The effects of four hypocaloric diets containing different levels of sucrose or high fructose corn syrup on weight loss and related parameters The Effect of Normally Consumed Amounts of Sucrose or High Fructose Corn Syrup on Lipid Profiles, Body Composition and Related Parameters in Overweight/Obese Subjects No difference between high-fructose and high-glucose diets on liver triacylglycerol or biochemistry in healthy overweight men. Effects of Two Energy-Restricted Diets Containing Different Fruit Amounts on Body Weight Loss and Macronutrient Oxidation 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 Impaired cellular insulin binding and insulin sensitivity induced by high-fructose feeding in normal subjects. Consumption of fructose-sweetened beverages for 10 weeks reduces net fat oxidation and energy expenditure in overweight/obese men and women Acute effects of feeding fructose, glucose and sucrose on blood lipid levels and systemic inflammation Dietary Fructose Reduction Improves Markers of Cardiovascular Disease Risk in Hispanic-American Adolescents with NAFLD Dietary glycemic load, carbohydrate, sugar, and colorectal cancer risk in men and women. Effects of fructose vs glucose on regional cerebral blood flow in brain regions involved with appetite and reward pathways. Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. Consumption of a Diet Low in Advanced Glycation End Products for 4 Weeks Improves Insulin Sensitivity in Overweight Women Effect of a High-Fructose Weight-Maintaining Diet on Lipogenesis and Liver Fat. Acute effects of fructose and glucose ingestion with and without caffeine in young and old humans. A pilot study on the impact of a low fructose diet and allopurinol on clinic blood pressure among overweight and prehypertensive subjects: a randomized placebo controlled trial. Coffee consumption attenuates short-term fructose-induced liver insulin resistance in healthy men. High-fructose corn syrup and sucrose have equivalent effects on energy-regulating hormones at normal human consumption levels. Fructose and insulin sensitivity in patients with type 2 diabetes. Effects of grain, fructose, and histidine on ruminal pH and fermentation products during an induced subacute acidosis protocol. Effects of a short-term overfeeding with fructose or glucose in healthy young males. Exercise performed immediately after fructose ingestion enhances fructose oxidation and suppresses fructose storage. Effects of high-fructose corn syrup and sucrose consumption on circulating glucose, insulin, leptin, and ghrelin and on appetite in normal-weight women.
Background The replacement of sucrose with HFCS in food products has been suggested as playing a role in the development of obesity as a public health issue . The objective of this study was to examine the effects of four equally hypocaloric diets containing different levels of sucrose or high fructose corn syrup ( HFCS ) . Methods This was a r and omized , prospect i ve , double blind trial , with overweight/obese participants measured for body composition and blood chemistry before and after the completion of 12 weeks following a hypocaloric diet .  The average caloric deficit achieved on the hypocaloric diets was 309 kcal . Results Reductions were observed in all measures of adiposity including body mass , BMI , % body fat , waist circumference and fat mass for all four hypocaloric groups , as well as reductions in the exercise only group for body mass , BMI and waist circumference . Conclusions Similar decreases in weight and indices of adiposity are observed when overweight or obese individuals are fed hypocaloric diets containing levels of sucrose or high fructose corn syrup typically consumed by adults in the United States The American Heart Association ( AHA ) has advocated that women and men not consume more than 100 and 150 kcal/day , respectively , from added sugars . These levels are currently exceeded by over 90 % of the adult population in the United States . Few data exist on longer-term metabolic effects when sucrose and High Fructose Corn Syrup ( HFCS ) , the principal sources of added dietary sugars , are consumed at levels typical of the general population . Sixty five overweight and obese individuals were placed on a eucaloric ( weight stable ) diet for 10-weeks , which incorporated sucrose- or HFCS-sweetened , low-fat milk at 10 % or 20 % of calories in a r and omized , double-blinded study . All groups responded similarly ( interaction p > 0.05 ) . There was no change in body weight in any of the groups over the 10-week study , or in systolic or diastolic blood pressure . Likewise , there were no changes in total cholesterol , triglycerides , low-density lipoprotein ( LDL ) , or apolipoprotein B ( Apo B ) . We conclude that ( 1 ) when consumed as part of a eucaloric diet fructose — when given with glucose ( as normally consumed ) does not promote weight gain or an atherogenic lipid profile even when consumed at two to four times the level recently recommended by the AHA . ( 2 ) There were no differences between HFCS and