Blood lipid distribution of hyperinsulinemic men consuming three levels of fructose. The effects of drinks made from simple sugars on blood pressure in healthy older people. Fructose ingestion acutely elevates blood pressure in healthy young humans. Effects of dietary fructose on plasma lipids in healthy subjects. 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. Fructose and insulin sensitivity in patients with type 2 diabetes. Mechanisms for the acute effect of fructose on postprandial lipemia. Effects on uric acid, body mass index and blood pressure in adolescents of consuming beverages sweetened with high-fructose corn syrup Effects of pure sugar vs. mixed starch fructose loads on food intake Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. Acute effects of feeding fructose, glucose and sucrose on blood lipid levels and systemic inflammation Fructose consumption and the risk of kidney stones. Low fructose and low salt diets increase mitochondrial DNA in white blood cells of overweight subjects. Dietary glycemic load, carbohydrate, sugar, and colorectal cancer risk in men and women. Short-term effects of various sugars on antinatriuresis and blood pressure changes in normotensive young men. Macronutrient disposal during controlled overfeeding with glucose, fructose, sucrose, or fat in lean and obese women. 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 An isocaloric glucose-fructose beverage's effect on simulated 100-km cycling performance compared with a glucose-only beverage. Brain functional magnetic resonance imaging response to glucose and fructose infusions in humans. Acute fructose administration improves oral glucose tolerance in adults with type 2 diabetes. Dietary sugars stimulate fatty acid synthesis in adults. Consumption of fructose-sweetened beverages for 10 weeks reduces net fat oxidation and energy expenditure in overweight/obese men and women Inulin supplementation prevents high fructose diet-induced hypertension in rats.
Twelve carbohydrate-sensitive men selected due to their abnormally high insulin responses to a sucrose load and 12 men with normal insulin responses were fed diets containing 0 , 7.5 , and 15 % fructose for 5 wk each in a cross-over design . The diets contained 43 % total carbohydrate , 42 % fat , and 15 % protein . Initial fasting total cholesterol and low-density lipoprotein cholesterol were higher in the hyperinsulinemic men than in the controls . Diastolic blood pressure was not affected by diet , but systolic blood pressure was slightly higher after the men consumed the 0 % fructose diet . Free fatty acids were not different . Total plasma cholesterol and low-density lipoprotein cholesterol were higher after the men consumed 7.5 and 15 % fructose than when they consumed the 0 % fructose diet . Plasma triglyceride increased significantly as fructose in the diets of the hyperinsulinemics increased , but was not affected in the controls . These changes in blood lipids are associated with heart disease The objective of the research was to determine the blood pressure ( BP ) lowering effects in older people of 50 g carbohydrate drinks with varying carbohydrate content using a r and omised , cross-over study with ten ( six females ) healthy older subjects ( mean age 72.20 ( sem 1.50 ) years ) .  BP , heart rate and glucometer-derived blood glucose levels were determined at baseline and following the ingestion of equal volumes ( 300 ml ) of water and carbohydrate drinks with varying nutrient content ( glucose , sucrose and fructose ) . A significant decline in BP over the first 60 min was seen following  glucose ( systolic BP ( SBP ) P<0.01 , diastolic BP ( DBP ) P<0.01 , mean arterial BP ( MAP ) P=0.03 ) and sucrose ( SBP P<0.01 , DBP P<0.01 , MAP P<0.01 ) ingestion , although the decrease occurred earlier after glucose than sucrose ingestion ( SBP 7.33 ( sem 2.19 ) v. 21.00 ( sem 4.30 ) min ( P=0.03 ) and MAP 11.22 ( sem 3.10 ) v. 17.00 ( sem 3.78 ) min ( P=0.03 ) ) . BP increased after water ingestion ( SBP P=0.04 , DBP P=0.18 , MAP P=0.02 ) but did not change after fructose ingestion ( SBP P=0.36 , DBP P=0.81 , MAP P=0.34 ) . Post hoc analyses revealed that the BP ( SBP , DBP and MAP ) decrease following glucose and sucrose ingestion were similar but significantly greater than following fructose or water ingestion . Sucrose , which is used widely ( table sugar ) , reduces BP as much as glucose . In contrast to this , fructose ingestion causes no change in BP . Further studies are required to determine if the substitution of glucose or sucrose with fructose may be beneficial in the medical management of older people with severe symptomatic postpr and ial hypotension 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 BACKGROUND About 9 % of average dietary energy intake in the United States comes from fructose . Such a high consumption raises concern about the metabolic effects of this sugar . OBJECTIVE The objective of this study was to determine the effect of dietary fructose on plasma lipids . DESIGN The