL insulin is responsible for! Insulin does not promote ‘growth’ in any manner. Insulin is responsible for getting more glucose into the cells so the glucose can be made into glycogen Glucose is a simpler molecule and it has been made into a more complex one, glycogen. THAT IS NOT GROWTH! Let glucose be akin to the individual link of a chain. Glucose is a chain link. Glucose is then bound to other chain links to become a longer chain. Does glucose driven by insulin ever become anything else? HELL NO! IT IS STILL A CHAIN! Break it down and nothing has been added or changed. Break a chain link anywhere and you still have nothing but chain links. And finally, glycogen levels in the cell are limited. The chain can only be so long and any additional links will not be added to the chain, but will leak back into the bloodstream for uptake by the fat cells.

Growth is defined as the size or stage of development or completed growth. When glucose is incorporated into glycogen has any stage of development been completed? NO! Glucose is always being chained into glycogen and glycogen is being broken down into glucose over and over. No end development or structure is ever reached. Using our analogy to the chain links, has the chain been developed into wall? Absolutely not! AA’s, with the assistance of the hormones IGF-1, and hGH actually develop into something different. You have many AA’s that must be joined to make a protein. You have many components required to build a wall, such as wood and bricks an mortar. When the wall is completed, can you break it down into individual components any longer? No, because it has been developed into a wall and attempt to break it down will not yield the individual components back, If you rip off a brick you are going to get mortar and maybe some wood on there as well. You can’t break it down because it has been developed into something else. That is growth.

But glucose is anabolic because glucose can be developed into fat, so your argument is false. Well, for one, if you want to take a chemical (insulin) that only has the job of causing anabolism of FAT CELLS, then I don’t know what to tell you. That argument, nevertheless can be invalidated as well. Glucose is broken down into a simpler molecule which enter the mitochondria. This molecule is added to a chain of fatty acids. The production of fatty acids is the addition of molecules. All you are creating is FA’s and the FA’s can never become anything else. Furthermore, the development is never completed which is a requirement of the definition of growth. You just get fatter and fatter as more links are added Has anything been changed? Can fat ever become a wall? No because glucose being added to FA’s is still just increasing the chain length and it never ceases meaning no stage of development has been reached and therefore it is not growth.


No changes or stages of development have been changed. Glucose has just been changed into a more complex form. Glucose has not caused anything to ‘grow’ but glycogen or the length of a FA chain.. We know this to be true because glucose is not involved in the building of protein structures except to supply the ATP via the mitochondria which the enzymes need to synthesize protein structures which in turn results in true growth. All insulin does is supply a molecule which is going to be broken down for energy use! That energy is what enhances protein synthesis.
Why do we need insulin at all? We really don’t except to keep the muscles glycogenated in order that they can supply the enzymes with enough ATP to continue protein synthesis. That is the goal.
We could, in all likelihood, just have a diet of strictly 80-90% protein and 20-10% fat. Such a diet would, nevertheless be hard on the kidneys and liver and would not be very tasty, either. I am not saying that large protein intake is going to cause kidney problems. High dietary protein requires a lot of water to process and this increases water intake and urinary output which does make the kidneys work harder, but that is not inducive to kidney problems.

- insulin is present we now know that it is going to inhibit lipolysis. That being said, why would you want to eat 5-6 meals a day? Every time you eat carbohydrates and get an insulin rise you are going to be inhibiting the lipolytic process. The only time you need an insulin rise is after a workout and in the recovery time period from 2-6 hours. But let’s say, for the sake of argument, that you still believe you need 5-6 meals a day.with carbs to stay anabolic because carbs rise insulin which is anabolic you have been told.

If nothing else, think about what that does to your fat buring. Insulin inhibits lipolysis so every time you eat you have a rise in insulin which is going to decrease your fat burning capacity for that day. The post workout carb pro drink is one meal and your regular meal is the second. 3-4 meals still exist which are raising insulin and stopping lipolysis.


Knowing that unused carbs are going to go towards fat, then why would you want to eat 5-6 meals a day.


I may have not made it clear, but I didn't mean to infer that you could both build muscle and lose fat at the same time of the day. You only want to have an insulin rise at one time of the day, which is when muscle cells are the most sensitive to insulin due to your workout. Why? because fat cells are much more sensitive to insulin at ALL other times than many other tissues and the fat cells will out compete and soak up the glucose. Add that to the fact that you CANNOT put anymore glycogen into the cell if it is fully glycogenated . Without a workout to increase the sensitivity of the muscle the fat would always get more. After a workout you now have muscle competing on a more even playing field for the glucose. All other times of the day you DON'T have any glucose in the blood so how could it not be catabolic to the fat cells. Insulin is anabolic to fat cells and lack of it is catabolic.

As for doing both at the same time I didn't think I was inferring that. As for the insulin having to be antagonized by another hormone, that is not the case. For one, insulin is not perpetual. Two, the controlling factor is the rate of reformation of TAG to the rate of lipolysis within the cell! This happens within the cell at all times IRREGARDLESS of the hormone condition or lack thereof. In other words, you don't need any glucagon or catabolic hormones, because when the cell can no longer match the rate of lipolysis becomes greater than the rate of TAG formation then FFA's build up and are released into the plasma. Now, glucagon and norep and all the hormones you cited can ACCELERATE the rate of FFA formation and release, but it still continues despite their absence.


The best explanation may be to look the body as an entire organism and not just the individual cells. All cells can be anabolic, however, IT IS IN THE BEST INTEREST OF THE ORGANISM FOR THE FAT CELLS TO BE CATABOLIC WITHOUT A STIMULI! The fat cells are the sacrificial lambs in our bodies. All other cells in the body are more important than a fat cell. It is their job to give themselves up for the greater good of the entire organism. They are always trying to be catabolic unless stimulated by insulin.



BTW, the magic chemical that can keep lipolysis going and desensitize fat cells to insulin and in presence of insulin is.........

IGF-1!!