Good Calories, Bad Calories

Some of these free fatty acids will be taken up by the tissues and organs and used as fuel. Perhaps as much as half of them will not. These will be incorporated in the liver back into triglycerides, loaded on lipoproteins,^*115 and shipped back again to the fat tissue. And so fatty acids are continuously slipping from the fat tissue into the circulation, while those fatty acids that aren’t immediately taken up and used for fuel are continuously being reconverted to triglycerides and transported back to the fat tissue for storage. “The storage of triglyceride fat in widely scattered adipose tissue sites is a remarkably dynamic process,” explained the University of Wisconsin endocrinologist Edgar Gordon in 1969, “with the stream of fatty acid carbon atoms flowing in widely fluctuating amounts, first in one direction and then the other in a finely adjusted minute by minute response to the fuel requirements of energy metabolism of the whole organism.”

This remarkably dynamic process, however, is regulated by a remarkably simple system. The flow of fatty acids out of the fat cells and into the circulation depends on the level of blood sugar available. The burning of this blood sugar by the cells—the oxidation of glucose—depends on the availability of fatty acids to be burned as fuel instead.

A single molecule plays the pivotal role in the system. It goes by a number of names, the simplest being glycerol phosphate. This glycerol-phosphate molecule is produced from glucose when it is used for fuel in the fat cells and the liver, and it, too, can be burned as fuel in the cells. But glycerol phosphate is also an essential component of the process that binds three fatty acids into a triglyceride. It provides the glycerol molecule that links the fatty acids together.^†116 In other words, a product of carbohydrate metabolism—i.e., burning glucose for fuel—is an essential component in the regulation of fat metabolism: storing fat in the fat tissue. In fact, the rate at which fatty acids are assembled into triglycerides, and so the rate at which fat accumulates in the fat tissue, depend primarily on the availability of glycerol phosphate. The more glucose that is transported into the fat cells and used to generate energy, the more glycerol phosphate will be produced. And the more glycerol phosphate produced, the more fatty acids will be assembled into triglycerides. Thus, anything that works to transport more glucose into the fat cells—insulin, for example, or rising blood sugar—will lead to the conversion of more fatty acids into triglycerides, and the storage of more calories as fat.

This brings us to the mechanisms that control and regulate the availability of fat and carbohydrates for fuel and regulate our blood sugar in the process.

The first is the triglyceride/fatty-acid cycle we just discussed. This cycle is regulated by the amount of blood sugar made available to the fat tissue. If blood sugar is ebbing, the amount of glucose transported into the fat cells will decrease; this limits the burning of glucose for energy, which in turn reduces the amount of glycerol phosphate produced. With less glycerol phosphate present, fewer fatty acids are bound up into triglycerides, and more of them remain free to escape into the circulation. As a result, the fatty-acid concentration in the bloodstream increases. The bottom line: as the blood-sugar level decreases, fatty-acid levels rise to compensate.

If blood-sugar levels increase—say, after a meal containing carbohydrates—then more glucose is transported into the fat cells, which increases the use of this glucose for fuel, and so increases the production of glycerol phosphate. This is turn increases the conversion of fatty acids into triglycerides, so that they’re unable to escape into the bloodstream at a time when they’re not needed. Thus, elevating blood sugar serves to decrease the concentration of fatty acids in the blood, and to increase the accumulated fat in the fat cells.