Effects of dietary fructose on plasma lipids in healthy subjects. Exercise performed immediately after fructose ingestion enhances fructose oxidation and suppresses fructose storage. The ingestion of a fructose-containing beverage combined with fat cream exacerbates postprandial lipidemia in young healthy women. Consumption of fructose-sweetened beverages for 10 weeks reduces net fat oxidation and energy expenditure in overweight/obese men and women Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. Simultaneous ingestion of fructose and fat exacerbates postprandial exogenous lipidemia in young healthy Japanese women. Fructose prefeeding reduces the glycemic response to a high-glycemic index, starchy food in humans. Plasma-triglycerides and exercise: A delicate balance Walking Reduces Postprandial Insulin Secretion in Obese Adolescents Consuming a High-Fructose or High-Glucose Diet. Sweetener augmentation of serum triacylglycerol during a fat challenge test in humans. Acute effects of feeding fructose, glucose and sucrose on blood lipid levels and systemic inflammation Postprandial hyperglycemia impairs vascular endothelial function in healthy men by inducing lipid peroxidation and increasing asymmetric dimethylarginine:arginine. A dose-response study of consuming high-fructose corn syrup-sweetened beverages on lipid/lipoprotein risk factors for cardiovascular disease in young adults. Altering source or amount of dietary carbohydrate has acute and chronic effects on postprandial glucose and triglycerides in type 2 diabetes: Canadian trial of Carbohydrates in Diabetes (CCD). Pitavastatin prevents postprandial endothelial dysfunction via reduction of the serum triglyceride level in obese male 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. Appetite hormones and energy intake in obese men after consumption of fructose, glucose and whey protein beverages Improvement of Postprandial Endothelial Function After a Single Dose of Exenatide in Individuals With Impaired Glucose Tolerance and Recent-Onset Type 2 Diabetes Atorvastatin and omega-3 fatty acids protect against activation of the coagulation system in patients with combined hyperlipemia. The rationale for paired pre- and postprandial self-monitoring of blood glucose: the role of glycemic variability in micro- and macrovascular risk Exenatide suppresses postprandial elevations in lipids and lipoproteins in individuals with impaired glucose tolerance and recent onset type 2 diabetes mellitus. Effect of xuezhikang, a cholestin extract, on reflecting postprandial triglyceridemia after a high-fat meal in patients with coronary heart disease. Dietary sugars stimulate fatty acid synthesis in adults.
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 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 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 / 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 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 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 The study objective was to determine whether a small dose of fructose administered before or simultaneously with a high glycemic index , starchy food decreases postpr and ial glycemic response .  Nondiabetic healthy adults ( n = 31 ; mean + /- SEM : age , 26 + /- 1 y ; weight , 66.1 + /- 2.6 kg ; body mass index , 23.3 + /- 0.6 kg/m(2 ) ) were studied in a r and omized crossover design . Treatments consisted of 50 g available carbohydrate from instant mashed potatoes fed alone ( control ) or with 10 g fructose fed 60 , 30 or 0 min before the potato meal . Capillary finger-stick blood sample s were analyzed for glucose concentration at -60 , -30 , 0 , 15 , 30 , 45 , 60 , 90 and 120 min relative to the ingestion of the potato meal . Compared with the control , the positive incremental area under the glucose curve was reduced 25 and 27 % ( P < 0.01 ) when fructose was fed either 60 or 30 min before the meal , respectively . In contrast to previous studies demonstrating that immediate administration of a small amount of fructose lowers the glycemic response to a glucose solution , we found that fructose must be consumed before a starchy food to reduce postpr and ial glycemia Summary Alimentary lipemia was studied in 12 healthy young men with and without exercise .  