sucrose on these parameters BACKGROUND & AIMS Diets high in fructose have been proposed to contribute to nonalcoholic fatty liver disease . We compared the effects of high-fructose and matched glucose intake on hepatic triacylglycerol ( TAG ) concentration and other liver parameters . DESIGN In a double-blind study , we r and omly assigned 32 healthy but central ly overweight men to groups that received either a high-fructose or high-glucose diet ( 25 % energy ) . These diets were provided during an initial isocaloric period of 2 weeks , followed by a 6-week washout period , and then again during a hypercaloric 2-week period . The primary outcome measure was hepatic level of TAG , with additional assessment s of TAG levels in serum and soleus muscle , hepatic levels of adenosine triphosphate , and systemic and hepatic insulin resistance . RESULTS During the isocaloric period of the study , both groups had stable body weights and concentrations of TAG in liver , serum , and soleus muscle . The high-fructose diet produced an increase of 22 ± 52 μmol/L in the serum level of uric acid , whereas the high-glucose diet led to a reduction of 23 ± 25 μmol/L ( P < .01 ) . The high-fructose diet also produced an increase of 0.8 ± 0.9 in the homeostasis model assessment of insulin resistance , whereas the high-glucose diet produced an increase of only 0.1 ± 0.7 ( P = .03 ) . During the hypercaloric period , participants in the high-fructose and high-glucose groups had similar increases in weight ( 1.0 ± 1.4 vs 0.6 ± 1.0 kg ; P = .29 ) and absolute concentration of TAG in liver ( 1.70 % ± 2.6 % vs 2.05 % ± 2.9 % ; P = .73 ) and serum ( 0.36 ± 0.75 vs 0.33 ± 0.38 mmol/L ; P = .91 ) , and similar results in biochemical assays of liver function . Body weight changes were associated with changes in liver biochemistry and concentration of TAGs . CONCLUSIONS In the isocaloric period , overweight men who were on a high-fructose or a high-glucose diet did not develop any significant changes in hepatic concentration of TAGs or serum levels of liver enzymes . However , in the hypercaloric period , both high-fructose and high-glucose diets produced significant increases in these parameters without any significant difference between the 2 groups . This indicates an energy-mediated , rather than a specific macronutrient-mediated , effect . Clinical trials.gov no : NCT01050140 The consumption of specific foods in energy-restricted diets may affect the weight loss process . The purpose of this research was to evaluate whether obese women following two hypocaloric diets with distinct fruit content differ in weight loss and metabolic responses .  Fifteen obese women were included , who were r and omly assigned to follow a low or a high-fruit energy-restricted diet for 8 weeks . The main outcome variables were weight and fat losses . Metabolic measurements concerning macronutrient oxidation were also assessed by using 13C labelled fructose and indirect calorimetry . The induced weight loss was similar for both diets ( 6.9 ± 2 % vs. 6.6 ± 2 % , p = 0.785 ) . Both experimental diets similarly improved the lipid plasma profile in the participants , but the cholesterol fall was higher in obese subjects receiving the diet containing more fruit . No statistical differences in lipids carbohydrates and 13C labelled fructose utilisation were observed , but protein oxidation was differently affected by the experimental diets . The compensatory effects of the associated fibre/fructose intake may explain the lack of a specific effect of the fruit amount on hypocaloric diets design ed to weight loss , although the increased fibre content from enriched fruit diets may be involved in the favourable effects on cholesterol plasma levels 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 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 Background / Objectives : The results of short-term studies in humans suggest that , compared with glucose , acute consumption of fructose leads to increased postpr and ial energy expenditure and carbohydrate oxidation and decreased postpr and ial fat oxidation . The objective of this study was to determine the potential effects of increased fructose consumption compared with isocaloric glucose consumption on substrate utilization and energy expenditure following sustained consumption and under energy-balanced conditions . Subjects/ Methods : As part of a parallel arm study , overweight/obese male and female subjects , 40–72 years , consumed glucose- or fructose-sweetened beverages providing 25 % of energy requirements for 10 weeks . Energy expenditure and substrate utilization were assessed using indirect calorimetry at baseline and during the 10th week of intervention . Results : Consumption of fructose , but not glucose , led to significant decreases of net postpr and ial fat oxidation and significant increases of net postpr and ial carbohydrate oxidation ( P<0.0001 for both ) . Resting energy expenditure ( REE ) decreased significantly from baseline values in subjects consuming fructose ( P=0.031 ) but