Effects of a short-term overfeeding with fructose or glucose in healthy young males. Effects of 4-week very-high-fructose/glucose diets on insulin sensitivity, visceral fat and intrahepatic lipids: an exploratory trial. Effects of fructose vs glucose on regional cerebral blood flow in brain regions involved with appetite and reward pathways. Moderate Amounts of Fructose Consumption Impair Insulin Sensitivity in Healthy Young Men Fructose and insulin sensitivity in patients with type 2 diabetes. Fructose ingestion acutely elevates blood pressure in healthy young humans. Dietary glycemic load, carbohydrate, sugar, and colorectal cancer risk in men and women. Exercise performed immediately after fructose ingestion enhances fructose oxidation and suppresses fructose storage. Consumption of fructose- but not glucose-sweetened beverages for 10 weeks increases circulating concentrations of uric acid, retinol binding protein-4, and gamma-glutamyl transferase activity in overweight/obese humans Dietary Fructose Reduction Improves Markers of Cardiovascular Disease Risk in Hispanic-American Adolescents with NAFLD The effects of glucose, fructose, and sucrose ingestion during exercise. Brain functional magnetic resonance imaging response to glucose and fructose infusions in humans. Differential effects of fructose versus glucose on brain and appetitive responses to food cues and decisions for food rewards Acute effects of feeding fructose, glucose and sucrose on blood lipid levels and systemic inflammation Effects of high-fructose corn syrup and sucrose consumption on circulating glucose, insulin, leptin, and ghrelin and on appetite in normal-weight women. Impaired cellular insulin binding and insulin sensitivity induced by high-fructose feeding in normal subjects. Effects of oral fructose and glucose on plasma GLP-1 and appetite in normal subjects
Consumption of simple carbohydrates has markedly increased over the past decades , and may be involved in the increased prevalence in metabolic diseases . Whether an increased intake of fructose is specifically related to a dysregulation of glucose and lipid metabolism remains controversial . We therefore compared the effects of hypercaloric diets enriched with fructose ( HFrD ) or glucose ( HGlcD ) in healthy men . Eleven subjects were studied in a r and omised order after 7 d of the following diets : ( 1 ) weight maintenance , control diet ; ( 2 ) HFrD ( 3.5 g fructose/kg fat-free mass ( ffm ) per d , + 35 % energy intake ) ; ( 3 ) HGlcD ( 3.5 g glucose/kg ffm per d , + 35 % energy intake ) . Fasting hepatic glucose output ( HGO ) was measured with 6,6 - 2H2-glucose . Intrahepatocellular lipids ( IHCL ) and intramyocellular lipids ( IMCL ) were measured by 1H magnetic resonance spectroscopy . Both fructose and glucose increased fasting VLDL-TAG ( HFrD : + 59 % , P < 0.05 ; HGlcD : + 31 % , P = 0.11 ) and IHCL ( HFrD : + 52 % , P < 0.05 ; HGlcD : + 58 % , P = 0.06 ) . HGO increased after both diets ( HFrD : + 5 % , P < 0.05 ; HGlcD : + 5 % , P = 0.05 ) . No change was observed in fasting glycaemia , insulin and alanine aminotransferase concentrations . IMCL increased significantly only after the HGlcD ( HFrD : + 24 % , NS ; HGlcD : + 59 % , P < 0.05 ) . IHCL and VLDL-TAG were not different between hypercaloric HFrD and HGlcD , but were increased compared to values observed with a weight maintenance diet . However , glucose led to a higher increase in IMCL than fructose An increasing amount of fructose in the diet is suggested to play a causal role in the pathogenesis of the metabolic syndrome , type 2 diabetes and fatty liver . Our aim was to investigate and compare the effects of very high fructose and very high glucose in hyperenergetic diets on glucose and lipid metabolism and on fat depots in healthy humans . We conducted an exploratory , prospect i ve , r and omised , single-blinded , intervention trial . Participants in addition to a balanced weight-maintaining diet received 150 g of fructose or glucose/d for 4 weeks . Insulin sensitivity was estimated from oral glucose tolerance tests . Visceral and subcutaneous abdominal fat was determined with MRI . Liver fat and intramyocellular lipids of the tibialis anterior muscle were measured with (1)H magnetic resonance spectroscopy . A total of twenty healthy subjects ( fructose group n 10 and glucose group n 10 ; twelve males and eight females ) completed the study . They had a mean age of 30·5 ( SEM 2·0 ) years