Three sets of experiments were performed . While continuous exercise of 90 min duration significantly reduced postpr and ial triglycerides by 26 % ( study I ) , this effect could not be observed when exercise was interrupted for 5 min after each 25 min ( study II ) . Plasma free fatty acid concentrations , in the latter experiment , were significantly higher ( by 311 % ) than during rest . When , in a third experiment continuous exercise was compared with intermittent physical activity , the latter condition significantly increased postpr and ial triglyceridemia , most probably due to precipitous rises of free fatty acids on each interruption of ergometry . It is concluded that in the third experiment the balance between triglyceride removal and triglyceride synthesis was shifted toward the latter . Whether exercise lowers , leaves unaltered , or raises plasma triglyceride levels may depend on subtle changes of experimental design BACKGROUND This study assessed if walking at a self-selected pace could improve postpr and ial glucose and insulin concentrations in obese adolescents consuming high-fructose ( HF ) or high-glucose ( HG ) diets . METHODS Seven obese male and female adolescents ( 18 ± 1 yr ) performed 4 , 15-day trials in a r and om order , including 1 ) HF-diet ( 50 g fructose/d added to normal diet ) while being sedentary , 2 ) HG-diet ( 50 g glucose/d ) while sedentary , 3 ) HF-diet with additional walking , and 4 ) HG-diet with additional walking . On the 15th day of each trial , the participants performed mixed meal testing in the laboratory in which they consumed three liquid shakes ( either HF or HG ) and during the HF and HG sedentary trials , the participants took < 4000 steps while in the laboratory but during the walking trials took ≥ 13,000 steps during testing . RESULTS Walking did not alter postpr and ial glucose concentrations . Although walking reduced insulin secretion by 34 % and 25 % during the HF- and HG-diet , respectively ( P < .05 ) , total insulin concentrations were only significantly reduced ( P > .05 ) with walking during the HF trial , possibly because walking enhanced insulin clearance to a greater extent during the HF-diet . CONCLUSIONS Walking reduces postpr and ial insulin secretion in obese adolescents consuming a high-fructose or high-glucose diet 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 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 Postpr and ial hyperglycemia induces  vascular endothelial dysfunction ( VED )  and increases future cardiovascular disease risk . We hypothesized that postpr and ial hyperglycemia would decrease vascular function in healthy men by inducing oxidative stress and proinflammatory responses and increasing asymmetric dimethylarginine : arginine ( ADMA : arginine ) , a biomarker that is predictive of reduced NO bio synthesis . In a r and omized , cross-over design , healthy men ( n = 16 ; 21.6 ± 0.8 y ) ingested glucose or fructose  ( 75 g  )  after an  overnight fast  . Brachial artery flow-mediated dilation ( FMD ) , plasma glucose and insulin , antioxidants , malondialdehyde ( MDA ) , inflammatory proteins , arginine , and ADMA were measured at regular intervals during the 3-h postpr and ial period . Baseline FMD did not differ between trials ( P > 0.05 ) . Postpr and ial FMD was reduced following the ingestion of glucose only . Postpr and ial MDA concentrations increased to a greater extent following the ingestion of glucose compared to fructose . Plasma arginine decreased and the ratio of ADMA : arginine increased to a greater extent following the ingestion of glucose . Inflammatory cytokines and cellular adhesion molecules were unaffected by the ingestion of either sugar . Postpr and ial AUC(0 - 3 h ) for FMD and MDA were inversely related ( r = -0.80 ; P < 0.05 ) , suggesting that hyperglycemia-induced lipid peroxidation suppresses postpr and ial vascular function . Collectively , these findings suggest that postpr and ial hyperglycemia in healthy men  reduces endothelium-dependent vasodilation by increasing lipid peroxidation independent of inflammation . Postpr and ial alterations in arginine and ADMA : arginine also suggest that acute hyperglycemia may induce VED by decreasing NO bioavailability through an oxidative stress-dependent