Pooled analyses show that although fructose may increase total cholesterol , uric acid , and postpr and ial triglycerides in isocaloric replacement for glucose , it does not appear to be any worse than glucose in its effects on other aspects of the lipid profile , insulin , or markers of nonalcoholic fatty liver disease .
It may also have important advantages over glucose for body weight , glycemic control , and blood pressure .
SUMMARY Depending on the cardiometabolic endpoint in question , fructose has variable effects when replacing glucose .
PURPOSE OF REVIEW Fructose is seen as uniquely contributing to the p and emics of obesity and its cardiometabolic complications .
Much of the evidence for this view derives from the unique biochemical , metabolic , and endocrine responses that differentiate fructose from glucose .
To underst and whether these proposed mechanisms result in clinical ly meaningful modification of cardiovascular risk in humans , we up date a series of systematic review s and meta-analyses of controlled feeding trials to assess the cardiometabolic effects of fructose in isocaloric replacement for glucose .
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
Pooled analyses show that although fructose may increase total cholesterol , uric acid , and postpr and ial triglycerides in isocaloric replacement for glucose , it does not appear to be any worse than glucose in its effects on other aspects of the lipid profile , insulin , or markers of nonalcoholic fatty liver disease .
It may also have important advantages over glucose for body weight , glycemic control , and blood pressure .
SUMMARY Depending on the cardiometabolic endpoint in question , fructose has variable effects when replacing glucose .
PURPOSE OF REVIEW Fructose is seen as uniquely contributing to the p and emics of obesity and its cardiometabolic complications .
Much of the evidence for this view derives from the unique biochemical , metabolic , and endocrine responses that differentiate fructose from glucose .
To underst and whether these proposed mechanisms result in clinical ly meaningful modification of cardiovascular risk in humans , we up date a series of systematic review s and meta-analyses of controlled feeding trials to assess the cardiometabolic effects of fructose in isocaloric replacement for glucose .