study was conducted in the General Clinical Research Center at Fairview-University of Minnesota Medical Center . The participants were 24 healthy adult volunteers ( 12 men and 12 women ; 6 of each sex were aged < 40 y and 6 of each sex were aged > /=40 y ) . All subjects received 2 isoenergetic study diets assigned by using a r and omized , balanced crossover design . One diet provided 17 % of energy as fructose . The other diet was sweetened with glucose and was nearly devoid of fructose . Each diet was fed for 6 wk . Both diets were composed of common foods and contained nearly identical amounts of carbohydrate , protein , fat , fiber , cholesterol , and saturated , monounsaturated , and polyunsaturated fatty acids . All meals were prepared in the metabolic kitchen of the General Clinical Research Center . RESULTS The responses to the study diets differed by sex . In men , the fructose diet produced significantly higher fasting , postpr and ial , and daylong plasma triacylglycerol concentrations than did the glucose diet . The daylong plasma triacylglycerol concentration after 6 wk of the fructose diet was 32 % greater in men than the corresponding concentration during the glucose diet ( P : < 0.001 ) . The fructose diet had no significant effect on fasting or postpr and ial plasma triacylglycerol concentrations in women . The fructose diet also had no persistent effect on fasting plasma cholesterol , HDL cholesterol , or LDL cholesterol in either men or women . CONCLUSIONS Dietary fructose was associated with increased fasting and postpr and ial plasma triacylglycerol concentrations in men . Diets high in added fructose may be undesirable , particularly for men . Glucose may be a suitable replacement sugar 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 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 BACKGROUND A high fructose intake can lead to postpr and ial hypertriacylglycerolemia . The underlying mechanism is unclear . OBJECTIVE The objective of the study was to investigate the mechanisms involved in fructose-induced hypertriacylglycerolemia and the contribution of de novo lipogenesis in an acute setting . DESIGN In a r and omized , crossover study , 14 subjects were given a fructose or glucose test meal after an overnight fast . [(2)H2]Palmitate and [U(13)C]d-fructose or [U(13)C]d-glucose were added to trace the h and ling of dietary fats and the fate of dietary sugars in the body . Blood sample s were taken before and after the meal . Respiratory exchange ratio was measured by using indirect calorimetry , and breath sample s were collected . RESULTS Plasma triacylglycerol and VLDL-triacylglycerol concentrations were significantly higher ( P = 0.001 for both ) , whereas the concentrations of insulin and [(2)H2]palmitate in nonesterified fatty acids were significantly lower after fructose than after glucose ( P = 0.002 and 0.03 , respectively ) . The respiratory exchange ratio was higher after fructose ( P = 0.04 ) ; significantly ( P = 0.003 ) more carbon from sugars was recovered in breath carbon dioxide over 6 h after fructose ( 30.5 % ) than after glucose ( 24.5 % ) . At 240 min , newly synthesized fatty acids from fructose made up approximately 0.4 % of circulating VLDL-triacylglycerol , whereas newly synthesized triacylglycerol-glycerol made up 38 % . Newly synthesized fatty acids and triacylglycerol-glycerol from glucose contributed almost none of VLDL-triacylglycerol ( P = 0.002 and 0.007 for glucose and fructose , respectively ) . CONCLUSIONS The lower insulin excursion after fructose may result in less activation of adipose tissue lipoprotein lipase , which led to impaired triacylglycerol clearance . The contribution of de novo lipogenesis to fructose-induced hypertriacylglycerolemia is small , but its effect on altering the partitioning of fatty acids toward esterification may be considerable Objective : The dietary intake of fructose-rich sugar-sweetened beverages ( SSB ) may have a significant role in raising serum uric acid ( SUA ) levels as well as the risk of contracting gout and cardiovascular risk factors . Our objective was to investigate the impact of SSB intake on SUA , body mass index ( BMI ) and systolic blood pressure ( SBP ) among adolescents in Taiwan . Methods : We evaluated data from 2727 representative adolescents who were multistage sample d from 36 Junior High schools in Taiwan . We cross-sectionally collected demographic , physical , dietary and anthropometric variables , and prospect ively measured clinical outcomes . Data were analyzed using multiple regression and logistic models adjusted for covariates . Results : We found that 87.7 % of adolescents were SSB drinkers , with 25.1 % drinking > 500 ml per day of such beverages . Increased SSB intake was associated with increased waist and hip circumferences , body fat , BMI , SBP and SUA . As compared with non-drinkers , SSB drinkers had a 3.2–4.9 elevated risk of obesity . The prevalence of hyperuricemia in heavy SSB  users ( 40.2–49.4 % ) was appreciably greater