Abstract and Introduction
Epidemiological studies indicate that the consumption of fructose-containing caloric sweeteners (FCCS: mainly sucrose and high-fructose corn syrup) is associated with obesity. The hypothesis that FCCS plays a causal role in the development of obesity however implies that they would impair energy balance to a larger extent than other nutrients, either by increasing food intake, or by decreasing energy expenditure. We therefore reviewed the literature comparing a) diet-induced thermogenesis (DIT) after ingestion of isocaloric FCCS vs glucose meals, and b) basal metabolic rate (BMR) or c) post-prandial energy expenditure after consuming a high FCCS diet for > 3 days vs basal,weight-maintenance low FCCS diet. Nine studies compared the effects of single isocaloric FCCS and glucose meals on DIT; of them, six studies reported that DIT was significantly higher with FCCS than with glucose, 2 reported a non-significant increase with FCCS, and one reported no difference. The higher DIT with fructose than glucose can be explained by the low energy efficiency associated with fructose metabolism. Five studies compared BMR after consumption of a high FCCS vs a low FCCS diet for > 3 days. Four studies reported no change after 4–7 day on a high FCCS diet, and only one study reported a 7% decrease after 12 week on a high FCCS diet. Three studies compared post-prandial EE after consumption of a high FCCS vs a low FCCS diet for > 3 days, and did not report any significant difference. One study compared 24-EE in subjects fed a weight-maintenance diet and hypercaloric diets with 50% excess energy as fructose, sucrose and glucose during 4 days: 24-EE was increased with all 3 hypercaloric diets, but there was no difference between fructose, sucrose and glucose. We conclude that fructose has lower energy efficiency than glucose. Based on available studies, there is presently no hint that dietary FCCS may decrease EE. Larger, well controlled studies are however needed to assess the longer term effects of FCCS on EE.
Sugar is a dispensable nutrient, which has been present in low amounts in the human diet throughout most of Man's history. Its consumption however has markedly increased in Europe and North America over the course of the nineteenth and twentieth centuries. In the USA, high-fructose corn syrup (HFCS) has become available since the 1970s, and has in part replaced sugar as a sweetener. Consumption of fructose-containing caloric sweeteners (FCCS), whether as sucrose extracted from cane or beet, or as mixtures of free glucose and fructose as in HFCS, nowadays accounts for about 20% of the average energy intake of the US population.[2,3] Based on the facts a) that the increase in obesity has roughly paralleled the increase in FCCS consumption over the past 50 years,[4,5] b) that FCCS can cause metabolic disorders when present in high amounts in rodents' or primates' diet, c) that adverse metabolic effects of high sucrose diets has been specifically linked to their fructose component in rodents, and d) that fructose is known to be converted into fat to some extent in liver cells, it has been proposed, both in the scientific literature and in the lay press, that FCCS represent a threat to metabolic health.[10–12]
Obesity results from the deposition of fat in subcutaneous and visceral adipose tissue, occurring usually over several months to years. Given that one kg of body fat contains approximately 8000 kcal, total body energy content increases progressively when people gain weight. This obligatorily implies that obesity results of an imbalance between food energy intake and energy expenditure (EE). The hypothesis that fructose, more than the other nutrients present in foods, is mainly responsible for obesity, therefore suggests that it disrupts the complex mechanisms regulating body weight and energy balance, either by increasing food intake or by decreasing EE, at least during periods of active weight gain. The aim of this review was therefore to bring together the results of human studies having assessed the effects of pure fructose or FCCS on EE, and to discuss which metabolic pathways may account for differences between FCCS and glucose.
24-hour EE (24-EE) can be partitioned into basal metabolic rate (BMR), adaptive thermogenesis (including diet-induced thermogenesis (DIT) and adaptive changes in resting metabolism occurring in response to nutritional and thermal factors), and energy expended for physical activity.[15,16] Given the lack of data regarding the effects of FCCS on EE during physical activity, this review focused exclusively on BMR and adaptive thermogenesis.
Nutr Metab. 2013;10(54) © 2013 BioMed Central, Ltd.