ABSTRACT
Fructose has been a part of the human diet for many thousands of years, and it is found in highest concentrations in fruits and to a lesser degree in vegetables. Cane, beet, and corn sugars are produced industrially, and their use results in significant quantities of added sugars entering the diet, about half of which is fructose [1]. Cane and beet sugars are comprised of the disaccharide sucrose (glucose bonded to fructose) and are commonly called table sugar or simple sugar. Corn sugars come from corn starch, and mainly consist of high fructose corn syrup 55 (HFCS 55; 55% fructose-41% glucose), HFCS 42 (42% fructose-52% glucose), and corn syrup (glucose and oligoglucose with trace amounts of fructose). During the last several decades, the prevalence of obesity and metabolic syndrome has risen dramatically on a global basis, but more so in the U.S. population. Because the prevalence is chronologically and statistically correlated with the increase of added sugar intakes, particularly HFCS in the U.S. (HFCS is not consumed significantly outside the U.S.), some have proposed the intake of HFCS or fructose as a free monosaccharide may be a cause of various adverse health consequences [2]. Conventional clinical trials and ecological studies have been conducted to assess the hypotheses, but not all results are found to be supportive. Conventional studies often cannot reveal details of interconnecting metabolic pathways when testing fructose
or fructose-containing sugars, but they also cannot clearly distinguish a mechanistic cause associated with an observed physiological consequence linked to the sugar consumed. This is because the ordinary diet contains multiple forms of saccharides which are inter-convertible in the body and share many steps of the carbohydrate metabolism pathways.
