Recently, much attention has been given to the potentially adverse
metabolic effects of the fructose fraction of these beverages. Fructose,
which is a constituent of both sucrose and HFCS in relatively equal parts
is preferentially metabolized to lipid in the liver, leading to increased
hepatic de novo lipogenesis, dyslipidemia and insulin resistance [89–92].
Fructose consumption has also been shown to promote accumulation of
visceral adiposity, which has extremely serious implications for T2DM
risk [22,93,94]. In a recent study comparing the effects of consuming
glucose or fructose sweetened beverages providing 25% of energy
requirements, after 10-weeks, both groups showed similarweight gain,
but only the fructose group showed a significant increase in visceral
adiposity [22]. In addition, while fasting plasma triglyceride levels only
increased in the glucose group, hepatic de novo lipogenesis, postprandial
triglycerides and markers of altered lipid metabolism and lipoprotein
remodeling such as fasting apoB and small LDL particles significantly
increased in the fructose group [22]. Moreover, fasting plasma glucose
and insulin levels increased and insulin sensitivity decreased in the
fructose group. Of note, Ghanimet al. did not find evidence of oxidative
or inflammatory stress following intake of 300 kcal of fructose or orange
juice while ROS generation and NF-kB binding was significantly increased
after intake of glucose [95]. However, quantities of fructose
contained in SSBs are far greater than those contained in these beverage
preloads [95].