Fructose metabolism and noncommunicable diseases: recent findings and new research perspectives.

Abstract

There is increasing concern that dietary fructose may contribute to the development of noncommunicable diseases. This review identifies major new findings related to fructose's physiological or adverse effects. Fructose is mainly processed in splanchnic organs (gut, liver, kidneys) to glucose, lactate, and fatty acids, which can then be oxidized in extrasplanchnic organs and tissues. There is growing evidence that splanchnic lactate production, linked to extrasplanchnic lactate metabolism, represents a major fructose disposal pathway during and after exercise. Chronic excess fructose intake can be directly responsible for an increase in intrahepatic fat concentration and for the development of hepatic, but not muscle insulin resistance. Although it has long been thought that fructose was exclusively metabolized in splanchnic organs, several recent reports provide indirect that some fructose may also be metabolized in extrasplanchnic cells, such as adipocytes, muscle, or brain cells; the quantity of fructose directly metabolized in extrasplanchnic cells, and its physiological consequences, remain however unknown. There is also growing evidence that endogenous fructose production from glucose occurs in humans and may have important physiological functions, but may also be associated with adverse health effects. Fructose is a physiological nutrient which, when consumed in excess, may have adverse metabolic effects, mainly in the liver (hepatic insulin resistance and fat storage). There is also concern that exogenous or endogenously produced fructose may be directly metabolized in extrasplanchnic cells in which it may exert adverse metabolic effects.