The simple explanation is that the insulin induced by the carbohydrates serves to deposit both fats and carbohydrates (fatty acids and glucose) as fat in the adipose tissue, and it keeps those calories fixed in the adipose tissue once they get there. As long as we respond to the carbohydrates by secreting more insulin, we continue to remove nutrients from our bloodstream in expectation of the arrival of more, so we remain hungry, or at least absent any feeling of satiation. It’s not so much that fat fills us up as that carbohydrates prevent satiety, and so we remain hungry.

The second observation is the carbohydrate craving associated with obesity. Here the metabolic background of hunger is established by chronic hyperinsulinemia rather than the immediate insulin secretion during a carbohydrate-rich meal. In both cases the insulin induces hunger or prevents satiety. In the case of hyperinsulinemia and obesity, however, this happens even between meals, when the cells should be living off a fuel mixture of predominantly fatty acids. Instead, the insulin traps the fat in the fat tissue, and it signals the cells to burn glucose. As far as the body is concerned, the elevated insulin is the indication that we’ve just eaten—“high levels of insulin herald the ‘fed’ state,” as George Cahill put it—and the signal that carbohydrates are available to be burned. But in this case, they’re not. Now the homeostatic system that evolved to maintain blood sugar in a healthy range establishes an internal environment in which the cells are primed to burn glucose for fuel, and only glucose can satisfy that demand, yet there’s no expendable glucose in the system. High insulin levels even prevent the liver from releasing the glucose that’s stored there as glycogen. As a result, it’s glucose that we crave. Even if we eat fat and protein—our cheese slices, for instance—the hyperinsulinemia will work to store these nutrients rather than allow them to be used for fuel.