Induction of metabolic syndrome by excess fructose consumption

Fructose is an important nutritive component of foods such as honey and fruit, but this easily available sweetener may contribute to increased caloric consumption from overeating. Fructose is now a major component of the Western diet, with increased consumption associated with obesity, metabolic syndrome, and cardiovascular disorders in observational and short-term intervention studies, mainly in animal models. Rodent studies have identifi ed possible mechanisms for the adverse effects of fructose when ingested in large amounts. Fructose promoted de novo lipogenesis, infl ammation, and increased sympathetic tone. These mechanisms induced hepatic insulin resistance, increased total and visceral fat mass with accumulation of ectopic fat in the liver and skeletal muscle, and dyslipidemia. Fructose reduced leptin and insulin signals for satiety, caused structural and functional damage to the heart and blood vessels, and disrupted the diversity of the gut microbiota. These early effects may initiate the development of the metabolic syndrome. Despite this evidence from rodents, there are few long-term intervention studies in humans, especially at a moderate dose. The defi nition of prudent fructose consumption is needed, but this will require carefully controlled dose–response studies in humans