and a mean BMI of 25·9 ( SEM 0·5 ) kg/m(2 ) . Insulin sensitivity appeared to decrease both in the fructose and glucose groups . TAG markedly increased in the fructose group . No strong alterations or treatment effects were found for liver fat , visceral fat , subcutaneous abdominal fat and intramyocellular lipids of the tibialis anterior muscle . In conclusion , the effects of very high fructose and very high glucose in hyperenergetic diets on glucose metabolism and body fat composition were not different in the healthy participants of the present study . However , elevation of plasma TAG seemed to be fructose-specific IMPORTANCE Increases in fructose consumption have paralleled the increasing prevalence of obesity , and high-fructose diets are thought to promote weight gain and insulin resistance . Fructose ingestion produces smaller increases in circulating satiety hormones compared with glucose ingestion , and central administration of fructose provokes feeding in rodents , whereas central ly administered glucose promotes satiety . OBJECTIVE To study neurophysiological factors that might underlie associations between fructose consumption and weight gain . DESIGN , SETTING , AND PARTICIPANTS Twenty healthy adult volunteers underwent 2 magnetic resonance imaging sessions at Yale University in conjunction with fructose or glucose drink ingestion in a blinded , r and om-order , crossover design . MAIN OUTCOME MEASURES Relative changes in hypothalamic regional cerebral blood flow ( CBF ) after glucose or fructose ingestion . Secondary outcomes included whole-brain analyses to explore regional CBF changes , functional connectivity analysis to investigate correlations between the hypothalamus and other brain region responses , and hormone responses to fructose and glucose ingestion . RESULTS There was a significantly greater reduction in hypothalamic CBF after glucose vs fructose ingestion ( -5.45 vs 2.84 mL/g per minute , respectively ; mean difference , 8.3 mL/g per minute [ 95 % CI of mean difference , 1.87 - 14.70 ] ; P = .01 ) . Glucose ingestion ( compared with baseline ) increased functional connectivity between the hypothalamus and the thalamus and striatum . Fructose  increased connectivity between the hypothalamus and thalamus but not the striatum . Regional CBF within the hypothalamus , thalamus , insula , anterior cingulate , and striatum ( appetite and reward regions ) was reduced after glucose ingestion compared with baseline ( P < .05 significance threshold , family-wise error [ FWE ] whole-brain corrected ) . In contrast , fructose  reduced regional CBF in the thalamus , hippocampus , posterior cingulate cortex , fusiform , and visual cortex ( P < .05 significance threshold , FWE whole-brain corrected ) . In whole-brain voxel-level analyses , there were no significant differences between direct comparisons of fructose vs glucose sessions following correction for multiple comparisons . Fructose vs glucose ingestion result ed in lower peak levels of serum glucose ( mean difference , 41.0 mg/dL [ 95 % CI , 27.7 - 54.5 ] ; P < .001 ) , insulin ( mean difference , 49.6 μU/mL [ 95 % CI , 38.2 - 61.1 ] ; P < .001 ) , and glucagon-like polypeptide 1 ( mean difference , 2.1 pmol/L [ 95 % CI , 0.9 - 3.2 ] ; P = .01 ) . CONCLUSION AND RELEVANCE In a series of exploratory analyses , consumption of fructose compared with glucose result ed in a distinct pattern of regional CBF and a smaller increase in systemic glucose , insulin , and glucagon-like polypeptide 1 levels OBJECTIVE Adverse effects of hypercaloric , high-fructose diets on insulin sensitivity and lipids in human subjects have been shown repeatedly . The implication s of fructose in amounts close to usual daily consumption , however , have not been well studied . This study assessed the effect of moderate amounts of fructose and sucrose compared with glucose on glucose and lipid metabolism . RESEARCH DESIGN AND METHODS Nine healthy , normal-weight male volunteers ( aged 21–25 years ) were studied in this double-blind , r and omized , cross-over trial . All subjects consumed four different sweetened beverages ( 600 mL/day ) for 3 weeks each : medium fructose ( MF ) at 40 g/day , and high fructose ( HF ) , high glucose ( HG ) , and high sucrose ( HS ) each at 80 g/day . Euglycemic-hyperinsulinemic clamps with [6,6]-2H2 glucose labeling were used to measure endogenous glucose production . Lipid profile , glucose , and insulin were measured