Fructosa y resistencia a la insulina

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  • Publicado : 16 de febrero de 2011
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Special Article

Fructose, weight gain, and the insulin resistance syndrome1–3
Sharon S Elliott, Nancy L Keim, Judith S Stern, Karen Teff, and Peter J Havel
ABSTRACT This review explores whether 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 disappearancedata 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 cells, the consumption of foods and beverages containingfructose 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 thereforeincrease 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, hypertriacylglycerolemia, and hypertension in animal models. The data in humans are less clear. Although there are existing data onthe 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. Am J Clin Nutr 2002;76:911–22. KEY WORDS Fructose, leptin,weight gain, insulin resistance, triacylglycerol, hypertension, obesity, review is responsible for the increased prevalence of moderate obesity, environmental elements—interacting with predisposing genetic factors—clearly must be involved (1). Identification of the acquired causes contributing to an increase in the prevalence of obesity is necessary to develop public health policy and dietary andphysical activity recommendations that are both comprehensive and effective in reversing the current trend. The purpose of this review is to explore whether the increased consumption of dietary fructose might be one of the environmental factors contributing to the development of obesity and the accompanying abnormalities of the insulin resistance syndrome. The insulin resistance syndrome is acluster of related variables that appears to be of major importance in the pathogenesis of coronary artery disease. The syndrome originally included resistance to insulin-stimulated glucose uptake, glucose intolerance, hyperinsulinemia, hypertension, dyslipidemia characterized by high triacylglycerol concentrations, and low concentrations of HDLs (6). More recently, the list of abnormalities has beenexpanded to include central obesity (7); small, dense LDLs (8); increased uric acid concentrations (9); higher circulating concentrations of plasminogen activator inhibitor 1 (10); and decreased circulating concentrations of adiponectin (11). In addition, a link between local adipose steroid metabolism and the insulin resistance syndrome has been suggested by reports that the activity of 11-hydroxysteroid dehydrogenase (EC 1.1.1.146) is increased in the adipose tissue of obese humans (12). Increased expression of this enzyme, specifically in adipose tissue, was shown recently to induce visceral obesity, insulin-resistant diabetes, and hyperlipidemia in a transgenic mouse model (13). The terms syndrome X, metabolic syndrome, and insulin resistance syndrome have been used in the literature...
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