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Fat burning 101 – where the lipolysis that matters happens
If you’re metabolically challenged, glucose levels are often higher than they should be, because there is a delivery problem. Now in the case of glucose, the problem stems from the fact that ………….
The GLUT4 gate doesn’t respond insulin.
So glucose levels accumulate in the blood and get up to all sorts of mischief.
But glucose is not the only nutrient which is NOT being delivered. Fats are higher too – this manifests as hypertriglyceremia. And it’s often the first manifestation of metabolic troubles.
A hint of metabolic troubles
High triglyceride levels are officially part of metabolic syndrome aka insulin resistance. But the connection between them and insulin is NOT OBVIOUS, because insulin doesn’t directly handle fats. But since insulin is in charge of putting away the groceries and fats are an important grocery, insulin definitely influences what happens to them.
However, in people who are insulin resistant, unlike with glucose, insulin has no problem putting away fat…..
Or does he ?
Heaps of “particles”
In the metabolically challenged there are an awful lot of fat containing particles doing the rounds.
The thinking is the liver is going crazy, shipping them out.
And an extension of this is…………….. the fats are high, because you’re eating too much fat.
But it’s not that simple. Cells must first take delivery of those triglycerides, before they can be burned for energy. The particles are big and bulky. And THERE IS NO GATE !
So it’s complicated….
Adding to the difficulties, there are two ways triglycerides can be delivered.
You either eat the fats or you take advantage of the fats that have been stored, for rainy days. Some of us have supplies that could last for 40 days and nights. Lol !
- If the fats are coming from dinner, they are being carried in chylomicrons, which are enormous conglomerates of triglycerides, assembled by the enterocytes in the intestine.
- If the fats are coming from stores, they’re being carried in lipoproteins, which are put together by the liver.
The lipoprotein we are most familiar with is LDL – this is where high concentrations of cholesterol are found. What happens to or doesn’t happen to these lipoproteins, gets an awful lot of attention. But, those LDL particles start off as the particles moving triglycerides around.
In this form, they are referred to as VLDL particles. The liver creates them, by packaging lots of triglycerides and small amounts of cholesterol, into a protein shell.
The cholesterol is primarily there to provide structural support.
So what happens to these lipoprotein particles as they whirl around the body at break neck speed ?
They get grabbed by hungry cells…..
GRABBED………….there is NO GATE !
And the hungry cells don’t have direct access to the lipoprotein particles, because the endothelial cells that line the capillaries, are “in the way”.
Now they’re not deliberately obstructing delivery.
In fact, they do what they can to help. So let’s look at how does the transaction play out…………
Ordering a fat delivery
The cell wanting a fat delivery, which could be a heart/muscle or fat cell, negotiates with their nearest endothelial cells, to take a delivery.
The way they negotiate is they make an order.
The order is made, when they ship their lipoprotein lipase enzyme (LPL for short) to the border. Now LPL has an entourage, (which includes lipase maturation factor 1) – which ensures that the LPL is attached to surface of the endothelial cell as it dangles from the side, it is able to flag down a passing lipoprotein.
LPL by the numbers
Now because fat cells are in the business of storing fat, they have a vast array of LPLs on stand by. These guys are typically deployed after dinner. Whereas heart cells and muscle cells, work more on a just in time, model. They deploy LPLs, according to their needs/desires.
For muscle cells, the demand for fat, peaks after a workout, not during one.
NOTE : During workouts they prefer to burn sugar – it’s easier. Click here to learn more.
Processing the order
The endothelial cell then locks onto the LPL via a special transporter protein, called glycosylphosphatidylinositol anchored high density lipoprotein binding protein 1 or GPIHBP1 for short. Eish, what a mouthful, let’s just call it the LPL chaperone.
Now the LPL chaperone is FLEXIBLE.
It allows the LPL to bounce from one side of the endothelial cell to the other and back again.
This helps LPL flag down a lipoprotein particle, when it swings by…
Catching me some fat
Amazingly the LPL with the help of his little chaperone, manages to stop the lipoprotein particle and board it. Once inside he grabs triglycerides and begins slicing and dicing them, to release individual fatty acids and strip the lipoprotein of all it’s triglycerides.
The individual fatty acids and glycerol, exit the lipoprotein.
The free fatty acids that are released are grabbed by the endothelial cell and passed across to the cell that put in the order.
Yes, some spills out.
But, most of it, goes to the cell, that placed the order or his associates.
Empty particles move on
When the lipoprotein has been stripped bare, LPL jumps off, releasing it, to continue on it’s rounds.
- In the case of the chylomicrons, they’re kaput and are referred to as chylomicron remnants. These remnants make their way back to the liver, where they are disassembled for parts.
- In the case of the VLDL particles, with most of the triglycerides gone, what is left is cholesterol – they have morphed to LDL particles. And now become public enemy number one.
The LDL particles proceed on their way, to deliver cholesterol to cells, who are making the call, for this important resource.
The fat fate
If the cell placing the order, was a fat cell, the fats that are taken up are dutifully stored for a rainy day.
NOTE : Fat cells don’t use the fatty acids for fuel. They run on carbs.
All other cells, accessing the fatty acids, use the majority of the fatty acids for fuel, although on occasion, they keep a small stash of fats on hand, for emergencies.
So what can go wrong ?
Lots if you’re insulin resistant.
The chemistry of fats is complicated. High fat levels are not because you stacked your plate with butter, meat, cream and eggs – your body made those fats.
When fats are burned, they’re consumed by FIRE, generating heat. It makes sense. But, this picture of fat burning, is not scientifically accurate…..
Busy fat cells sometime need to take a break, so built into the fat cell’s milieu, is an enzyme or two, that “neutralizes” the testosterone squeeze.