in fasting sample s. RESULTS Hepatic suppression of glucose production during the clamp was significantly lower after HF ( 59.4 ± 11.0 % ) than HG ( 70.3 ± 10.5 % , P < 0.05 ) , whereas fasting glucose , insulin , and C-peptide did not differ between the interventions . Compared with HG , LDL cholesterol and total cholesterol were significantly higher after MF , HF , and HS , and free fatty acids were significantly increased after MF , but not after the two other interventions ( P < 0.05 ) . Subjects ’ energy intake during the interventions did not differ significantly from baseline intake . CONCLUSIONS This study clearly shows that moderate amounts of fructose and sucrose significantly alter hepatic insulin sensitivity and lipid metabolism compared with similar amounts of glucose The effect of dietary fructose ( 20 % of carbohydrate calories , 45 - 65 g day-1 for 4 weeks ) on glycaemic control , serum lipid , lipoprotein and apoprotein A-I and A-II concentrations and on insulin sensitivity was studied in 10 type 2 diabetic patients . The study was done in a r and omized , double-blind fashion with crystalline fructose or placebo administered evenly during 4 meals or snacks per day . The patients were hospitalized throughout the study periods . The fasting plasma glucose concentration decreased during the fructose ( from 10.7 + /- 1.4 mmol l-1 to 8.0 + /- 0.8 mmol l-1 , P < 0.02 ) and the control diet ( from 10.1 + /- 0.9 mmol l-1 to 8.0 + /- 0.7 mmol l-1 , P < 0.05 ) . The mean diurnal blood glucose concentration also fell both during the fructose ( from 10.8 + /- 0.5 mmol l-1 to 8.4 + /- 0.3 mmol l-1 , P < 0.001 ) and the control diet ( from 10.3 + /- 0.3 mmol l-1 to 8.8 + /- 0.9 mmol l-1 , P < 0.01 ) . The HbA1 concentration improved ( P < 0.02 ) only during the fructose diet . Insulin sensitivity increased by 34 % ( P < 0.05 ) during the fructose diet , but remained unchanged during the control period . Serum insulin , triglyceride , apoprotein A-I and A-II concentrations , body weight , blood pressure and blood lactate remained unchanged during both diets . In conclusion , substitution of moderate amounts of fructose for complex carbohydrates can improve glycaemic control and insulin sensitivity in patients with type 2 diabetes Overconsumption of fructose , particularly in the form of soft drinks , is increasingly recognized as a public health concern . The acute cardiovascular responses to ingesting fructose have not , however , been well-studied in humans . In this r and omized crossover study , we compared cardiovascular autonomic regulation after ingesting water and drinks containing either glucose or fructose in 15 healthy volunteers ( aged 21 - 33 yr ) . The total volume of each drink was 500 ml , and the sugar content 60 g. For 30 min before and 2 h after each drink , we recorded beat-to-beat heart rate , arterial blood pressure , and cardiac output . Energy expenditure was determined on a minute-by-minute basis . Ingesting the fructose drink significantly increased blood pressure , heart rate , and cardiac output but not total peripheral resistance . Glucose ingestion result ed in a significantly greater increase in cardiac output than fructose but no change in blood pressure and a concomitant decrease in total peripheral resistance . Ingesting glucose and fructose , but not water , significantly increased blood pressure variability and decreased cardiovagal baroreflex sensitivity . Energy expenditure increased by a similar amount after glucose and fructose ingestion , but fructose elicited a significantly greater increase in respiratory quotient . These results show that ingestion of glucose and fructose drinks is characterized by specific hemodynamic responses . In particular , fructose ingestion elicits an increase in blood pressure that is probably mediated by an increase in cardiac output without compensatory peripheral vasodilatation Hyperinsulinemia may explain excess colorectal cancer among individuals who are overweight or inactive . Recent studies have observed elevated colorectal cancer risk among individuals with elevated insulin levels 2 hours after oral glucose challenge or with elevated plasma C-peptide levels . The effect of consuming a high glycemic diet on colorectal risk , however , remains uncertain . Two prospect i ve cohort studies , the Nurses ' Health Study and the Health Professionals Follow-up Study , contributed up to 20 years of follow-up . After exclusions , 1,809 incident colorectal cancers were available for analyses .  