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.