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: PUFA of the n−6 and n−3 series have beneficial effects on key risk factors of coronary heart disease ( CHD ) . Our earlier studies on the intake of FA and on the FA composition of plasma and platelet phospholipids suggested the need to improve the n−3 PUFA nutritional status in the Indian population . The present long-term study was conducted on 80 middle-aged Indian subjects ( 40 men and 40 women ) using the subjects ' own home-prepared diets to evaluate the effects of dietary n−3 PUFA on biochemical indices of CHD risk .  Substitution of Blend G ( equal proportions of groundnut and canola oils ) for groundnut oil or substitution of Blend S ( equal proportions of sunflower and canola oils ) for sunflower oil  increased α-linolenic acid ( ALNA ) fourfold and decreased the linoleic acid (LA)/ALNA ratio from 35 to 6 and 65 to 9 , respectively . Twelve subjects ( six men and six women ) who received Blend G were switched back to groundnut oil and were administered 0.3 g daily of long-chain ( LC ) n−3 PUFA from fish oil . At the end of the trial period for both blends in both sexes , plasma lipid and apolipoprotein levels had not changed , and ADP-induced aggregation had decreased . In plasma and platelet phospholipids , LA as well as LCn-3 PUFA had increased , suggesting competition between LA and ALNA for metabolism into the respective LC-PUFA . Fish oil supplementation  increased LCn-3 PUFA in plasma and platelet phospholipids , decreased ADP-induced platelet aggregation , and increased plasma cholesterol . On the basis of the increased LCn-3 PUFA in plasma phospholipids , it was calculated that 0.75 % energy ( en% ) ( 2.2 g ) ALNA ( from vegetable oils ) may be required to increase LCn-3 PUFA to about the same extent as 0.1 en% ( 0.3 g ) LCn-3 PUFA ( from fish oils ) . Since both n−6 and n−3 PUFA play a critical role in fetal growth and development and in the programming of diet-related chronic diseases in adults , an improvement in the n−3 PUFA nutritional status in cereal-based diets through long-term use of cooking oils containing 25–40 % LA and 4 % ALNA may contribute to the prevention of CHD in Indians High linoleic acid ( LA ) intakes have been suggested to reduce alpha-linolenic acid [ ALA , 18:3(n-3 ) ] metabolism to eicosapentaenoic acid [ EPA , 20:5(n-3 ) ] and docosahexaenoic acid [ DHA , 22:6(n-3 ) ] , and favor high arachidonic acid [ ARA , 20:4(n-6 ) ] . We used a r and omized cross-over study with men ( n = 22 ) to compare the effect of replacing vegetable oils high in LA with oils low in LA in foods , while maintaining constant ALA , for 4 wk each , on plasma ( n-3 ) fatty acids . Nonvegetable sources of fat , except fish and seafoods , were unrestricted . We determined plasma phospholipid fatty acids at wk 0 , 2 , 4 , 6 , and 8 , and triglycerides , cholesterol , serum CRP , and IL-6 , and platelet aggregation at wk 0 , 4 , and 8 .  LA and ALA intakes were 3.8 + /- 0.12 % and 1.0 + /- 0.05 % , and 10.5 + /- 0.53 % and 1.1 + /- 0.06 % energy with LA : ALA ratios of 4:0 and 10:1 during the low and high LA diets , respectively . The plasma phospholipid LA was higher and EPA was lower during the high than during the low LA diet period ( P < 0.001 ) , but DHA declined over the 8-wk period ( r = -0.425 , P < 0.001 ) . The plasma phospholipid ARA : EPA ratios were ( mean + /- SEM ) 20.7 + /- 1.52 and 12.9 + /- 1.01 after 4 wk consuming the high or low LA diets , respectively ( P < 0.001 ) ; LA was inversely associated with EPA ( r = -0.729 , P < 0.001 ) but positively associated with ARA : EPA ( r = 0.432 , P < 0.001 ) . LA intake did not influence ALA , ARA , DPA , DHA , or total , LDL or HDL cholesterol , CRP or IL-6 , or platelet aggregation . In conclusion , high LA intakes decrease plasma phospholipid EPA and increase the ARA : EPA ratio , but do not favor higher ARA Dietary alpha-linolenic acid ( ALA ) can be converted to long-chain ( n-3 ) PUFA in humans and may potentially reproduce the beneficial effects of eicosapentaenoic ( EPA ) and docosahexaenoic ( DHA ) acids on risk factors for coronary heart disease ( CHD ) . This study compared the effects of increased intakes of ALA with those of dietary EPA and DHA on blood coagulation and fibrinolytic factors in fasting subjects . A placebo-controlled , parallel study was conducted in 150 moderately hyperlipidemic subjects , age 25 - 72 y. Subjects were r and omly