Purpose of review
Fructose is consumed in significant amounts in Western diets. An increase in fructose consumption over the past 10–20 years has been linked with a rise in obesity and metabolic disorders. Fructose/sucrose produces deleterious metabolic effects in animal models. This raises concern regarding the short-term and long-term effects of fructose and its risk in humans.
In rodents, fructose stimulates lipogenesis
and leads to hepatic and extrahepatic insulin resistance
, dyslipidaemia and high blood pressure. Insulin resistance
appears to be related to ectopic lipid deposition. In humans, short-term fructose feeding increases de-novo lipogenesis
and blood triglycerides and causes hepatic insulin resistance
. There is presently no evidence for fructose-induced muscle insulin resistance
in humans. The cellular mechanisms underlying the metabolic effects of fructose involve production of reactive oxygen species, activation of cellular stress pathways and possibly an increase in uric acid synthesis.
Consuming large amounts of fructose can lead to the development of a complete metabolic syndrome in rodents. In humans, fructose consumed in moderate to high quantities in the diet increases plasma triglycerides and alters hepatic glucose homeostasis, but does not appear to cause muscle insulin resistance
or high blood pressure in the short term. Further human studies are required to delineate the effects of fructose in humans.