Mechanisms for the acute effect of fructose on postprandial lipemia. The ingestion of a fructose-containing beverage combined with fat cream exacerbates postprandial lipidemia in young healthy women. Acute effects of feeding fructose, glucose and sucrose on blood lipid levels and systemic inflammation Simultaneous ingestion of fructose and fat exacerbates postprandial exogenous lipidemia in young healthy Japanese women. Consumption of fructose-sweetened beverages for 10 weeks reduces net fat oxidation and energy expenditure in overweight/obese men and women Effects of dietary fructose on plasma lipids in healthy subjects. Effects of meals rich in either monounsaturated or saturated fat on lipid concentrations and on insulin secretion and action in subjects with high fasting triglyceride concentrations. Exercise performed immediately after fructose ingestion enhances fructose oxidation and suppresses fructose storage. Sweetener augmentation of serum triacylglycerol during a fat challenge test in humans. Increased postprandial glycaemia, insulinemia, and lipidemia after 10 weeks’ sucrose-rich diet compared to an artificially sweetened diet: a randomised controlled trial Two consecutive high-fat meals affect endothelial-dependent vasodilation, oxidative stress and cellular microparticles in healthy men. alpha-Dicarbonyls increase in the postprandial period and reflect the degree of hyperglycemia. High-fructose corn syrup and sucrose have equivalent effects on energy-regulating hormones at normal human consumption levels. Effects of 4-week very-high-fructose/glucose diets on insulin sensitivity, visceral fat and intrahepatic lipids: an exploratory trial. Differential effects of saturated and monounsaturated fats on postprandial lipemia and glucagon-like peptide 1 responses in patients with type 2 diabetes. Moderate Amounts of Fructose Consumption Impair Insulin Sensitivity in Healthy Young Men Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women.
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 AIM To investigate the acute effects of the ingestion of a fructose-containing beverage combined with fat on postpr and ial lipoprotein metabolism . METHODS Twelve young healthy Japanese women with apolipoprotein E phenotype 3/3 were enrolled in this study . At each of four sessions , the subjects ingested one of four sugar beverages containing fructose and /or glucose ( total : 0.5 g/kg body weight ) combined with OFTT cream ( 1 g/kg , 0.35 g/kg as fat ) in a r and omized crossover design . The four sugar beverages were as follows : 100 % ( w/w ) fructose ( F100 ) , 90 % fructose + 10 % glucose ( F90G10 ) , 55 % fructose + 45 % glucose ( F55G45 ) and 100 % glucose ( G100 ) . Venous blood sample s were obtained at baseline and 0.5 , one , two , four and six hours after ingestion . RESULTS The serum concentrations of TG in the F100 , F90G10 and F55G45 trials were significantly higher than each fasting value at two and four hours , and returned to baseline at six hours , except in the F100 trial . The concentrations at four hours and the incremental areas under the curve for the hepatic triglyceride-rich lipoprotein-triglyceride ( VLDL-TG(TM ) ) levels in the F100 and F90G10 trials were significantly higher and larger , respectively , than those observed in the G100 trial . Meanwhile , the concentrations of RLP-TG and apolipoprotein B-48 peaked at two hours in the G100 trial , versus four hours in the other trials , and did not return to baseline at six hours , except in the G100 trial . At four hours , the ⊿apoB48 tended to be higher in the F100 trial than in the G100 trial . CONCLUSIONS The ingestion of a high-fructose-containing beverage with fat cream delays the clearance of chylomicron and its remnant derived from the intestine and enhances the secretion of triglyceride-rich lipoprotein particles from the liver , thereby inducing postpr and ial lipidemia , even in young healthy women 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 AIM To investigate the acute effects of the simultaneous ingestion of fructose and fat on postpr and ial lipoprotein metabolism in healthy young women . METHODS Nine young healthy Japanese women with a normal weight ( body mass index : 18.5≤- < 25 kg/m(2 ) ) , a normal