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Zuckley et al. (2007) have recently repeated the same study design to compare hormonal and
appetitive responses to HFCS and sucrose in obese and overweight women. Preliminary indings
showed that these responses to HFCS and sucrose do not differ signiicantly in persons carrying
excess body weight. Similar blood glucose and hormones, as well as appetite ratings and ad libitum
energy intake, were seen with the consumption of HFCS and sucrose.
Monsivais et al. (2007) worked on a preliminary study that compared cola sweetened with
sucrose, HFCS-55, HFCS-42, or aspartame; 1%-fat milk; and a no-beverage control in 37 adults in
a randomized paired design. Hunger and satiety ratings did not differ signiicantly among the bever-
age treatments. Relative to the two no-energy treatments, energy intake compensation was similar
among the four energy-containing drinks at the meal 140 min later. This study examined typical
HFCS loads and found similar appetite responses compared with isocaloric beverages.
Prospective epidemiologic data in adults have associated increases in SSBs with weight gain
(Schulze et al. 2004). Together, these studies imply that increased energy intake by sweetened bev-
erages is not compensated for in subsequent intake, which may lead to overconsumption.
However, these studies do not determine whether HFCS may be more of a factor in weight
gain than other caloric sweeteners nor do they speciically address the implications of total dietary
HFCS from all sources on energy intake and body weight.
Stanhope and Havel (2008) have investigated two hypotheses regarding the effects of fruc-
tose consumption: (1) the endocrine effects of fructose consumption favor a positive energy bal-
ance and (2) fructose consumption promotes the development of an atherogenic lipid proile. In
previous short- and long-term studies, they showed that the consumption of fructose-sweetened
beverages with three meals results in lower 24-h plasma concentrations of glucose, insulin, and
leptin in humans than does the consumption of glucose-sweetened beverages. They have also
tested whether the prolonged consumption of high-fructose diets leads to increased caloric intake
or decreased energy expenditure, thereby contributing to weight gain and obesity. Results from
a study conducted in rhesus monkeys produced equivocal results. Carefully controlled and ade-
quately powered long-term studies are required to address these hypotheses. In both short- and
long-term studies, they showed that the consumption of fructose-sweetened beverages substan-
tially increases postprandial triacylglycerol concentrations compared with glucose-sweetened bev-
erages. In the long-term studies, apolipoprotein B concentrations were also increased in subjects
consuming fructose but not in those consuming glucose. Data from a short-term study compar-
ing the consumption of beverages sweetened with fructose, glucose, HFCS, and sucrose suggest
that HFCS and sucrose increase postprandial triacylglycerol to an extent comparable with that
induced by 100% fructose alone. Increased consumption of fructose-sweetened beverages along
with increased prevalence of obesity, metabolic syndrome, and type 2 diabetes underscores the
importance of investigating the metabolic consequences of fructose consumption in carefully con-
trolled experiments.
Similarly, Stanhope et al. (2008) carried out a short-term study suggesting that consuming
HFCS- and sucrose-sweetened beverages increases postprandial triacylglycerol concentrations to
the same degree as fructose alone. Similar results in both short- and long-term studies have shown
that fructose consumption substantially increases postprandial triacylglycerol concentrations (Teff
et al. 2004; Swarbrick et al. 2008).
11.5.8 honey and Weight Gain
Honey is a naturally occurring sweetener that contains simple and complex sugars, as well as
vitamins, minerals, acids, and enzymes. Limited clinical studies have shown that honey has a lower
GI than sucrose (Shambaugh et al. 1990) and that honey, sucrose, and fructose do have differential
effects on blood glucose levels (Samanta et al. 1985; Al-Waili 2003, 2004).
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