The important thing about sucrose and HFCS is that they are the main sources of fructose in the American diet. As we saw in the previous post, when fructose is metabolized in the liver, it is most likely to be broken down into glycerol 3-phosphate and acyl-coA, which are then assembled into triglycerides, i.e., fat.
Eat fructose, create fat. But that's not the end of the story. Fructose increases glucose metabolism in the liver by mobilizing an enzyme called glucokinase. The liver takes up more glucose than it normally would, and the excess glucose is also synthesized into fat.
In addition to fructose-induced lipogenesis, other long-term effects of fructose have been observed in experimental animals and in humans. Although fructose produces a very small insulin response, long-term use of fructose nevertheless induces insulin resistance, which eventually results in fructose-induced hypertension. Somewhat surprisingly, the low concentration of insulin released after fructose ingestion also means that there is a low satiety response to fructose. It is possible to consume a great deal of fructose without feeling full. Finally, fructose is 10-17 times more effective than glucose in producing Advanced Glycation Endproducts--the crosslinked matrix of proteins and sugars that accumulates in our tissues and stiffens them.
In 1960, the average American consumed approximately 110 pounds of sweeteners per year, mostly in the form of cane and beet sugar. Since then, the use of table sugar has declined, but the use of high fructose corn syrup has more than replaced it. Americans now consume an average of over 140 pounds of sweeteners per year. Because half of those sweeteners by weight is composed of fructose, the potential negative health effects are worth serious consideration.