Insulin stimulates the transport of glucose into the fat cells, thereby effectively controlling the production of glycerol phosphate, the fixing of free fatty acids as triglycerides, and all that follows. The one fundamental requirement to increase the flow of fatty acids out of adipose tissue—to increase lipolysis—and so decrease the amount of fat in our fat tissue, is to lower the concentration of insulin in the bloodstream. In other words, the release of fatty acids from the fat cells and their diffusion into the circulation require “only the negative stimulus of insulin deficiency,” as Yalow and Berson wrote. By the same token, the one necessary requirement to shut down the release of fat from the fat cells and increase fat accumulation is the presence of insulin. When insulin is secreted, or the level of insulin in the circulation is abnormally elevated, fat accumulates in the fat tissue. When insulin levels are low, fat escapes from the fat tissue, and the fat deposits shrink.
All other hormones will work to release fatty acids from the fat tissue, but the ability of these hormones to accomplish this job is suppressed almost entirely by the effect of insulin and blood sugar. These hormones can mobilize fat from the adipose tissue only when insulin levels are low—during starvation, or when the diet being consumed is lacking in carbohydrates. (If insulin levels are high, that implies that there is plenty of carbohydrate fuel available.) In fact, virtually anything that increases the secretion of insulin will also suppress the secretion of hormones that release fat from the fat tissue. Eating carbohydrates, for example, not only elevates insulin but inhibits growth-hormone secretion; both effects lead to greater fatty-acid storage in the fat tissue.