Dietary glycemic load ( GL ) was calculated as a function of glycemic index ( postpr and ial blood glucose response as compared with a reference food ) , carbohydrate content , and frequency of intake of individual foods reported on food frequency question naires . Multivariable Cox proportional hazards models were used to adjust for potential confounders . Intakes of dietary carbohydrate , GL , overall glycemic index , sucrose , and fructose were not associated with  colorectal cancer risk in women . A small increase in risk was observed in men with high dietary GL ( multivariate relative risk , 1.32 ; 95 % confidence interval , 0.98 - 1.79 ; highest versus lowest quintile ) , sucrose or fructose ( multivariate relative risk , 1.37 ; 95 % confidence interval , 1.05 - 1.78 ; highest versus lowest quintile of fructose , P = 0.008 ) . Associations were slightly stronger among men with elevated body mass index ( > or = 25 kg/m(2 ) ) . Results among women were similar after stratifying by body mass index or physical activity . High intakes of GL , fructose , and sucrose were related to an elevated  colorectal cancer risk among men . For women , however , these factors did not seem to increase the risk of colorectal cancer BACKGROUND Exercise prevents the adverse effects of a  high-fructose diet through mechanisms that remain unknown . OBJECTIVE We assessed the hypothesis that exercise prevents fructose-induced increases in very-low-density lipoprotein ( VLDL ) triglycerides by decreasing the fructose conversion into glucose and VLDL-triglyceride and fructose carbon storage into hepatic glycogen and lipids . DESIGN Eight healthy men were studied on 3 occasions after 4 d consuming a  weight-maintenance , high-fructose diet . On the fifth day , the men ingested an oral (13)C-labeled fructose load ( 0.75 g/kg ) , and their total fructose oxidation ( (13)CO2 production ) , fructose storage ( fructose ingestion minus (13)C-fructose oxidation ) , fructose conversion into blood (13)C glucose ( gluconeogenesis from fructose ) , blood VLDL-(13)C palmitate ( a marker of hepatic de novo lipogenesis ) , and lactate concentrations were monitored over 7 postpr and ial h. On one occasion , participants remained lying down throughout the experiment [ fructose treatment alone with no exercise condition ( NoEx ) ] , and on the other 2 occasions , they performed a 60-min exercise either 75 min before fructose ingestion [ exercise , then fructose condition ( ExFru ) ] or 90 min after fructose ingestion [ fructose , then exercise condition ( FruEx ) ] . RESULTS Fructose oxidation was significantly ( P < 0.001 ) higher in the FruEx ( 80 % ± 3 % of ingested fructose ) than in the ExFru ( 46 % ± 1 % ) and NoEx ( 49 % ± 1 % ) . Consequently , fructose storage was lower in the FruEx than in the other 2 conditions ( P < 0.001 ) . Fructose conversion into blood (13)C glucose , VLDL-(13)C palmitate , and postpr and ial plasma lactate concentrations was not significantly different between conditions . CONCLUSIONS Compared with sedentary conditions , exercise performed immediately after fructose ingestion increases fructose oxidation and decreases fructose storage . In contrast , exercise performed before fructose ingestion does not significantly alter fructose oxidation and storage . In both conditions , exercise did not abolish fructose conversion into glucose or its incorporation into VLDL triglycerides . This trial was registered at clinical trials.gov as NCT01866215 Background Prospect i ve studies in humans examining the effects of fructose consumption on biological markers associated with the development of metabolic syndrome are lacking . Therefore we investigated the relative effects of 10 wks of fructose or glucose consumption on plasma uric acid and RBP-4 concentrations , as well as liver enzyme ( AST , ALT , and GGT ) activities in men and women . Methods As part of a parallel arm study , older ( age 40–72 ) , overweight and obese male and female subjects ( BMI 25–35 kg/m2 ) consumed glucose- or fructose-sweetened beverages providing 25 % of energy requirements for 10 wks . Fasting and 24-h blood collection s were performed at baseline and following 10 wks of intervention and plasma concentrations of uric acid , RBP-4 and liver enzyme activities were measured . Results Consumption of fructose , but not glucose , led to significant increases of 