***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: 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 Using a within-subjects design , we gave over-weight and normal-weight subjects a 500-mL drink of fructose , glucose , or aspartame diluted in lemon-flavored water or plain water in a r and omized fashion at about weekly intervals . Food intake was assessed at a buffet lunch that began 38 min after the preload was completed . Blood was drawn throughout and assayed for concentrations of glucose , insulin , glucagon , and free fatty acid . When subjects drank the fructose preload , they subsequently ate fewer overall calories and fewer grams of fat than when they drank any of the other preloads . The aspartame load did not stimulate intake beyond the plain-water control . The effects of the oxidation of fructose as a possible mechanism for the reduction in food intake is discussed . The effects of insulin in stimulating intake are also discussed 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 Aims /hypothesisType 2 diabetes is regarded as inevitably progressive , with irreversible beta cell failure . The hypothesis was tested that both beta cell failure and insulin resistance can be reversed by dietary restriction of energy intake . Methods Eleven people with type 2 diabetes ( 49.5 ± 2.5 years , BMI 33.6 ± 1.2 kg/m2 , nine male and two female ) were studied before and after 1 , 4 and 8 weeks of a 2.5 MJ ( 600 kcal)/day diet . Basal hepatic glucose output , hepatic and peripheral insulin sensitivity and beta cell function were measured . Pancreas and liver triacylglycerol content was measured using three-point Dixon magnetic resonance imaging . An age- , sex- and weight-matched group of eight non-diabetic participants was studied . Results After 1 week of restricted energy intake , fasting plasma glucose normalised in the diabetic group ( from 9.2 ± 0.4 to 5.9 ± 0.4 mmol/l ; p = 0.003 ) . Insulin suppression of hepatic glucose output improved from 43 ± 4 % to 74 ± 5 % ( p = 0.003 vs baseline ; controls 68 ± 5 % ) . Hepatic triacylglycerol content fell from 12.8 ± 2.4 % in the diabetic group to 2.9 ± 0.2 % by week 8 ( p = 0.003 ) . The first-phase insulin response increased during the study period ( 0.19 ± 0.02 to 0.46 ± 0.07 nmol min−1 m−2 ; p < 0.001 ) and approached control values ( 0.62 ± 0.15 nmol min−1 m−2 ; p = 0.42 ) . Maximal insulin response became supranormal at 8 weeks ( 1.37 ± 0.27 vs controls 1.15 ± 0.18 nmol min−1 m−2 ) . Pancreatic triacylglycerol decreased from 8.0 ± 1.6 % to 6.2 ± 1.1 % ( p = 0.03 ) . Conclusions /interpretationNormalisation of both beta cell function and hepatic insulin sensitivity in type 2 diabetes was achieved by dietary energy restriction alone . This was associated with decreased pancreatic and liver triacylglycerol stores . The abnormalities underlying type 2 diabetes are reversible by reducing dietary energy intake OBJECTIVE : The overall aims of the ADDITION study are to evaluate whether screening for prevalent undiagnosed Type 2 diabetes is feasible , and whether subsequent optimised intensive treatment of diabetes , and associated risk factors , is feasible and beneficial . DESIGN : Population -based screening in three European countries followed by an open , r and omised controlled trial . SUBJECTS AND METHODS : People aged 40–69 y in the community , without known diabetes , will be offered a r and om capillary blood glucose screening test by their primary care physicians , followed , if equal to or greater than 5.5 mmol/l , by fasting and 2-h post-glucose-challenge blood glucose measurements . Three thous and newly diagnosed patients will subsequently receive conventional treatment ( according to current national guidelines ) or intensive multifactorial treatment ( lifestyle advice , prescription of aspirin and ACE-inhibitors , in addition to protocol -driven tight control of blood glucose , blood pressure and cholesterol ) . Patients allocated to intensive treatment will be further r and omised to centre-specific interventions to motivate adherence to lifestyle changes and medication . Duration of follow-up is planned for 5 y. Endpoints will include mortality , macrovascular and microvascular complications , patient health status and satisfaction , process-of-care indicators and costs Background Recent studies have demonstrated a relationship between fructose consumption and risk of developing metabolic syndrome . Mechanisms by which dietary fructose mediates metabolic changes are poorly understood . This study compared the effects of fructose , glucose and sucrose consumption on post-postpr and ial lipemia and low grade inflammation measured as hs-CRP . Methods This was a r and omized , single blinded , cross-over trial involving healthy subjects ( n = 14 ) . After an overnight fast , participants were given one of 3 different isocaloric drinks , containing 50 g of either fructose or glucose or sucrose dissolved in water .  Blood sample s were collected at baseline , 30 , 60 and 120 minutes post intervention for the analysis of blood lipids , glucose , insulin and high sensitivity C-reactive protein ( hs-CRP ) . Results Glucose and sucrose supplementation initially result ed in a significant increase in glucose and insulin levels compared to fructose supplementation and returned to near baseline values within 2 hours . Change in plasma cholesterol , LDL and HDL-cholesterol ( measured as area under curve , AUC ) was significantly higher when participants consumed fructose compared with glucose or sucrose ( P < 0.05 ) . AUC for plasma triglyceride levels however remained unchanged regardless of the dietary intervention . Change in AUC for hs-CRP was also significantly higher in subjects consuming fructose compared with those consuming glucose ( P < 0.05 ) , but not sucrose ( P = 0.07 ) . Conclusion This study demonstrates that fructose as a sole source of energy modulates plasma lipids and hsCRP levels in healthy individuals . The significance of increase in HDL-cholesterol with a concurrent increase in LDL-cholesterol and elevated hs-CRP levels remains to be delineated when considering health effects of feeding fructose-rich diets . Registration number for clinical Objective : 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 bever 
    Output:
    
Results : Replacement of either glucose or sucrose by fructose result ed in significantly lowered peak postpr and ial blood glucose , particularly in people with prediabetes and type 1 and type 2 diabetes .
Similar results were obtained for insulin .
Peak postpr and ial blood triglyceride concentrations did not significantly increase .
Conclusions : Strong evidence exists that substituting fructose for glucose or sucrose in food or beverages lowers peak postpr and ial blood glucose and insulin concentrations .
Isoenergetic replacement does not result in a substantial increase in blood triglyceride concentrations