not in those consuming glucose . Conclusions : Increased consumption of fructose for 10 weeks leads to marked changes of postpr and ial substrate utilization including a significant reduction of net fat oxidation . In addition , we report that REE is reduced compared with baseline values in subjects consuming fructose-sweetened beverages for 10 weeks 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 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 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 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 Previous studies indicate that leptin secretion is regulated by insulin-mediated glucose metabolism . Because fructose , unlike glucose , does not stimulate insulin secretion , we hypothesized that meals high in fructose would result in lower leptin concentrations than meals containing the same amount of glucose . Blood sample s were collected every 30 - 60 min for 24 h from 12 normal-weight women on 2 r and omized days during which the subjects consumed three meals containing 55 , 30 , and 15 % of total kilocalories as carbohydrate , fat , and protein , respectively , with 30 % of kilocalories as either a fructose-sweetened [ high fructose ( HFr ) ] or glucose-sweetened [ high glucose ( HGl ) ] beverage . Meals were isocaloric in the two treatments . Postpr and ial glycemic excursions were reduced by 66 + /- 12 % , and insulin responses were 65 + /- 5 % lower ( both P < 0.001 ) during HFr consumption . The area under the curve for leptin during the first 12 h ( -33 + /- 7 % ; P < 0.005 ) , the entire 24 h ( -21 + /- 8 % ; P < 0.02 ) , and the diurnal amplitude ( peak - nadir ) ( 24 + /- 6 % ; P < 0.0025 ) were reduced on the HFr day compared with the HGl day . In addition , circulating levels of the orexigenic gastroenteric hormone , ghrelin , were suppressed by approximately 30 % 1 - 2 h after ingestion of each HGl meal ( P < 0.01 ) , but postpr and ial suppression of ghrelin was significantly less pronounced after HFr meals ( P < 0.05 vs. HGl ) . Consumption of HFr meals produced a rapid and prolonged elevation of plasma triglycerides compared with the HGl day ( P < 0.005 ) . Because insulin and leptin , and possibly ghrelin , function as key signals to the central nervous system in the long-term regulation of energy balance , decreases of circulating insulin and leptin and increased ghrelin concentrations , as demonstrated in this study , could lead to increased caloric intake and ultimately contribute to weight gain and obesity during chronic consumption of diets high in fructose OBJECTIVE High-heat cooking of food induces the formation of advanced glycation end products ( AGEs ) , which are thought to impair glucose metabolism in type 2 diabetic patients . High intake of fructose might additionally affect endogenous formation of AGEs . This parallel intervention study investigated whether the addition of fructose or cooking methods influencing the AGE content of food affect insulin sensitivity in overweight individuals . RESEARCH DESIGN AND METHODS Seventy-four overweight women were r and omized to follow either a high- or low-AGE diet for 4 weeks , together with consumption of either fructose or glucose drinks .  Glucose and insulin concentrations — after fasting and 2 h after an oral glucose tolerance test — were measured before and after the intervention . Homeostasis model assessment of insulin resistance ( HOMA-IR ) and insulin sensitivity index were calculated . Dietary and urinary AGE concentrations were measured ( liquid chromatography t and em mass spectrometry ) to estimate AGE intake and excretion . RESULTS When adjusted for changes in anthropometric measures during the intervention , the low-AGE diet decreased urinary AGEs , fasting insulin concentrations , and HOMA-IR , compared with the high-AGE diet . Addition of fructose did not affect any outcomes . CONCLUSIONS Diets with high AGE content may increase the development of insulin resistance . AGEs can be reduced by modulation of cooking methods but is unaffected by moderate fructose intake CONTEXT Consumption of high-fructose diets promotes hepatic fatty acid synthesis ( de novo lipogenesis [ DNL ] ) and an atherogenic lipid profile . It is unclear whether these effects occur independent of positive energy balance and weight gain . OBJECTIVES We compared the effects of a high-fructose , ( 25 % of energy content ) weight-maintaining diet to those of an isocaloric diet with the same macronutrient distribution but in which complex carbohydrate ( CCHO ) was substituted for fructose . DESIGN , SETTING , AND PARTICIPANTS Eight healthy men were studied as in patients for consecutive 9-day periods . Stable isotope tracers were used to measure fractional hepatic DNL and endogenous glucose production ( EGP ) and its suppression during a euglycemic-hyperinsulinemic clamp . Liver fat was measured by magnetic resonance spectroscopy . RESULTS Weight remained stable . Regardless of the order in which the diets were fed , the high-fructose diet was associated with both higher DNL ( average , 18.6 ± 1.4 % vs 11.0 ± 1.4 % for CCHO ; P = .001 ) and higher liver fat ( median , + 137 % of CCHO ; P = .016 ) in all participants . Fasting EGP and insulin-mediated glucose disposal did not differ significantly , but EGP during hyperinsulinemia was greater ( 0.60 ± 0.07 vs 0.46 ± 0.06 mg/kg/min ; P = .013 ) with the high-fructose diet , suggesting blunted suppression of EGP . CONCLUSION Short-term high-fructose intake was associated with increased DNL and liver fat in healthy men fed weight-maintaining diets Aging is associated with a decline in energy expenditure ( EE ) , glucose intolerance , and a reduction in body nitrogen content . In addition , a reduction in the thermic response to glucose but not to fructose or protein has been reported in the elderly . The present study was conducted to further examine nutrient-induced thermogenesis and the effects of specific sugars on amino acid metabolism in relation to age . After 3 days on a weight-maintaining , 250-g carbohydrate diet , 16 healthy non-obese men and women in two age groups ( 18 to 29 and 66 to 80 years ) consumed on 4 different days 500 mL of either a 75-g fructose or 75-g glucose solution , with or without 300 mg caffeine or vitamin C as a placebo .  Blood substrate and hormone levels and EE , using indirect calorimetry , were measured at timed intervals for 3 hours after consumption of the drinks . There was no difference in the carbohydrate-induced increase in EE in either young or old even after adjustments for body weight and fat-free mass ( FFM ) . An approximately 20-fold increase in serum caffeine levels increased EE in both groups ( P < .003 ) , but had minimal effects on substrate and hormone responses . In contrast to glucose , fructose induced a marked elevation in plasma alanine from combined basal levels of 301 + /- 24 to approximately 500 + /- 18 mumol/L ( mean + /- SEM ) in both groups ( P < .001 ) . However , both fructose and glucose ingestion result ed in a similar decline in branched-chain and aromatic amino acids . ( ABSTRACT TRUNCATED AT 250 WORDS Fructose and sodium intake have been associated with hypertension and metabolic syndrome . Although various mechanisms are involved , fructose causes hypertension partly through rising intracellular and serum uric acid . To date , there are no studies in adults that have evaluated the impact of low fructose diets and allopurinol on prehypertensive and overweight subjects . The objective of this study was to compare the effect of low fructose diet and allopurinol or placebo on blood pressure ( BP ) and metabolic syndrome components The study was a controlled clinical trial and consisted of two phases ; in the first phase of intervention ( 4 weeks ) , patients were r and omized to either low fructose diet ( 34 patients ) or control diet ( 38 patients ) . In the second phase of intervention ( weeks 4 - 8 ) , the same groups continued with the same diet prescriptions but were further r and omized to receive placebo or allopurinol ( 300 mg/d ) . Clinic and 24-hour ambulatory BP , anthropometric measures , and laboratory data were determined at baseline , weeks 4 and 8 . Seventy-two patients were included in the trial . At the end of the dietary phase , both diet groups significantly reduced their BP , but there were no between-group differences . Compared to placebo , at the end of follow-up , subjects in the allopurinol group had a lower clinic systolic blood pressure and this was significant within- and between-group comparisons . The percentage of dippers was higher in the allopurinol group , and weight was reduced significantly despite the absence of caloric restriction Allopurinol was associated with a significant reduction in clinic BP , an increase in the percentage of dippers , and significant weight loss . Larger studies with longer follow-up are needed to confirm our findings BACKGROUND Epidemiologic and experimental data have suggested that chlorogenic acid , which is a polyphenol contained in green coffee beans , prevents diet-induced hepatic steatosis and insulin resistance . OBJECTIVE We assessed whether the consumption of chlorogenic acid-rich coffee attenuates the effects of short-term fructose overfeeding , dietary conditions known to increase intrahepatocellular lipids ( IHCLs ) , and blood triglyceride concentrations and to decrease hepatic insulin sensitivity in healthy humans . DESIGN Effects of 3 different coffees were assessed in 10 healthy volunteers in a r and omized , controlled , crossover trial . IHCLs , hepatic glucose production ( HGP ) ( by 6,6-d2 glucose dilution ) , and fasting lipid oxidation were measured after 14 d of consumption of caffeinated coffee high in chlorogenic acid ( C-HCA ) , decaffeinated coffee high in chlorogenic acid , or decaffeinated coffee with regular amounts of chlorogenic acid ( D-RCA ) ; during the last 6 d of the study , the weight-maintenance diet of subjects was supplemented with 4 g fructose · kg(-1 ) · d(-1 ) ( total energy intake ± SD : 143 ± 1 % of weight-maintenance requirements ) . All participants