24-h uric acid profiles ( P < 0.0001 ) and RBP-4 concentrations ( P = 0.012 ) , as well as plasma GGT activity ( P = 0.04 ) . Fasting plasma uric acid concentrations increased in both groups ; however , the response was significantly greater in subjects consuming fructose ( P = 0.002 for effect of sugar ) . Within the fructose group male subjects exhibited larger increases of RBP-4 levels than women ( P = 0.024 ) . Conclusions These findings suggest that consumption of fructose at 25 % of energy requirements for 10 wks , compared with isocaloric consumption of glucose , may contribute to the development of components of the metabolic syndrome by increasing circulating uric acid , GGT activity , suggesting alteration of hepatic function , and the production of RBP-4 Nonalcoholic fatty liver disease ( NAFLD ) is now thought to be the most common liver disease worldwide . Cardiovascular complications are a leading cause of mortality in NAFLD . Fructose , a common nutrient in the westernized diet , has been reported to be associated with increased cardiovascular risk , but its impact on adolescents with NAFLD is not well understood . We design ed a 4-week r and omized , controlled , double-blinded beverage intervention study . Twenty-four overweight Hispanic-American adolescents who had hepatic fat > 8 % on imaging and who were regular consumers of sweet beverages were enrolled and r and omized to calorie-matched study -provided fructose only or glucose only beverages . After 4 weeks , there was no significant change in hepatic fat or body weight in either group . In the glucose beverage group there was significantly improved adipose insulin sensitivity , high sensitivity C-reactive protein ( hs-CRP ) , and low-density lipoprotein ( LDL ) oxidation . These findings demonstrate that reduction of fructose improves several important factors related to cardiovascular disease despite a lack of measurable improvement in hepatic steatosis . Reducing dietary fructose may be an effective intervention to blunt atherosclerosis progression among NAFLD patients and should be evaluated in longer term clinical trials The purpose of this study was to compare the physiological , sensory , and exercise performance responses to ingestion of 6 % glucose , 6 % fructose , and 6 % sucrose solutions during cycling exercise . Twelve subjects completed three sessions consisting of 115 min of intermittent cycle ergometer exercise at 65 - 80 % of VO2max followed by a timed performance bout requiring the completion of 600 pedal revolutions . During each of five 4-min rest periods , subjects consumed 3 ml.kg LBM-1 of one of the beverages . Beverages were presented in counterbalanced , double-blind fashion . Heart rate , VO2 , plasma urate , plasma lactate , respiratory exchange ratio , and carbohydrate combustion rates changed similarly among beverage treatment . However , fructose was associated with lower plasma glucose and serum insulin , a larger loss of plasma volume , greater gastrointestinal distress and relative perceived exertion ratings , and higher plasma or serum concentrations of free fatty acids , fructose , and cortisol values than sucrose or glucose ( P less than 0.05 ) . Compared to sucrose and glucose , fructose feeding also result ed in lower lactate and HR values during the performance bout ( P less than 0.05 ) . Mean + /- SE cycling performance times were faster with sucrose and glucose than with fructose : 419.4 + /- 21.0 s , 423.9 + /- 21.2 s , and 488.3 + /- 21.1 s , respectively ( P less than 0.05 ) . Relative to 6 % solutions of sucrose and glucose , ingestion of a 6 % fructose beverage is associated with gastrointestinal distress , compromised physiological response , and reduced exercise capacity AIMS In animals , intracerebroventricular glucose and fructose have opposing effects on appetite and weight regulation . In humans , functional brain magnetic resonance imaging ( fMRI ) studies during glucose ingestion or infusion have demonstrated suppression of hypothalamic signalling , but no studies have compared the effects of glucose and fructose . We therefore sought to determine if the brain response differed to glucose vs. fructose in humans independently of the ingestive process . METHODS Nine healthy , normal weight subjects underwent blood oxygenation level dependent ( BOLD ) fMRI measurements during either intravenous ( IV ) glucose ( 0.3 mg/kg ) , fructose ( 0.3 mg/kg ) or saline , administered over 2 min in a r and omized , double-blind , crossover study . Blood was sample d every 5 min during a baseline period and following infusion for 60 min in total for glucose , fructose , lactate and insulin levels . RESULTS No significant brain BOLD signal changes were detected in response to IV saline .  