WARNING: THERE’S, LIKE, SCIENCE AND STUFF IN HERE…CONSIDER YOURSELF WARNED.
As I have already explained, calories are not the means by which we get fat. So if not calories, then what?
In a nutshell, the hormone responsible for fat accumulation is insulin. Insulin is “regulated” by the amount of dietary carbohydrates, the more carbs, the more insulin. Protein also impacts insulin levels, but not to the same degree as carbs. Insulin works to simultaneously regulate the storage and use of fat and protein. It works to make sure your muscles and organs have enough protein to repair damage, and it also works to make sure those cells have enough energy for daily use.
How does insulin “decide” how to do that?
That’s a little more involved. Let’s talk fat and enzymes.
Fat exists in two forms: fatty acids and triglycerides. Fatty acids are small enough to enter and exit cellular membranes. Triglycerides are not. Triglycerides are formed in cells by three fatty acids combining with a glycerol molecule. Once that triglyceride is formed, it cannot exit the cell unless it is acted upon by some other chemical or molecule to break it down to its requisite components.
Two enzymes are primarily responsible for how fat is used by cells (stored or burned). Lipoprotein Lipase (LPL) is an enzyme that hangs out on the outside of cell walls and breaks down the triglycerides into their component form fatty acids. It then pulls fatty acids into the cells. If LPL is on a muscle cell, the fat is used for fuel. If LPL is on a fat cell, then the fat is used to make the fat cell fatter. Insulin is the primary regulator for LPL on fat cells, especially belly fat cells. The more insulin in the blood stream, the more active the LPL is on fat cells, and the more fatty acids are shuttled into fat cells. Bigger fat cells continue to get bigger as the levels of insulin continue to increase, because more insulin is triggering more LPL on fat cells…so it’s a downward spiral. Not only that, but insulin decreases LPL activity on muscle cells. It, basically, tells muscle cells to stop using fat as a fuel source and to use carbs instead. This causes even more fat to be stored in our fat cells.
The second enzyme that insulin influences is Hormone Sensitive Lipase (HSL). As LPL works to make fat cells bigger, HSL does the opposite. It works to make fat cells smaller. It does this by working inside fat cells to break down triglycerides into fatty acids and releasing those fatty acids into the blood stream to be used for fuel. This is the “miracle enzyme” of fat loss. And insulin represses it. Larger amounts of insulin mean lower activity of HSL. That’s the bad news. The worse news is it only takes a little insulin to do this. So even a small increase in insulin can repress HSL activity. And that just sucks.
Insulin also activates a mechanism in fat cells to pump glucose into the cells. This allows the fat cells to increase the amount of glucose it burns. One of the byproducts of glucose metabolism is glycerol. These newly formed glycerol molecules float around the cells and combine with the fatty acids to form triglycerides, which cannot leave the fat cells, so it results in more stored fat (bigger fat cells).
Insulin also works to make sure there are enough fat cells to store all the excess fat. If fat cells are getting too full, insulin makes more. It also sends signals to the liver, telling the liver not to burn fatty acids, but to form them into triglycerides and to move them back to the fat cells.
So it would seem that everything insulin does, with regard to fat loss or fat accumulation, is designed to make us increase fat storage and decrease fat usage. In a nutshell, insulin works very hard to make people fatter.
This also shows that the primary factor responsible for fat accumulation is increased levels of insulin. If that is lowered, more fat can be mobilized from cells and used as fuel. That’s best accomplished in a ketogenic lifestyle.