mechanism . Additional work is warranted to define whether inhibiting lipid peroxidation and restoring arginine metabolism would mitigate hyperglycemia-mediated decreases in vascular function BACKGROUND National Health and Nutrition Examination Survey data show an increased risk of cardiovascular disease ( CVD ) mortality with an increased intake of added sugar . OBJECTIVE We determined the dose-response effects of consuming beverages sweetened with high-fructose corn syrup ( HFCS ) at zero , low , medium , and high proportions of energy requirements ( Ereq ) on circulating lipid/lipoprotein risk factors for CVD and uric acid in adults [ age : 18 - 40 y ; body mass index ( in kg/m(2 ) ) : 18 - 35 ] . DESIGN We conducted a parallel-arm , nonr and omized , double-blinded intervention study in which adults participated in 3.5 inpatient days of baseline testing at the University of California Davis Clinical and Translational Science Center 's Clinical Research Center . Participants then consumed beverages sweetened with HFCS at 0 % ( aspartame sweetened , n = 23 ) , 10 % ( n = 18 ) , 17.5 % ( n = 16 ) , or 25 % ( n = 28 ) of Ereq during 13 outpatient days and during 3.5 inpatient days of intervention testing at the research center . We conducted 24-h serial blood collection s during the baseline and intervention testing periods . RESULTS Consuming beverages containing 10 % , 17.5 % , or 25 % Ereq from HFCS produced significant linear dose-response increases of lipid/lipoprotein risk factors for CVD and uric acid : postpr and ial triglyceride ( 0 % : 0 ± 4 ; 10 % : 22 ± 8 ; 17.5 % : 25 ± 5 : 25 % : 37 ± 5 mg/dL , mean of Δ ± SE , P < 0.0001 effect of HFCS-dose ) , fasting LDL cholesterol ( 0 % : -1.0 ± 3.1 ; 10 % : 7.4 ± 3.2 ; 17.5 % : 8.2 ± 3.1 ; 25 % : 15.9 ± 3.1 mg/dL , P < 0.0001 ) , and 24-h mean uric acid concentrations ( 0 % : -0.13 ± 0.07 ; 10 % : 0.15 ± 0.06 ; 17.5 % : 0.30 ± 0.07 ; 25 % : 0.59 ± 0.09 mg/dL , P < 0.0001 ) . Compared with beverages containing 0 % HFCS , all 3 doses of HFCS-containing beverages increased concentrations of postpr and ial triglyceride , and the 2 higher doses increased fasting and /or postpr and ial concentrations of non-HDL cholesterol , LDL cholesterol , apolipoprotein B , apolipoprotein CIII , and uric acid . CONCLUSIONS Consuming beverages containing 10 % , 17.5 % , or 25 % Ereq from HFCS produced dose-dependent increases in circulating lipid/lipoprotein risk factors for CVD and uric acid within 2 wk . These results provide mechanistic support for the epidemiologic evidence that the risk of cardiovascular mortality is positively associated with consumption of increasing amounts of added sugars . This trial was registered at clinical trials.gov as NCT01103921 BACKGROUND AND AIMS Nutrition recommendations for type 2 diabetes ( T2DM ) are partly guided by the postpr and ial responses elicited by diets varying in carbohydrate ( CHO ) . We aim ed to explore whether long-term changes in postpr and ial responses on low-glycemic-index ( GI ) or low-CHO diets were due to acute or chronic effects in T2DM . METHODS AND RESULTS Subjects with diet-alone-treated T2DM were r and omly assigned to high-CHO/high-GI ( H ) , high-CHO/low-GI ( L ) , or low-CHO/high-monounsaturated-fat ( M ) diets for 12-months . At week-0 ( Baseline ) postpr and ial responses after H-meals ( 55 % CHO , GI = 61 ) were measured from 0800 h to 1600 h. After 12 mo subjects were r and omly assigned to H-meals or study diet meals ( L , 57 % CHO , GI = 50 ; M , 44 % CHO , GI = 61 ) . This yielded 5 groups : H diet with H-meals ( HH , n = 34 ) ; L diet with H- ( LH , n = 17 ) or L-meals ( LL , n = 16 ) ; and M diet with H- ( MH , n = 18 ) or M meals ( MM , n = 19 ) . Postpr and ial glucose fluctuations were lower in LL than all other groups ( p < 0.001 ) . Changes in postpr and ial-triglycerides differed among groups ( p < 0.001 ) . After 12 mo in HH and MM both fasting- and postpr and ial-triglycerides were similar to Baseline while in MH postpr and ial-triglycerides were significantly higher than at Baseline ( p = 0.028 ) . In LH , triglycerides were consistently ( 0.18 - 0.34 mmol/L ) higher than Baseline throughout the day , while in LL the difference from Baseline varied across the day from 0.04 to 0.36 mmol/L ( p < 0.001 ) . CONCLUSION Low-GI and low-CHO diets have both acute and chronic effects on postpr and ial glucose and triglycerides in T2DM subjects . Thus , the composition of the acute test-meal and the habitual diet should be considered when interpreting the nutritional implication s of different postpr and ial responses Obesity is a well-established risk factor for the development and progression of coronary heart disease . Moreover , endothelial dysfunction is an early event in atherosclerosis and is known to be associated with postpr and ial hypertriglyceridemia . The purpose of this study was to determine whether a statin might have an effect on postpr and ial hypertriglyceridemia , and thereby on endothelial function in obese subjects . Twenty-four obese male subjects were recruited for this study . They were r and omly assigned to receive pitavastatin ( 2 mg/day ) or placebo for 2 weeks . The oral fat loading test using OFTT cream was performed pre- and post-treatment , in which the lipid profile and flow-mediated dilation ( FMD ) were assessed before and 4 h after an oral fat load . In the oral fat loading test conducted pretreatment , the oral fat load induced a marked increase of the serum triglyceride ( TG ) level and decrease in FMD in the pitavastatin and placebo group . In the test conducted post-treatment , the increase in postpr and ial TG was attenuated ( + 183 vs. + 81 mg/dL , P < 0.001 ) and decrease in postpr and ial FMD was completely abolished ( −1.1 vs. + 0.1 % , P < 0.01 ) by pitavastatin treatment . Moreover , there was a good correlation between the change in postpr and ial TG and the change in postpr and ial FMD after the 2 weeks of treatment ( r = −0.737 , P < 0.001 ) . Pitavastatin might prevent endothelial dysfunction caused by postpr and ial hypertriglyceridemia within 2 weeks of therapy in obese subjects 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 Objective : To investigate appetite responses over 4 h to fructose beverages in obese men , relative to glucose and whey protein . Second , to investigate the effect of combining whey and fructose on postpr and ial appetite hormones . Design : R and omized , double-blind crossover study of four beverages ( 1.1 MJ ) containing 50 g of whey , fructose , glucose or 25 g whey+25 g fructose . Blood sample s and appetite ratings were collected for 4 h then a buffet meal was offered . Subjects : Twenty-eight obese men ( age : 57.0±1.6 years , body mass index : 32.5±0.6 kg/m2 )  Measurements : Plasma ghrelin ( total ) , glucagon-like peptide-1 ( GLP-1 7–36 ) , cholecystokinin-8 , glucose , insulin and appetite ratings were assessed at baseline and 30 , 45 , 60 , 90 , 120 , 180 , 240 min after beverages , followed by measurement of ad libitum energy intake . Results : Fructose  produced lower glycaemia and insulinaemia compared to the glucose treatment ( P<0.0001 ) ; whereas postpr and ial ghrelin , GLP-1 and cholecystokinin responses were similar after both treatments . Whey protein produced a prolonged ( 2–4 h ) suppression of ghrelin ( P=0.001 ) and elevation of GLP-1 ( P=0.002 ) and cholecystokinin ( P=0.003 ) that were reduced when combined with fructose , while glucose and insulin responses were similar . Energy intake after 4 h was independent of beverage type ( glucose 4.7±0.2 MJ ; fructose 4.9±0.3 MJ ; whey 4.6±0.3 MJ ; whey/fructose 4.8±0.3 MJ ; P>0.05 ) . Conclusion : In obese men  , fructose- and glucose-based beverages had similar effects on appetite and associated regulatory hormones , independent of the differing glycaemic and insulinaemic responses . The contrasting profile of plasma ghrelin , GLP-1 and cholecystokinin after whey protein consumption did not impact on ad libitum intake 4 h later and was attenuated when 50 % of whey was replaced with fructose OBJECTIVE Endothelial dysfunction is frequently present in individuals with insulin resistance or type 2 diabetes and can be induced by high-fat or high-carbohydrate meals . Because exenatide reduces postpr and ial glucose and lipid excursions , we hypothesized that it may also improve postpr and ial endothelial function . RESEARCH DESIGN AND METHODS In a double-blinded r and omized crossover design , postpr and ial endothelial function was examined in 28 individuals with impaired glucose tolerance or