ovarian cycle and an apolipoprotein E 3/3 phenotype were enrolled as participants and studied on four occasions . At each session , the subjects ingested one of four beverages containing either glucose or fructose ( 0.5 g/kg body weight each ) with or without OFTT cream ( 1 g/kg , 0.35 g/ kg as fat ) in a r and omized crossover design . Blood sample s were collected at baseline and at 0.5 , 1 , 2 , 4 and 6 hours after ingestion . RESULTS The ingestion of fructose combined with fat led to significantly higher rises in the serum triglyceride ( TG ) , remnant-like particle (RLP)-TG , remnant lipoprotein-cholesterol ( RemL-C ) and apolipoprotein B-48 ( apoB48 ) concentrations with delayed peaks compared with that observed following ingestion of the other three types of beverages . The incremental area under the curve (ΔAUC)-TG and ΔAUC-apoB48 were larger than those observed for the ingestion of fat only . The serum RLP-TG and apoB48 concentrations returned to the fasting levels ( 0 hours ) at the end of the test ( 6 hours ) following the ingestion of fat only ; however , these concentrations did not return to the fasting levels following the intake of fructose combined with fat . CONCLUSIONS These findings suggest a delay in the clearance of intestinal TG-rich lipoproteins , namely chylomicron and its remnant , following the ingestion of fructose combined with fat . The simultaneous ingestion of fructose and fat markedly enhances postpr and ial exogenous lipidemia in young healthy Japanese women 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 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 BACKGROUND The nature of dietary fats and fasting concentrations of triglycerides affect postpr and ial hypertriglyceridemia and glucose homeostasis . OBJECTIVES The objectives were to examine the effects of meals enriched in monounsaturated fatty acids ( MUFAs ) or saturated fatty acids ( SFAs ) on postpr and ial lipid , glucose , and insulin concentrations and to examine the extent of β cell function and insulin sensitivity in subjects with high fasting triglyceride concentrations . DESIGN Fourteen men with fasting hypertriglyceridemia and normal glucose tolerance were given meals ( ≈10 kcal/kg body weight ) containing MUFAs , SFAs , or no fat . Blood sample s were collected at baseline and hourly over 8 h for analysis . RESULTS The high-fat meals significantly increased postpr and ial concentrations of triglycerides , nonesterified fatty acids , and insulin and postpr and ial indexes of β cell function . However , postpr and ial indexes of insulin sensitivity decreased significantly . These effects were significantly attenuated with MUFAs relative to SFAs . CONCLUSIONS MUFAs postpr and ially buffered β cell hyperactivity and insulin intolerance relative to SFAs in subjects with high fasting triglyceride concentrations . These data suggest that , in contrast with SFAs , MUFA-based strategies may provide cardiovascular benefits to persons at risk by limiting lipid and insulin excursions and may contribute to optimal glycemic control after meal challenges 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 High concentrations of fructose enhance postpr and ial lipemia following lipid loading whereas glucose exerts a negative or minimal effect . This study evaluated the effect of lower sweetener concentrations and the contribution of their sweetness level and palatability . METHODS At each of four test sessions , twelve male and ten female healthy adults ingested one of four milkshakes containing 108 g dairy cream alone or supplemented with 30 g fructose , 17.5 g glucose or 1 g aspartame .  