Dietary fructose and the metabolic syndromeMiller, Abigale; Adeli, KhosrowCurrent Opinion in Gastroenterology: March 2008 - Volume 24 - Issue 2 - p 204–209 doi: 10.1097/MOG.0b013e3282f3f4c4 Nutrition: Edited by David H. Alpers and William F. Stenson Abstract Author InformationAuthors Article MetricsMetrics Purpose of review Fructose, a naturally found sugar in many fruits, is now commonly used as an industrial sweetener and is excessively consumed in Western diets. High fructose intake is increasingly recognized as causative in development of prediabetes and metabolic syndrome. The mechanisms underlying fructose-induced metabolic disturbances are unclear but are beginning to be unravelled. This review presents recent findings in this field and an overall mechanistic insight into the metabolic effects of dietary fructose and its role in metabolic syndrome. Recent findings Recent animal studies have confirmed the link between fructose feeding and increased plasma uric acid, a potentially causative factor in metabolic syndrome. Advanced glycation end products are also implicated because of their direct protein modifications and indirect effects on inflammation and oxidative stress. Human studies have demonstrated fructose's ability to change metabolic hormonal response, possibly contributing to decreased satiety. Summary There is much evidence from both animal models and human studies supporting the notion that fructose is a highly lipogenic nutrient that, when consumed in high quantities, contributes to tissue insulin insensitivity, metabolic defects, and the development of a prediabetic state. Recently evidence has helped to decipher the mechanisms involved in these metabolic changes. Molecular Structure & Function, Research Institute, The Hospital for Sick Children, and Department of Biochemistry, University of Toronto, Toronto, Ontario, Canada Correspondence to Khosrow Adeli, Division of Clinical Biochemistry, The Hospital for Sick Children, Toronto, Ontario, M5G 1X8, Canada Tel: +1 416 813 8682; fax: +1 416 813 6257; e-mail: email@example.com © 2008 Lippincott Williams & Wilkins, Inc.