recent-onset type 2 diabetes after a single injection of exenatide or placebo given just before a high-fat meal . Endothelial function was determined with peripheral arterial tonometry pre- and postpr and ially . RESULTS Postpr and ial endothelial function was higher after exenatide compared with placebo ( P = 0.0002 ) . In the placebo phase , postpr and ial change in endothelial function was inversely associated with mean postpr and ial concentrations of triglycerides ( r = −0.62 , P = 0.0004 ) . Changes in postpr and ial triglyceride concentrations explained 64 % of exenatide 's effect on postpr and ial endothelial function . CONCLUSIONS Exenatide  ameliorates postpr and ial endothelial dysfunction after a high-fat meal Activation of factor (F)VII by tissue factor may represent a critical event during plaque rupture in acute coronary syndromes . Patients with combined hyperlipemia are at high risk for developing coronary heart disease and their tendency to thrombosis may be accelerated during postpr and ial hyperlipemia . In the present double-blind , placebo-controlled parallel study , 42 patients with combined hyperlipemia and serum triglycerides between 2.0 and 15.0 mmol L(-1 ) and serum cholesterol > 5.3 mmol L-1 at the end of a 3-month dietary run-in period were treated with atorvastatin at 10 mg day-1 for at least 10 weeks . During the last 5 weeks the patients were r and omized into two groups receiving 1.68 g day(-1 ) omega-3 fatty acids ( omega-3 FA ) or placebo ( corn oil ) . The fasting levels of FVII antigen ( FVII-Ag ) and FVII coagulant activity ( FVII : C ) were high compared with healthy males . The fasting levels of activated FVII ( FVIIa ) and FVII-Ag correlated both to serum triglycerides and apolipoprotein A1 ( apoA1 ) . FVIIa and FVII : C increased during postpr and ial hyperlipemia . This increase of FVIIa correlated to the fasting triglyceride and apoA1 levels , but not to the degree of postpr and ial hypertriglyceridemia . The concentrations of fasting FVIIa in these patients were reduced in parallel with a reduction of fasting triglycerides by treatment with atorvastatin + placebo . This treatment also reduced the postpr and ial level of FVIIa . omega-3 FA in addition to atorvastatin further reduced FVIIa concentrations , fasting and postpr and ially , and also significantly reduced FVII : C and FVII-Ag during postpr and ial hyperlipemia . Prothrombin fragment 1 + 2 ( F1 + 2 ) increased during postpr and ial hyperlipemia . This increase was significantly reduced after treatment with atorvastatin plus omega-3 FA . The increase of F1 + 2 measured as incremental area under the curve ( iAUC ) during postpr and ial hyperlipemia correlated to the fasting levels of FVIIa , FVII : C and FVII-Ag and also to the levels of these factors during postpr and ial lipemia . In conclusion , patients with combined hyperlipemia are at risk for activation of the coagulation system , particularly during postpr and ial lipemia . This activation may be significantly reduced by statins and omega-3 FA ABSTRACT Background : Decisions regarding diabetes management traditionally have been driven by the results of fasting plasma glucose measurement or measurement of glycosylated hemoglobin ( A1C ) , yet glycemic control remains far from optimal in many individuals with diabetes . Mounting evidence implicates glycemic variability , manifested predominantly as postpr and ial glycemic spikes , as a key factor in the development of macrovascular complications . Recent studies suggest that newer therapies specifically targeting postpr and ial hyperglycemia can significantly reduce postpr and ial glucose levels and improve overall glycemic control . Methods : A Medline search was performed using the term ‘ postchallenge ’ or ‘ postpr and ial ’ , together with glucose or diabetes . After excluding review articles and case studies , we review ed primary articles , meta-analyses , and references therein and selected those that best addressed this topic . Selection bias may be considered a potential limitation of this approach . Findings : Although not conclusively demonstrated by prospect i ve studies , a wealth of evidence suggests that postpr and ial hyperglycemia should not be ignored as an important target for preventing complications