were also studied without coffee supplementation , either with 4 g fructose · kg(-1 ) · d(-1 ) ( high fructose only ) or without high fructose ( control ) . RESULTS Compared with the control diet , the high-fructose diet significantly increased IHCLs by 102 ± 36 % and HGP by 16 ± 3 % and decreased fasting lipid oxidation by 100 ± 29 % ( all P < 0.05 ) . All 3 coffees significantly decreased HGP . Fasting lipid oxidation increased with C-HCA and D-RCA ( P < 0.05 ) . None of the 3 coffees significantly altered IHCLs . CONCLUSIONS Coffee consumption attenuates hepatic insulin resistance but not the increase of IHCLs induced by fructose overfeeding . This effect does not appear to be mediated by differences in the caffeine or chlorogenic acid content . This trial was registered at clinical trials.gov as NCT00827450 Intake of high-fructose corn syrup ( HFCS ) has been suggested to contribute to the increased prevalence of obesity , whereas a number of studies and organizations have reported metabolic equivalence between HFCS and sucrose . We hypothesized that HFCS and sucrose would have similar effects on energy-regulating hormones and metabolic substrates at normal levels of human consumption and that these values would not change over a 10-week , free-living period at these consumption levels . This was a r and omized , prospect i ve , double-blind , parallel group study in which 138 adult men and women consumed 10 weeks of low-fat milk sweetened with either HFCS or sucrose at levels of the 25th , 50th , and 90th percentile population consumption of fructose ( the equivalent of 40 , 90 , or 150 g of sugar per day in a 2000-kcal diet ) . Before and after the 10-week intervention , 24-hour blood sample s were collected . The area under the curve ( AUC ) for glucose , insulin , leptin , active ghrelin , triglyceride , and uric acid was measured . There were no group differences at baseline or posttesting for all outcomes ( interaction , P > .05 ) . The AUC response of glucose , active ghrelin , and uric acid did not change between baseline and posttesting ( P > .05 ) , whereas the AUC response of insulin ( P < .05 ) , leptin ( P < .001 ) , and triglyceride ( P < .01 ) increased over the course of the intervention when the 6 groups were averaged . We conclude that there are no differences in the metabolic effects of HFCS and sucrose when compared at low , medium , and high levels of consumption 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 The effects of grain , fructose , and histidine on ruminal pH and fermentation products were studied in dairy cattle during an induced subacute acidosis protocol . Thirty Holstein heifers were r and omly allocated to 5 treatment groups : ( 1 ) control ( no grain ) ; ( 2 ) grain [ fed at a crushed triticale dry matter intake ( DMI ) of 1.2 % of body weight ( BW ) ] ; ( 3 ) grain ( 0.8 % of BW DMI)+fructose ( 0.4 % of BW DMI ) ; ( 4 ) grain ( 1.2 % of BW DMI)+histidine ( 6 g/head ) ; and ( 5 ) grain ( 0.8 % of BW DMI)+fructose ( 0.4 % of BW DMI)+histidine ( 6 g/head ) in a partial factorial arrangement . Heifers were fed 1 kg of grain daily with ad libitum access to ryegrass silage and alfalfa hay for 10 d. Feed was withheld for 14 h before challenge day , on which heifers were fed 200 g of alfalfa hay and then the treatment diets immediately thereafter . Rumen sample s were collected 5 min after diet ingestion , 60 min later , and at 3 subsequent 50-min intervals . Grain decreased ruminal pH and increased ammonia , total volatile fatty acid ( VFA ) , acetate , butyrate , propionate , and valerate concentrations compared with controls . The addition of grain had no effect on ruminal D- and L-lactate concentrations . Fructose markedly decreased ruminal pH and markedly increased D- and L-lactate concentrations . Fructose increased total VFA and butyrate and decreased valerate concentrations . Although histidine did not have a marked effect on ruminal fermentation , increased concentrations of histamine were observed following feeding . This study demonstrates that the substitution of some grain for fructose can lower ruminal pH and increase VFA and lactate concentrations , warranting further investigation into the role of sugars on the risk of acidosis in dairy cattle 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 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 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
The weight-increasing effect of fructose in hypercaloric trials may have been attributable to excess energy rather than fructose itself .
Fructose does not seem to cause weight gain when it is substituted for other carbohydrates in diets providing similar calories .
Free fructose at high doses that provided excess calories modestly increased body weight , an effect that may be due to the extra calories rather than the fructose .
BACKGROUND The contribution of fructose consumption in Western diets to overweight and obesity in population s remains uncertain .
PURPOSE To review the effects of fructose on body weight in controlled feeding trials .