human
***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 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 
    Output:
    
agent
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 .
***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 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 
    Output:
    