of diabetes . Conclusions : Improved detection and management of postpr and ial hyperglycemia and glycemic variability is necessary to optimize glycemic control . Meal-based self-monitoring of blood glucose ( SMBG ) has been shown to improve glycemic control as part of a comprehensive management strategy by helping patients underst and the effects of food choices , physical activity , and medications on blood glucose concentrations . SMBG can also help healthcare professionals recognize postpr and ial hyperglycemia , guide therapeutic adjustments and receive more timely feedback regarding medication changes . The arrival of new therapies that specifically target postpr and ial hyperglycemia offer healthcare professionals the opportunity to optimally manage diabetes OBJECTIVE Chronic exenatide treatment in type 2 diabetes is associated with improved glucose control and fasting lipid levels , as well as weight loss . Less established is whether exenatide directly reduces postpr and ial lipid and lipoprotein levels without the reduction in body weight or fasting glucose and triglycerides levels that frequently occur with prolonged therapy . Therefore , the effect of a single injection of exenatide on postpr and ial lipids , remnant lipoproteins , and apolipoproteins was studied . METHODS A double-blinded , r and omized , placebo-controlled , crossover study was conducted in 35 subjects ( 31 men and 4 women ) with impaired glucose tolerance ( n=20 ) or recent onset type 2 diabetes ( n=15 ) . A single subcutaneous injection of exenatide ( 10 microg ) or normal saline was administered just prior to a high-calorie , fat-enriched breakfast meal . Concentrations of triglycerides ( TG ) , apolipoproteins B-48 and CIII , non-esterified fatty acids ( NEFA ) , and remnant lipoprotein ( RLP ) cholesterol and TG in serum or plasma were measured prior to the injection and for up to 8 h postpr and ially . RESULTS Exenatide markedly reduced postpr and ial elevation of TG , apolipoproteins B-48 and CIII , RLP-cholesterol and RLP-triglyceride ( all p<0.001 ) . Postpr and ial declines in NEFA were less pronounced but persisted longer with exenatide compared to placebo ( p<0.05 ) . These effects of exenatide were not affected either by glucose tolerance status or by treatment with statins . CONCLUSION These results demonstrate that exenatide acutely and profoundly inhibits postpr and ial excursions of proatherogenic lipids and lipoproteins and may offer additional cardiovascular risk reduction ( NCT00974272 ) The effect of xuezhikang on postpr and ial triglyceride ( TG ) level was investigated in patients with coronary heart disease ( CHD ) after a high-fat meal ( 800 cal ; 50 g fat ) . Fifty CHD patients were r and omly divided into two groups to accept xuezhikang ( xuezhikang group ) 1200 mg/day ( 600 mg twice daily ) or not ( control group ) on the base of routine therapy which included aspirin , metoprolol and fosinopril and nitrates during the whole 6 weeks following-up . Xuezhikang significantly reduced fasting serum total cholesterol ( TC ) ( -20 % ) , low-density lipoprotein cholesterol ( LDL-C , -34 % ) , TG ( -32 % ) and apoB ( -27 % ) levels , and raised fasting high-density lipoprotein cholesterol ( HDL-C , 18 % ) and apoA-I ( 13 % ) levels ( P<0.001 ) . The postpr and ial serum TG levels at 2 , 4 and 6 h decreased 32 , 38 and 43 % , respectively , in xuezhikang group ( P<0.001 ) . The TG area under the curve over the fasting TG level ( TG-AUC ) significantly decreased in CHD patients accepted xuezhikang with normal ( less than 1.7 mmol/l ) and elevated ( 1.74 to 2.92 mmol/l ) fasting TG levels by 45 and 50 % , respectively ( P<0.001 ) . Routine therapy had no significant effect on the fasting and postpr and ial lipid and apolipoprotein levels . The change of TG-AUC was significantly related to the changes of fasting TG , TC , LDL-C , and HDL-C levels after the treatment , which were related to the changes of fasting apoA-I and apoB levels significantly ( P<0.001 ) . Xuezhikang was shown to be beneficial in the treatment of reflecting postpr and ial triglyceridemia in CHD patients with normal and mildly elevated fasting TG levels 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
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 .