Blood sample s were collected at baseline , two , four , six and eight hours after ingestion . Sensory discrimination tests were conducted after the last two sessions . RESULTS Fructose and glucose led to 37 % ( p = 0.03 ) and 59 % ( p = 0.08 ) rises in triacylglycerol area under the curve ( TG AUC ) when compared to the plain milkshake , respectively . Although the sweetened shakes were equisweet and were more palatable than the plain shake , the TG rise after the aspartame milkshake did not differ from the plain milkshake . CONCLUSIONS These data indicate that low levels of glucose and fructose consumed with lipid enhance postpr and ial lipemia . Sweetness and palatability did not account for the effect Background The importance of exchanging sucrose for artificial sweeteners on risk factors for developing diabetes and cardiovascular diseases is not yet clear . Objective To investigate the effects of a diet high in sucrose versus a diet high in artificial sweeteners on fasting and postpr and ial metabolic profiles after 10 weeks . Design Healthy overweight subjects were r and omised to consume drinks and foods sweetened with either sucrose ( ∼2 g/kg body weight ) ( n = 12 ) or artificial sweeteners ( n = 11 ) as supplements to their usual diet . Supplements were similar on the two diets and consisted of beverages ( ∼80 weight% ) and solid foods ( yoghurts , marmalade , ice cream , stewed fruits ) . The rest of the diet was free of choice and ad libitum . Before ( week 0 ) and after the intervention ( week 10 ) fasting blood sample s were drawn and in week 10 , postpr and ial blood was sample d during an 8-hour meal test ( breakfast and lunch ) . Results After 10 weeks postpr and ial glucose , insulin , lactate , triglyceride , leptin , glucagon , and GLP-1 were all significantly higher in the sucrose compared with the sweetener group . After adjusting for differences in body weight changes and fasting values ( week 10 ) , postpr and ial glucose , lactate , insulin , GIP , and GLP-1 were significantly higher and after further adjusting for differences in energy and sucrose intake , postpr and ial lactate , insulin , GIP , and GLP-1 levels were still significantly higher on the sucrose-rich diet . Conclusion A sucrose-rich diet consumed for 10 weeks result ed in significant elevations of postpr and ial glycaemia , insulinemia , and lipidemia compared to a diet rich in artificial sweeteners in slightly overweight healthy subjects BACKGROUND A large body of evidence has accumulated indicating a relation between postpr and ial hyperglycemia and hypertriglyceridemia , and the risk of cardiovascular disease . OBJECTIVE We studied possible mechanisms underlying the postpr and ial proatherogenic state by exposing healthy males to two consecutive high-fat mixed meals . PATIENTS / METHODS Seventeen healthy males [ age 25.4 + /- 3 years , body mass index 23.6 + /- 2 kg m(-2 ) ] were studied during two r and omized visits . During the meal visit , subjects consumed st and ardized meals ( 50 g of fat , 55 g of carbohydrates and 30 g of proteins ) as breakfast and 4 h later as lunch . During the control visit , subjects remained fasted . Prior to each blood collection ( before and every 2 h after the first meal ) , flow-mediated dilation ( FMD ) of the brachial artery was measured . RESULTS Although within the normal range , postpr and ial plasma glucose and triacylglycerol concentrations increased significantly , especially after the second meal , as compared with baseline ( 4.8 + /- 0.3 to 5.4 + /- 0.4 , 0.8 + /- 0.2 to 1.7 + /- 0.7 mmol L(-1 ) , respectively ; both P < 0.05 ) and the fasting visit . After the second meal , FMD was significantly impaired ( 6.9 % vs. 3.7 % , P < 0.05 ) whereas oxidized low-density lipoprotein (oxLDL)/LDL cholesterol ratio and malondialdehyde concentrations were markedly elevated ( both P < 0.01 ) . Finally , an increase in total microparticle ( MP ) numbers was observed during the meal visit ( P < 0.05 ) . CONCLUSIONS In healthy males , after two consecutive fat-rich meals , mild elevations in plasma glucose and triacylglycerol were paralleled by impaired FMD , increased markers of oxidative stress and circulating MPs , in particular , after the second meal . These findings may have consequences for subjects with postpr and ial dysmetabolism , including those with Type 2 diabetes OBJECTIVE Chronic hyperglycemia is known to increase tissue glycation and diabetic complications , but controversy exists regarding the independent role of increased postpr and ial glucose excursions . To address this question , we have studied the effect of postpr and ial glycemic excursions ( PPGEs ) on levels of methylglyoxal ( MG ) and 3-deoxyglucosone ( 3-DG ) , two highly reactive precursors of advanced glycation end products ( AGEs ) . RESEARCH DESIGN AND METHODS We performed 4-month crossover studies on 21 subjects with type 1 diabetes and compared the effect of premeal insulin lispro or regular insulin on PPGEs and MG/3-DG excursions . PPGE was determined after st and ard test meal ( STMs ) and by frequent postpr and ial glucose monitoring .  