than that for non-users ( 24.2 % ) . Adolescents who consumed > 500 ml per day of heavy high-fructose corn syrup ( HFCS ) containing beverages had a 0.42 mg dl−1 higher SUA level and a 2.0–2.1 increased risk of developing hyperuricemia than non-drinkers . The consumption of HFCS-rich beverages was also found to interact with obesity in determining higher levels of SUA ( 2.2–2.4 mg dl−1 increases ) . Conclusion : High SSB consumption has a notable effect on increased levels of BMI and SUA . The intake of HFCS-rich beverages and BMI were likely to interactively strengthen SUA levels among obese adolescents Using a within-subject design , we gave subjects three different 520 - 530 kcal preloads in the form of puddings in a r and omized fashion at weekly intervals . The puddings contained either 50 g of fructose or glucose as the sole carbohydrate source in a protein and fat mixture , or 50 g fructose plus 15 g of starch .  Food intake was assessed 2.25 h after the preload was completed . Blood was drawn throughout and assayed for concentrations of glucose and insulin . When the preload contained fructose alone as the sole source of carbohydrate , subjects ate significantly fewer calories and less fat than when the preload contained glucose alone . When starch was added to the fructose preload , there was no significant reduction in calorie and fat intake . Effects on food intake paralleled the rise in plasma insulin levels produced by the different preloads . Implication s for use of fructose as an adjunct to weight control efforts are discussed 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 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 Fructose consumption has markedly increased over the past decades . This intake may increase the urinary excretion of calcium , oxalate , uric acid , and other factors associated with kidney stone risk . We prospect ively examined the relationship between fructose intake and incident kidney stones in the Nurses ' Health Study I ( NHS I ) ( 93,730 older women ) , the Nurses ' Health Study II ( NHS II ) ( 101,824 younger women ) , and the Health Professionals Follow-up Study ( 45,984 men ) . Food frequency question naires were used to assess free fructose and sucrose intake every 4 years . Total-fructose intake was calculated as free fructose plus half the intake of sucrose , and expressed as percentage of total energy . Cox proportional hazard regressions were adjusted for age , body mass index ( BMI ) , thiazide use , caloric intake , and other dietary factors . We documented 4902 incident kidney stones  during a combined 48 years of follow-up . The multivariate relative risks of kidney stones significantly increased for participants in the highest compared to the lowest quintile of total-fructose intake for all three study groups . Free-fructose intake was also associated with increased risk . Non-fructose carbohydrates were not associated with increased risk in any cohort . Our study suggests that fructose intake is independently associated with an increased risk of incident kidney stones OBJECTIVE To evaluate the effect of sodium and fructose restriction on mitochondrial DNA ( mtDNA ) content and systemic oxidative stress in a sample of overweight and pre hypertensive subjects . MATERIAL / METHODS Data and blood sample s were collected from 36 overweight and pre hypertensive patients r and omly assigned to either an isocaloric ( with respect to baseline ) low sodium-fructose diet or an isocaloric low sodium diet . Patients were followed for 8 weeks . We measured mitochondrial DNA ( mtDNA ) content from peripheral blood white cells by Real-time PCR and plasma malondialdehyde ( MDA ) and 2,4-dinitrophenylhydrazine ( DNPH ) as markers of reactive oxygen species ( ROS ) . RESULTS Compared to baseline , at week 8 there was a continued and significant increase in mtDNA in both the low sodium diet group [ 2.4 vs. 13.1 ( relative copy number ) , p<0.05 ] and the low sodium diet-fructose group ( 1.9 vs. 147.2 , p<0.05 ) . By week 8 there was a continued decrease in plasma DNPH levels in the low sodium diet group ( 4.6 vs. 2.6 , p<0.05 ) and in the low sodium diet-fructose group ( 5.8 vs. 2.2 , p<0.05 ) . No significant differences were found with MDA . CONCLUSION Our studies suggest that simple dietary measures such as reducing salt with or without restricting fructose can increase mtDNA and improve markers of oxidative stress 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 This is a report of the effects of sugars on salt metabolism and on blood pressure .  