Submitted to: American Journal of Clinical Nutrition
Publication Type: Peer reviewed journal
Publication Acceptance Date: 4/8/2002
Publication Date: 4/8/2002
Citation: Elliott, S.S., Keim, N.L., Stern, J., Teff, K., Havel, P.J. 2002. FRUCTOSE, WEIGHT GAIN, AND THE INSULIN RESISTANCE SYNDROME. American Journal of Clinical Nutrition 76:911-922, 2002. Interpretive Summary: In the United States, the incidence of obesity has increased dramatically in the past decade. One striking dietary change that has occurred in the same time frame is the increased consumption of of the simple sugar fructose. In this review we explored the possibility that the increased consumption of fructose might be a contributing factor to weight gain, the development of obesity, and some of the medical problems associated with obesity: the reduced capacity to maintain blood glucose levels in the normal range; the increase in the circulating levels of the hormone insulin, but a decrease in its effectiveness; an increase in blood lipid levels; and elevated blood pressure. In animal experiments, when dietary fructose increases, blood pressure and circulating levels of blood glucose, insulin, and triglycerides increase, and at extremely high levels of fructose intake, body weight and fatness increases. In humans, the effects of consuming large amounts of fructose are less certain, although the results of some studies are similar to those observed in the animal experiments. More research is needed to better understand if fructose contributes to the development of obesity when consumed in levels typical of the American diet.
Technical Abstract: Fructose consumption might be a contributing factor to the development of obesity and the accompanying metabolic abnormalities observed in the insulin resistance syndrome. The per capita disappearance data for fructose from the combined consumption of sucrose and high-fructose corn syrup have increased by 26%, from 64 g/d in 1970 to 81 g/d in 1997. Both plasma insulin and leptin act in the central nervous system in the long-term regulation of energy homeostasis. Because fructose does not stimulate insulin secretion from pancreatic beta cells, the consumption of foods and beverages containing fructose produces smaller postprandial insulin excursions than does consumption of glucose containing carbohydrate. Because leptin production is regulated by insulin responses to meals, fructose consumption also reduces circulating leptin concentrations. The combined effects of lowered circulating leptin and insulin in individuals who consume diets that are high in dietary fructose could therefore increase the likelihood of weight gain and its associated metabolic sequelae. In addition, fructose, compared with glucose, is preferentially metabolized to lipid in the liver. Fructose consumption induces insulin resistance, impaired glucose tolerance, hyperinsulinemia, hypertriayclglycerolemia, and hypertension in animal models. The data in humans are less clear. Although there are existing data on the metabolic and endocrine effects of dietary fructose that suggest that increased consumption of fructose may be detrimental in terms of body weight and adiposity and the metabolic indexes associated with the insulin resistance syndrome, much more research is needed to fully understand the metabolic effect of dietary fructose in humans.