HbA1c and postpr and ial MG and D-lactate were measured by HPLC , whereas 3-DG was determined by gas chromatography/mass spectroscopy . RESULTS Treatment with insulin lispro result ed in a highly significant reduction in PPGEs relative to the regular insulin-treated group ( P = 0.0005 ) . However , HbA1c levels were similar in the two groups , and no relationship was observed between HbA1c and PPGE ( P = 0.93 ) . Significant postpr and ial increases in MG , 3-DG , and D-lactate occurred after the STM . Excursions of MG and 3-DG were highly correlated with levels of PPGE ( R = 0.55 , P = 0.0002 and R = 0.61 , P = 0.0004 ; respectively ) , whereas a significant inverse relationship was seen between PPGE and D-lactate excursions ( R = 0.40 , P = 0.01 ) . Conversely , no correlation was observed between HbAlc and postpr and ial MG , 3-DG , or D-lactate levels . CONCLUSIONS Increased production of MG and 3-DG occur with greater PPGE , whereas HbA1c does not reflect these differences . Reduced PPGE also leads to increased production of D-lactate , indicating a role for increased detoxification in reducing MG levels . The higher postpr and ial levels of MG and 3-DG observed with greater PPGE may provide a partial explanation for the adverse effects of glycemic lability and support the value of agents that reduce glucose excursions 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 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 BACKGROUND Postpr and ial lipemia is important in the development of coronary artery disease because of elevated postpr and ial triacylglycerol-rich plasma lipoproteins and suppressed HDL-cholesterol concentrations . We showed in healthy subjects a possible association between postpr and ial lipid metabolism and the responses of the duodenal incretin hormones glucagon-like peptide 1 ( GLP-1 ) and gastric inhibitory polypeptide after meals rich in saturated and monounsaturated fatty acids ( oleic acid ) , respectively . OBJECTIVE The objective was to compare the postpr and ial responses ( 8 h ) of glucose , insulin , fatty acids , triacylglycerol , gastric inhibitory polypeptide , and GLP-1 to saturated- and monounsaturated-rich test meals . DESIGN Twelve overweight patients with type 2 diabetes ingested 3 meals r and omly : an energy-free soup with 50 g carbohydrate ( control meal ) , the control meal plus 100 g butter , and the control meal plus 80 g olive oil .  Triacylglycerol responses were measured in total plasma and in a chylomicron-rich and a chylomicron-poor fraction . RESULTS No significant differences in the glucose , insulin , or fatty acid responses to the 2 fat-rich meals were seen . The plasma triacylglycerol and chylomicron triacylglycerol responses were highest after the butter meal .  HDL-cholesterol concentrations decreased significantly after the butter meal but did not change significantly after the olive oil meal .  GLP-1 responses were highest after the olive oil meal . CONCLUSIONS Olive oil induced lower triacylglycerol concentrations and higher HDL-cholesterol concentrations than did butter , without eliciting significant changes in glucose , insulin , or fatty acids . Furthermore , olive oil induced higher concentrations of GLP-1 , which may indicate a relation between fatty acid composition , incretin responses , and triacylglycerol metabolism postpr and ially in patients with type 2 diabetes 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 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
Pooled analyses show that fructose in isocaloric exchange for other carbohydrate does not increase postpr and ial triglycerides , although an effect can not be excluded under all conditions .
Fructose providing excess energy does increase postpr and ial triglycerides .
BACKGROUND In the absence of consistent clinical evidence , concerns have been raised that  fructose  raises postpr and ial triglycerides .
PURPOSE A systematic review and meta- analysis was conducted to assess the effect of  fructose on postpr and ial triglycerides .