Twenty young men , none of whom had a personal or family history of hypertension , were orally hydrated after an overnight fast and required to lie recumbent for 6 h except for urinary voiding and blood pressure measurements which were performed at 1/2 h intervals . Venous blood sample s were drawn at hourly intervals . The volunteers were kept constantly hydrated by giving them water to drink equivalent to the volumes of urine voided . Two hours from the start of the experiment each subject was given one of the following sugars : glucose , fructose , sucrose , galactose , lactose , or water alone . After oral hydration the subjects appeared to develop natriuresis and kaliuresis . This was quickly abolished by ingestion of either glucose , fructose , sucrose , or lactose , but not by galactose or water alone . Fructose was the most potent antinatriuretic agent . Both glucose and sucrose significantly elevated systolic blood pressure . This lasted for 2 h after glucose ingestion and 1 h after sucrose ingestion BACKGROUND Previous short-term studies ( < or = 6 h ) showed differences in energy expenditure ( EE ) and macronutrient oxidation in response to overfeeding with different types of dietary carbohydrate . This finding could have implication s for obesity . OBJECTIVE We used 96-h continuous whole-body calorimetry in 8 lean and 5 obese women to assess metabolic disposal ( energy dissipation and glycogen or fat storage ) of a controlled excess of dietary energy supplied as different carbohydrate sources or as fat . DESIGN Five dietary treatments were applied in r and om order : energy balance ( control ) and overfeeding by 50 % of energy requirements with fat ( O(fat ) ) or predominantly with glucose , fructose , or sucrose ( O(cho ) ) .  Macronutrient oxidation rates were assessed from nonprotein gaseous exchanges . Net macronutrient balances were calculated as cumulative differences between intake and oxidation . RESULTS Increased EE in response to overfeeding dissipated 7.9 % of the energy excess with a variation in EE of < 1.7 % across overfeeding treatments ( NS ) . EE during the O(fat ) treatment significantly exceeded that during the control treatment in the lean but not in the obese women . There were no significant differences between lean and obese women in macronutrient oxidation or balances , so data were pooled . O(cho ) induced glycogen storage on day 1 ( approximately 100 g ) but thereafter progressively stimulated carbohydrate oxidation so that balance was reached on days 3 and 4 . Fat oxidation was proportionately suppressed . Of the excess carbohydrate , 74 % was oxidized ; there were no significant differences between the various O(cho ) treatments . O(fat ) stimulated fat oxidation by 18 % and suppressed carbohydrate oxidation . On average , 12 % of the excess energy was stored as glycogen and 88 % as fat ; there was no significant difference between overfeeding treatments . CONCLUSION There was no significant difference in fat balance during controlled overfeeding with fat , fructose , glucose , or sucrose 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 A number of recent research studies have demonstrated that providing glucose and fructose together in a beverage consumed during exercise results in significantly higher oxidation rates of exogenous carbohydrate ( CHO ) than consuming glucose alone . However , there is insufficient evidence to determine whether the increased exogenous CHO oxidation improves endurance performance . The purpose of this study was to determine whether consuming a beverage containing glucose and fructose ( GF ) would result in improved cycling performance compared with an isocaloric glucose-only beverage ( G ) .  Nine male competitive cyclists ( 32.6 + /- 5.8 years , peak oxygen uptake 61.5 + /- 7.9 ml x kg(-1 ) x min(-1 ) ) completed a familiarization trial and then 2 simulated 100-km cycling time trials on an electronically braked Lode cycle ergometer separated by 5 - 7 d. During the r and omly ordered experimental trials , participants received 36 g of CHO of either G or GF in 250 ml of water every 15 min . All 9 participants completed the 100-km time trial significantly faster when they received the GF beverage than with G ( 204.0 + /- 23.7 vs. 220.6 + /- 36.6 min ; p = .023 ) . There was no difference at any time point between trials for blood glucose or for blood lactate . Total CHO oxidation increased significantly from rest during exercise but was not statistically significant between the GF and G trials , although there was a trend for CHO oxidation to be higher with GF in the latter stages of the time trial . Consumption of a CHO beverage containing glucose and fructose results in improved 100-km cycling performance compared with an isocaloric glucose-only beverage 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 OBJECTIVE In normal adults , a small ( catalytic ) dose of fructose administered with glucose decreases the glycemic response to a glucose load , especially in those with the poorest glucose tolerance . We hypothesized that an acute catalytic dose of fructose would also improve glucose tolerance in individuals with type 2 diabetes . RESEARCH DESIGN AND METHODS Five adults with type 2 diabetes underwent an oral glucose tolerance test ( OGTT ) on two separate occasions , at least 1 week apart . Each OGTT consisted of 75 g glucose with or without the addition of 7.5 g fructose ( OGTT + F or OGTT - F ) , in r and om order . Arterialized blood sample s