BOLD signal in the cortical control areas increased during glucose infusion ( p = 0.002 ) , corresponding with increased plasma glucose and insulin levels . In contrast , BOLD signal decreased in the cortical control areas during fructose infusion ( p = 0.006 ) , corresponding with increases of plasma fructose and lactate . Neither glucose nor fructose infusions significantly altered BOLD signal in the hypothalamus . CONCLUSION In normal weight humans , cortical responses as assessed by BOLD fMRI to infused glucose are opposite to those of fructose . Differential brain responses to these sugars and their metabolites may provide insight into the neurologic basis for dysregulation of food intake during high dietary fructose intake Significance Fructose compared with glucose may be a weaker suppressor of appetite . Here we sought to determine the effects of fructose versus glucose on brain , hormone , and appetitive responses to food cues and food-approach behavior . We show that the ingestion of fructose compared with glucose result ed in smaller increases in plasma insulin levels and greater brain responses to food cues in the visual cortex and left orbital frontal cortex . Ingestion of fructose versus glucose also led to greater hunger and desire for food and a greater willingness to give up long-term monetary rewards to obtain immediate high-calorie foods . These findings suggest that ingestion of fructose relative to glucose activates brain regions involved in attention and reward processing and may promote feeding behavior . Prior studies suggest that fructose compared with glucose may be a weaker suppressor of appetite , and neuroimaging research shows that food cues trigger greater brain reward responses in a fasted relative to a fed state . We sought to determine the effects of ingesting fructose versus glucose on brain , hormone , and appetitive responses to food cues and food-approach behavior . Twenty-four healthy volunteers underwent two functional magnetic resonance imaging ( fMRI ) sessions with ingestion of either fructose or glucose in a double-blinded , r and om-order cross-over design . fMRI was performed while participants viewed images of high-calorie foods and nonfood items using a block design . After each block , participants rated hunger and desire for food . Participants also performed a decision task in which they chose between immediate food rewards and delayed monetary bonuses . Hormones were measured at baseline and 30 and 60 min after drink ingestion . Ingestion of fructose relative to glucose result ed in smaller increases in plasma insulin levels and greater brain reactivity to food cues in the visual cortex ( in whole-brain analysis ) and left orbital frontal cortex ( in region-of-interest analysis ) . Parallel to the neuroimaging findings , fructose versus glucose led to greater hunger and desire for food and a greater willingness to give up long-term monetary rewards to obtain immediate high-calorie foods . These findings suggest that ingestion of fructose relative to glucose results in greater activation of brain regions involved in attention and reward processing and may promote feeding behavior Background Recent studies have demonstrated a relationship between fructose consumption and risk of developing metabolic syndrome . Mechanisms by which dietary fructose mediates metabolic changes are poorly understood . This study compared the effects of fructose , glucose and sucrose consumption on post-postpr and ial lipemia and low grade inflammation measured as hs-CRP . Methods This was a r and omized , single blinded , cross-over trial involving healthy subjects ( n = 14 ) . After an overnight fast , participants were given one of 3 different isocaloric drinks , containing 50 g of either fructose or glucose or sucrose dissolved in water .  