Most systematic review s and meta-analyses from controlled feeding trials have shown that fructose-containing sugars in isocaloric exchange for other carbohydrates do not show evidence of harm and , in the case of fructose , may even have advantages for glycaemic control , especially at small doses .
Nevertheless , trials in which fructose-containing sugars supplement diets with excess energy have shown adverse effects , effects that appear more attributable to the excess energy than the sugar .
There is no unequivocal evidence that fructose intake at moderate doses is directly related with adverse metabolic effects , although there is potentially cause for concern where fructose is provided at high doses or contributes excess energy to diets .
Concerns are growing regarding the role of dietary sugars in the development of obesity and cardiometabolic diseases , including diabetes .
High-fructose corn syrup ( HFCS ) and sucrose are the most important dietary sweeteners .
Both HFCS and sucrose have overlapping metabolic actions with adverse effects attributed to their fructose moiety .
Ecological studies have linked the rise in fructose availability with the increases in obesity and diabetes worldwide .
This link has been largely underpinned by animal models and select human trials of fructose overfeeding at high levels of exposure .
Impaired cellular insulin binding and insulin sensitivity induced by high-fructose feeding in normal subjects.
We have studied whether the sucrose-induced reduction of insulin sensitivity and cellular insulin binding in normal man is related to the fructose or the glucose moiety . Seven young healthy subjects were fed their usual diets plus 1000 kcal extra glucose per day and eight young healthy subjects were fed their usual diets with addition of 1000 kcal extra fructose per day . The dietary regimens continued for 1 week . Before change of diet there were no statistically significant differences between body weight and fasting plasma concentrations of glucose , insulin , and ketone bodies in the two groups studied . High-glucose feeding caused no significant changes in insulin binding or insulin sensitivity whereas high-fructose feeding was accompanied by a significant reduction both of insulin binding ( P less than 0.05 ) and insulin sensitivity ( P less than 0.05 ) . The changes in insulin binding and insulin sensitivity correlated linearly ( r = 0.52 , P less than 0.01 ) . We conclude that fructose seems to be responsible for the impaired insulin binding and insulin sensitivity induced by sucrose
Most systematic review s and meta-analyses from controlled feeding trials have shown that fructose-containing sugars in isocaloric exchange for other carbohydrates do not show evidence of harm and , in the case of fructose , may even have advantages for glycaemic control , especially at small doses .
Nevertheless , trials in which fructose-containing sugars supplement diets with excess energy have shown adverse effects , effects that appear more attributable to the excess energy than the sugar .
There is no unequivocal evidence that fructose intake at moderate doses is directly related with adverse metabolic effects , although there is potentially cause for concern where fructose is provided at high doses or contributes excess energy to diets .
Concerns are growing regarding the role of dietary sugars in the development of obesity and cardiometabolic diseases , including diabetes .
High-fructose corn syrup ( HFCS ) and sucrose are the most important dietary sweeteners .
Both HFCS and sucrose have overlapping metabolic actions with adverse effects attributed to their fructose moiety .
Ecological studies have linked the rise in fructose availability with the increases in obesity and diabetes worldwide .
This link has been largely underpinned by animal models and select human trials of fructose overfeeding at high levels of exposure .