were collected from a heated dorsal h and vein twice before ingestion of the carbohydrate and every 15 min for 3 h afterward . RESULTS The area under the curve ( AUC ) of the plasma glucose response was reduced by fructose administration in all subjects ; the mean AUC during the OGTT + F was 14 % less than that during the OGTT - F ( P < 0.05 ) . The insulin AUC was decreased 21 % with fructose administration ( P = 0.2 ) . Plasma glucagon concentrations declined similarly during OGTT - F and OGTT + F. The incremental AUC of the blood lactate response during the OGTT - F was approximately 50 % of that observed during the OGTT + F ( P < 0.05 ) . Neither nonesterified fatty acid nor triglyceride concentrations differed between the two OGTTs . CONCLUSIONS Low-dose fructose improves the glycemic response to an oral glucose load in adults with type 2 diabetes , and this effect is not a result of stimulation of insulin secretion The goal of this study was to determine the magnitude by which acute consumption of fructose in a morning bolus would stimulate lipogenesis ( measured by infusion of 13C1-acetate and analysis by GC-MS ) immediately and after a subsequent meal . Six healthy subjects [ 4 men and 2 women ; aged ( mean + /- SD ) 28 + /- 8 y ; BMI , 24.3 + /- 2.8 kg/m(2 ) ; and serum triacylglycerols ( TG ) , 1.03 + /- 0.32 mmol/L ] consumed carbohydrate boluses of sugars  ( 85 g each ) in a r and om and blinded order , followed by a st and ardized lunch 4 h later . Subjects completed a control test of glucose ( 100:0 ) and a mixture of 50:50 glucose : fructose and one of 25:75 ( wt : wt ) . Following the morning boluses , serum glucose and insulin after 100:0 were greater than both other treatments ( P < 0.05 ) and this pattern occurred again after lunch . In the morning , fractional lipogenesis was stimulated when subjects ingested fructose and peaked at 15.9 + /- 5.4 % after the 50:50 treatment and at 16.9 + /- 5.2 % after the 25:75 treatment , values that were greater than after the 100:0 treatment ( 7.8 + /- 5.7 % ; P < 0.02 ) . When fructose was consumed , absolute lipogenesis was 2-fold greater than when it was absent ( 100:0 ) . Postlunch , serum TG were 11 - 29 % greater than 100:0 and TG-rich lipoprotein-TG concentrations were 76 - 200 % greater after 50:50 and 25:75 were consumed ( P < 0.05 ) . The data demonstrate that an early stimulation of lipogenesis after fructose , consumed in a mixture of sugars , augments subsequent postpr and ial lipemia . The postlunch blood TG elevation was only partially due to carry-over from the morning . Acute intake of fructose stimulates lipogenesis and may create a metabolic milieu that enhances subsequent esterification of fatty acids flowing to the liver to elevate TG synthesis postpr and ially 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 & AIMS The aim of this experiment was to evaluate the potential beneficial effect of supplementation with different inulin-type fructan fractions against common features of the metabolic syndrome in a rat model of this syndrome ( fructose-fed rat ) . METHODS Forty Wistar rats were r and omly divided into five groups and the animals received for 4 weeks either a semi-purified starch or fructose-based diet , or diets in which fructose was partially substituted with various fructans : 10 g/100 g of long-chain inulin or oligofructose , or an oligofructose-enriched inulin . After this period , blood pressure was measured and sample s of blood and tissues were collected for selected biochemical analyses . RESULTS As compared to the starch-fed group , the fructose-fed rats presented : hypertriglyceridemia , hypertension , increased susceptibility to heart peroxidation and renal damages . Long-chain inulin and oligofructose-enriched inulin supplementation prevented fructose induced elevated blood pressure , susceptibility to heart peroxidation and renal damages . All inulin-type fructans containing diets prevented fructose induced hypertriglyceridemia . CONCLUSIONS These results suggest that supplementation with inulin-type fructans is efficient against fructose induced hypertension and that effects are most pronounced for long-chain inulin and oligofructose-enriched inulin . We hypothesize that the anti-hypertensive effect of inulin could be explained by the reduction of the high fructose induced oxidative stress
The hypercaloric fructose feeding trials found no significant overall mean arterial blood pressure effect of fructose in comparison with other carbohydrates .
Contrary to previous concerns , we found that isocaloric substitution of fructose for other carbohydrates did not adversely affect blood pressure in humans
Concerns have been raised about the adverse effect of  fructose  on blood pressure .
International dietary guidelines , however , have not addressed fructose intake directly .
A systematic review and meta- analysis was conducted to assess the effect of fructose in isocaloric exchange for other carbohydrates on  systolic , diastolic , and mean arterial blood pressures .