Blood sample s were collected at baseline , 30 , 60 and 120 minutes post intervention for the analysis of blood lipids , glucose , insulin and high sensitivity C-reactive protein ( hs-CRP ) . Results Glucose and sucrose supplementation initially result ed in a significant increase in glucose and insulin levels compared to fructose supplementation and returned to near baseline values within 2 hours . Change in plasma cholesterol , LDL and HDL-cholesterol ( measured as area under curve , AUC ) was significantly higher when participants consumed fructose compared with glucose or sucrose ( P < 0.05 ) . AUC for plasma triglyceride levels however remained unchanged regardless of the dietary intervention . Change in AUC for hs-CRP was also significantly higher in subjects consuming fructose compared with those consuming glucose ( P < 0.05 ) , but not sucrose ( P = 0.07 ) . Conclusion This study demonstrates that fructose as a sole source of energy modulates plasma lipids and hsCRP levels in healthy individuals . The significance of increase in HDL-cholesterol with a concurrent increase in LDL-cholesterol and elevated hs-CRP levels remains to be delineated when considering health effects of feeding fructose-rich diets . Registration number for clinical OBJECTIVE Fructose has been implicated in obesity , partly due to lack of insulin-mediated leptin stimulation and ghrelin suppression . Most work has examined effects of pure fructose , rather than high-fructose corn syrup ( HFCS ) , the most commonly consumed form of fructose . This study examined effects of beverages sweetened with HFCS or sucrose ( Suc ) , when consumed with mixed meals , on blood glucose , insulin , leptin , ghrelin , and appetite . METHODS Thirty lean women were studied on two r and omized 2-d visits during which HFCS- and Suc-sweetened beverages were consumed as 30 % of energy on isocaloric diets during day 1 while blood was sample d. On day 2 , food was eaten ad libitum . Subjects rated appetite at design ated times throughout visits . RESULTS No significant differences between the two sweeteners were seen in fasting plasma glucose , insulin , leptin , and ghrelin ( P > 0.05 ) . The within-day variation in all four items was not different between the two visits ( P > 0.05 ) . Net areas under the curve were similar for glucose , insulin , and leptin ( P > 0.05 ) . There were no differences in energy or macronutrient intake on day 2 . The only appetite variable that differed between sweeteners was desire to eat , which had a higher area under the curve the day after Suc compared with HFCS . CONCLUSION These short-term results suggest that , when fructose is consumed in the form of HFCS , the measured metabolic responses do not differ from Suc in lean women . Further research is required to examine appetite responses and to determine if these findings hold true for obese individuals , males , or longer periods 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 Oral glucose is a potent stimulant of glucagon-like peptide-1 ( GLP-1 ) secretion . The effect of oral fructose on GLP-1 secretion in humans is unknown . The aims of this study were to determine ( i ) whether oral fructose stimulates GLP-1 secretion and ( ii ) the comparative effects of oral glucose and fructose on appetite . On 3 separate days , 8 fasting healthy males received , in single-blind r and omized order ( i ) 75 g glucose , ( ii ) 75 fructose , or ( iii ) 75 g glucose followed by 75 g fructose I h later . Venous glucose , insulin and GLP-1 were measured . Appetite was assessed by visual analog question naires and intake of a buffet meal . Whereas glucose and fructose both increased plasma glucose , insulin and GLP-1 ( P < 0.000 ) ] for all ) , the response to glucose was much greater ( P < 0.005 for all ) . There was no increase in plasma GLP-1 when fructose was given after glucose . There was no difference in food intake after oral glucose or fructose . We conclude that oral fructose ( 75 g ) stimulates GLP-1 ( and insulin ) secretion , but the response is less than that to 75 g glucose . These observations suggest that neither GLP-1 nor insulin play a major role in the regulation of satiation
Fructose consumption did not significantly affect fasting glucose or insulin .
A priori subgroup analyses showed no evidence of effect modification on any end point .
Isocaloric exchange of fructose for other carbohydrate improves long-term glycemic control , as assessed by glycated blood proteins , without affecting insulin in people with diabetes .
OBJECTIVE The effect of fructose on cardiometabolic risk in humans is controversial .
We conducted a systematic review and meta- analysis of controlled feeding trials to clarify the effect of fructose on glycemic control in individuals with diabetes .