title: Mechanisms for the acute effect of fructose on postprandial lipemia. Effects of dietary fructose on plasma lipids in healthy subjects. Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women.
abstract: 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 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 CONTEXT Elevated nonfasting triglycerides indicate the presence of remnant lipoproteins , which may promote atherosclerosis . OBJECTIVE To test the hypothesis that very high levels of nonfasting triglycerides predict myocardial infa rct ion ( MI ) , ischemic heart disease ( IHD ) , and death . DESIGN , SETTING , AND PARTICIPANTS A prospect i ve cohort study of 7587 women and 6394 men from the general population of Copenhagen , Denmark , aged 20 to 93 years , followed up from baseline ( 1976 - 1978 ) until 2004 . MAIN OUTCOME MEASURES Hazard ratios ( HRs ) for incident MI , IHD , and total death according to baseline nonfasting triglyceride level categories of 1 to 1.99 mmol/L ( 88.5 - 176.1 mg/dL ) , 2 to 2.99 mmol/L ( 177.0 - 264.6 mg/dL ) , 3 to 3.99 mmol/L ( 265.5 - 353.0 mg/dL ) , 4 to 4.99 mmol/L ( 354.0 - 441.6 mg/dL ) , and 5 mmol/L or more ( > or = 442.5 mg/dL ) vs triglyceride levels of less than 1 mmol/L ( < 88.5 mg/dL ) . RESULTS With increasing levels of nonfasting triglycerides , levels of remnant lipoprotein cholesterol increased . During a mean follow-up of 26 years , 1793 participants ( 691 women and 1102 men ) developed MI , 3479 ( 1567 women and 1912 men ) developed IHD , and 7818 ( 3731 women and 4087 men ) died . For MI , among women , the age-adjusted HRs and multifactorially adjusted HRs ( aHRs ) for each respective category per 1-mmol/L increase in nonfasting triglyceride levels were 2.2 ( aHR , 1.7 ) , 4.4 ( aHR , 2.5 ) , 3.9 ( aHR , 2.1 ) , 5.1 ( aHR , 2.4 ) , and 16.8 ( aHR , 5.4 ) ; for both , P for trend < .001 . For MI , among men , the values were 1.6 ( aHR , 1.4 ) , 2.3 ( aHR , 1.6 ) , 3.6 ( aHR , 2.3 ) , 3.3 ( aHR , 1.9 ) , and 4.6 ( aHR , 2.4 ) ; for both , P for trend < .001 . For IHD , among women , the values were 1.7 ( aHR , 1.4 ) , 2.8 ( aHR , 1.8 ) , 3.0 ( aHR , 1.8 ) , 2.1 ( aHR , 1.2 ) , and 5.9 ( aHR , 2.6 ) ; for both , P for trend < .001 . For IHD , among men , the values were 1.3 ( aHR , 1.1 ) , 1.7 ( aHR , 1.3 ) , 2.1 ( aHR , 1.3 ) , 2.0 ( aHR , 1.2 ) , and 2.9 ( aHR , 1.5 ) ; P for trend < .001 for age-adjusted and P for trend = .03 for multifactorially adjusted . For total death , among women , the values were 1.3 ( aHR , 1.3 ) , 1.7 ( aHR , 1.6 ) , 2.2 ( aHR , 2.2 ) , 2.2 ( aHR , 1.9 ) , and 4.3 ( aHR , 3.3 ) ; for both , P for trend < .001 . For total death , among men , the values were 1.3 ( aHR , 1.2 ) , 1.4 ( aHR , 1.4 ) , 1.7 ( aHR , 1.5 ) , 1.8 ( aHR , 1.6 ) , and 2.0 ( aHR , 1.8 ) ; for both , P for trend < .001 . CONCLUSION In this general population cohort , elevated nonfasting triglyceride levels were associated with increased risk of MI , IHD , and death in men and women CONTEXT The association of triglycerides with incident cardiovascular disease  remains controversial . Although triglyceride levels are typically obtained in the fasting state , postpr and ial hypertriglyceridemia may play an important role in atherosclerosis . OBJECTIVE To determine the association of  triglyceride levels ( fasting vs nonfasting ) and risk of future cardiovascular events . DESIGN , SETTING , AND PARTICIPANTS Prospect i ve study of 26,509 initially healthy US women ( 20,118 fasting and 6391 nonfasting ) participating in the Women 's Health Study , enrolled between November 1992 and July 1995 and undergoing follow-up for a median of 11.4 years .  Triglyceride levels  were measured in blood sample s obtained at time of enrollment . MAIN OUTCOME MEASURE Hazard ratios for incident cardiovascular events ( nonfatal myocardial infa rct ion , nonfatal ischemic stroke , coronary revascularization , or cardiovascular death ) . RESULTS At baseline , triglyceride levels in fasting as well as nonfasting women correlated with traditional cardiac risk factors and markers of insulin resistance . During a median follow-up of 11.4 years , 1001 participants experienced an incident cardiovascular event ( including 276 nonfatal myocardial infa rct ions , 265 ischemic strokes , 628 coronary revascularizations , and 163 cardiovascular deaths ) , for an overall rate of 3.46 cardiovascular events per 1000 person-years of follow-up . After adjusting for age , blood pressure , smoking , and use of hormone therapy , both fasting and nonfasting triglyceride levels predicted cardiovascular events . Among fasting participants , further adjustment for levels of total and high-density lipoprotein cholesterol and measures of insulin resistance weakened this association ( fully adjusted hazard ratio [ 95 % confidence interval ] for increasing tertiles of triglyceride levels : 1 [ reference ] , 1.21 [ 0.96 - 1.52 ] , and 1.09 [ 0.85 - 1.41 ] [ P = .90 for trend ] ) . In contrast , nonfasting triglyceride levels maintained a strong independent relationship with cardiovascular events in fully adjusted models ( hazard ratio [ 95 % confidence interval ] for increasing tertiles of levels : 1 [ reference ] , 1.44 [ 0.90 - 2.29 ] , and 1.98 [ 1.21 - 3.25 ] [ P = .006 for trend ] ) . In secondary analyses stratified by time since participants ' last meal , triglyceride levels measured 2 to 4 hours postpr and ially had the strongest association with cardiovascular events ( fully adjusted hazard ratio [ 95 % confidence interval ] for highest vs lowest tertiles of levels , 4.48 [ 1.98 - 10.15 ] [ P<.001 for trend ] ) , and this association progressively decreased with longer periods of fasting . CONCLUSIONS In this cohort of initially healthy women , nonfasting triglyceride levels were associated with incident cardiovascular events , independent of traditional cardiac risk factors , levels of other lipids , and markers of insulin resistance ; by contrast , fasting triglyceride levels showed little independent relationship
target: 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: 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 .