Consumption of simple sugars (monosaccharides) such as fructose has risen markedly in the American diet since the 1970s. This is due in large part to the development of high fructose corn syrup (HFCS), which is produced by the enzymatic conversion of glucose (also known as dextrose) to fructose (Hanover and White 1993). The most popular form of HFCS is comprised of 55% fructose (Hanover and White 1993; Park and Yetley 1993). Compared to sucrose, fructose is preferred by food manufacturers for several reasons: fructose is sweeter, and HFCS can be easily produced at a low cost. It has also been found to enhance flavors of foods such as caramel and chocolate (Park and Yetley 1993; Bray, Nielsen et al. 2004).

Fructose comprises approximately 8% of the total daily energy intake in the United States (Park and Yetley 1993; Havel 2005). This percentage includes both naturally occurring sources, such as fruits and vegetables, and added sources such as HFCS, sucrose (50% fructose), concentrated fruit juices, andcrystalline fructose. Food consumption surveys conducted in 2006 indicate that teenagers (ages 12-18 years) consume the most fructose. Approximately 12.17% of their total energy intake is from fructose, the highest percentage of which comes from non-alcoholic, non-100% juice beverages (NHANES, unpublished). The per capita use of HFCS ncreased from 0.23 kg in 1970 to 28.4 kg in 1997 (Putnam, Allshouse et al. 2002).

Increased consumption of HFCS is positively correlated with the increase in obesity in the United States (Elliott, Keim et al. 2002; Bray, Nielsen et al. 2004). Ingesting a high amount of fructose can produce obesity and related problems for a number of reasons. The main organ in the body that metabolizes fructose is the liver (Topping and Mayes 1972). This metabolism produces glyceraldehyde and dihydroxyacetone phosphate, which enter the gluconeogenic pathway. Phosphofructokinase (PFK) is the rate-limiting enzyme that determines the level of glucose production. Fructose metabolites enter the pathway after the PFK step, which results in uncontrolled production of triacylglyceride (TG) precursors and glucose (Kelley, Allan et al. 2004; Basciano, Federico et al. 2005; Havel 2005). Consequently, the liver produces TGs, which are in turn metabolized into free fatty acids (FFA). Another product of fructose metabolism acetyl-CoA, is a precursor for FFA (Havel 2005). Accumulation of these fats in the liver leads to a number of hepatic diseases, including nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) (Cave, Deaciuc et al. 2007). This increase in FFA in the liver also results in the elevation of blood levels of TGs and FFA (Sleder, Chen et al. 1980; Zavaroni, Chen et al. 1982; Bantle, Raatz et al. 2000). Circulating FFA stimulate insulin release (Crespin, Greenough et al. 1969). Insulin, in turn, perpetuates the buildup of FFA, as insulin reduces oxidation (lipolysis) of FFA (Cave, Deaciuc et al. 2007). Increases in FFA can cause insulin insensitivity by escalating intramyocellular lipids (Elliott, Keim et al. 2002).

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