Abstract
The prevalence of obesity is increasing worldwide. Increasing body weight together with decreasing physical activity is expected to increase the incidence of several diseases related to lifestyle, such as adult type diabetes and vascular atherosclerotic diseases. It has been postulated that increasing consumption of fructose may be a contributory factor in the development of obesity and the accompanying metabolic abnormalities. Most studies supporting these hypotheses, however, are animal studies, which suggest that consumption of high amounts of fructose may stimulate lipogenesis and thus alter lipid metabolism and increase body weight. This review explores the effects of dietary fructose on lipid metabolism in humans, with the conclusion that the data so far do not support any significant specific adverse effect of fructose apart from its energy content. A small amount of fructose may even improve glucose tolerance, and studies to date on diabetic subjects indic ate that isocaloric replacement of some glucose-based carbohydrates with fructose may improve metabolic control. Keywords: cholesterol; diabetes; fructose; oral glucose tolerance; triglycerides
Highlights
The general overall view of physicians and nutritionists on fructose as a dietary component has changed during the past few decades
The hepatic metabolism of fructose in high doses favours lipogenesis, and this may be linked with both hyperlipidaemia and increased body fat stores
Whereas hepatic glucose metabolism is limited by the capacity to store glucose as glycogen and by the inhibition of glycolysis, fructose uptake is not inhibited and consumption of fructose may result in greater increases in circulating lactate than would a comparable amount of glucose (2)
Summary
The general overall view of physicians and nutritionists on fructose as a dietary component has changed during the past few decades. The hepatic metabolism of fructose in high doses favours lipogenesis, and this may be linked with both hyperlipidaemia and increased body fat stores. Fructose is phosphorylated to fructose-1-phosphate, which may be converted to glycerol-3-phosphate or metabolized to acetyl-coenzyme A and incorporated into fatty acids through de novo lipogenesis (5). Through this pathway triglycerides can be formed. Whereas hepatic glucose metabolism is limited by the capacity to store glucose as glycogen and by the inhibition of glycolysis, fructose uptake is not inhibited and consumption of fructose may result in greater increases in circulating lactate than would a comparable amount of glucose (2)
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