High-fructose corn syrup (HFCS) accounts for as much as 40% of caloric sweeteners used in the United States. Some studies have shown that short-term access to HFCS can cause increased body weight, but the findings are mixed. The current study examined both short- and long-term effects of HFCS on body weight, body fat, and circulating triglycerides. In Experiment 1, male Sprague-Dawley rats were maintained for short term (8 wks) on (1) 12-h/day of 8% HFCS, (2) 12-h/day 10% sucrose, (3) 24-h/day HFCS, all with ad libitum rodent chow, or (4) ad libitum chow alone. Rats with 12-h access to HFCS gained significantly more body weight than animals given equal access to 10% sucrose, even though they consumed the same number of total calories but fewer calories from HFCS than sucrose. In Experiment 2, the long-term effects of HFCS on body weight and obesogenic parameters, as well as gender differences, were explored. Over the course of 6 or 7 months, both male and female rats with access to HFCS gained significantly more body weight than control groups.
This increase in body weight with HFCS was accompanied by an increase in adipose fat, notably in the abdominal region, and elevated circulating triglyceride levels. Translated to humans, these results suggest that excessive consumption of HFCS may contribute to the incidence of obesity. The introduction of high-fructose corn syrup (HFCS) as a cost-effective sweetener in the American diet has gradually led to a great increase in its use. From 1970 to 1990, consumption of HFCS increased more than 1000% and currently accounts for 40% of all added caloric sweeteners (Bray et al., 2004; Bray, 2010). The increase in HFCS use was accompanied by a decline in sucrose use during the same time period (Anderson, 2007). One common source of HFCS is caloric beverages (i.e., soft-drinks, colas). It is also a primary ingredient in baked goods, many cereals, breads, canned fruits, jams and jellies, desserts, and fruit juices (Hanover and White, 1993). It is estimated that nearly 7% of daily caloric consumption in the United States is from HFCS, an estimate that has been labeled as conservative (Bray et al., 2004). Other studies indicate that over 10% of daily calories come from fructose, of which 75% (in adults) and 82% (in children) is attributed to added sweeteners rather than naturally occurring fructose (Vos et al., 2008). Given its prevalence in the American diet, it is crucial to understand the behavioral and physiological effects of dietary HFCS.
The rise in obesity that has occurred since the introduction of HFCS into the American diet suggested a link between the two (Bray, 2008; Elliott et al., 2002). However, many have refuted the conjecture that HFCS alone is at fault, suggesting that sugars in general are the problem (Melanson et al., 2008). Some studies indicate that HFCS and sucrose elicit similar post-metabolic profiles (Melanson et al., 2008; Stanhope et al., 2008), but there are differences in how these sugars are metabolized and utilized in the body. HFCS-55 is 55% fructose, 42% glucose and 3% higher saccharides (White, 2008). Meals high in fructose have been shown to reduce circulating insulin and leptin levels in women (Teff et al., 2004). Thus, intake of HFCS would presumably not produce the degree of insulin or supplement for a balanced lifestyle leptin-induced satiety that would ensue with a meal of sucrose, potentially fueling overeating. The question investigated here is whether or not a standard diet supplemented with HFCS can cause obesity in male and female out-bred rats.
Male and female Sprague-Dawley rats were obtained from Taconic Farms (Germantown, NY) and housed individually on a reversed 12-h light: 12-h dark cycle. 10/group) were fed either (1) ad libitum chow, (2) 24-h HFCS and chow, (3) 12-h HFCS and ad libitum chow, or (4) 12-h sucrose with ad libitum chow for 8 weeks (2 months). We selected these schedules to allow comparison of intermittent and continuous access, as our previous publications show limited (12-h) access to sucrose precipitates binge-eating behavior (Avena et al., 2006). The 12-h groups had access to sugar (HFCS or sucrose) starting 4 h into the dark phase each day. These sugars were selected because they are the primary sweeteners in many soft-drinks. HFCS was an 8% solution (Nature’s Flavors®, Formula 55, v/v dissolved in tap water, 0.24 Kcal/mL), and sucrose was given as a 10% solution (Domino® Granulated Pure Cane Sugar, w/v, dissolved in tap water, 0.4 Kcal/mL). 5001, PMI, St. Louis, MO, 3.02 kcal/g). All animals had water available ad libitum (see Table 1 supplement for a balanced lifestyle complete list of diets). Summary of experiments, diets and final body weight.
Science continues to prove that the old adage "you are what you eat" is profoundly true. This is because you have trillions of microorganisms living in your gut, which are directly responsible for nearly every aspect of your health. These microbes make up what’s called your "gut microbiota." They are especially influential in determining your likelihood of gaining excessive weight, becoming obese, and developing obesity-related diseases like diabetes, heart disease, and premature death. The gut microbiome (the expressed genes of your gut microbiota) plays a major role in your metabolism through energy production, storage, and expenditure. So, it’s no surprise that science has found a strong connection between gut microbiome imbalance and metabolic syndrome. Yikes! If you have the wrong mix of microbes, it could be making it tough for you to get your health on track! Did you know: Scientists can actually look at your gut microbiome composition and tell with 90% accuracy if you are obese or lean. That’s pretty impressive, isn’t it?