assigned to one of five interventions and consumed a total intake of 0.8 or 1.7g/d EPA+DHA , 4.5 or 9.5g/d ALA or control ( linoleic acid ; LA ) for 6 mo . Fatty acids were incorporated into 25 g of fat spread , which replaced the subject 's normal spread and three capsules . Long-term supplementation with either dietary EPA+DHA or estimated biologically equivalent amounts of ALA did not affect factors VIIa , VIIc , VIIag , XIIa , XIIag , fibrinogen concentrations , plasminogen activator inhibitor-1 or tissue plasminogen activator activity compared with the control . ( n-3 ) PUFA of plant or marine origin do not differ from one another or from LA in their effect on a range of blood coagulation and fibrinolytic factors Both ( n-3 ) long-chain PUFA ( LCPUFA ) and linoleic acid [ LA , 18:2(n-6 ) ] improve cardiovascular disease ( CVD ) risk factors , but a high-LA intake may weaken the effect of ( n-3 ) LCPUFA . In a controlled , double-blind , 2 x 2-factorial 8-wk intervention , we investigated whether fish oil combined with a high- or low-LA intake affects overall CVD risk profile .  Healthy men ( n = 64 ) were r and omized to 5 mL/d fish oil capsules ( FO ) [ mean intake 3.1 g/d ( n-3 ) LCPUFA ] or olive oil capsules ( control ) and to oils and spreads with either a high ( S/B ) or a low ( R/K ) LA content , result ing in a 7.3 g/d higher LA intake in the S/B groups than in the R/K groups . Diet , ( n-3 ) LCPUFA in peripheral blood mononuclear cells , blood pressure ( BP ) , heart rate ( HR ) , and plasma CVD risk markers were measured before and after the intervention . FO lowered fasting plasma triacylglycerol ( TAG ) ( P < 0.001 ) by 51 % and 19 % in the FO+R/K-group and FO+S/B-group , respectively , which was also reflected in postpr and ial TAG measured after the intervention ( P < 0.01 ) . Although a fat x FO interaction was found for monocyte chemoattractant protein-1 , neither the FO nor fat intervention affected fasting plasma cholesterol , glucose , insulin , fibrinogen , C-reactive protein , interleukin-6 , vascular cell adhesion molecule-1 , P-selectin , oxidized LDL , cluster of differentiation antigen 40 lig and ( CD40L ) , adiponectin , or fasting or postpr and ial BP or HR after adjustment for body weight changes . In conclusion , neither fish oil supplementation nor the LA intake had immediate pronounced effects on the overall CVD risk profile  in healthy men , but fish oil lowered plasma TAG in healthy subjects with initially low concentrations Excess ectopic fat storage is linked to type 2 diabetes . The importance of dietary fat composition for ectopic fat storage in humans is unknown . We investigated liver fat accumulation and body composition during overfeeding saturated fatty acids ( SFAs ) or polyunsaturated fatty acids ( PUFAs ) . LIPOGAIN was a double-blind , parallel-group , r and omized trial . Thirty-nine young and normal-weight individuals were overfed muffins high in SFAs ( palm oil ) or n-6 PUFAs ( sunflower oil ) for 7 weeks .  Liver fat , visceral adipose tissue ( VAT ) , abdominal subcutaneous adipose tissue ( SAT ) , total adipose tissue , pancreatic fat , and lean tissue were assessed by magnetic resonance imaging . Transcriptomics were performed in SAT . Both groups gained similar weight . SFAs , however , markedly increased liver fat compared with PUFAs and caused a twofold larger increase in VAT than PUFAs . Conversely , PUFAs caused a nearly threefold larger increase in lean tissue than SFAs . Increase in liver fat directly correlated with changes in plasma SFAs and inversely with PUFAs . Genes involved in regulating energy dissipation , insulin resistance , body composition , and fat-cell differentiation in SAT were differentially regulated between diets , and associated with increased PUFAs in SAT . In conclusion , overeating SFAs promotes hepatic and visceral fat storage , whereas excess energy from PUFAs may instead promote lean tissue in healthy humans Background Dietary alpha-linolenic acid ( ALA ) has been associated with reduced risk of development of atherosclerosis . Adiponectin is a hormone specifically secreted by adipocytes and considered to have anti-atherogenic properties . Aim of the study We examined the effect of increased dietary intake of ALA on plasma concentration of adiponectin . Methods Thirty-five non-diabetic , dyslipidemic men , 38–71 years old , were r and omly allocated to take either 15 ml of flaxseed oil rich in ALA ( 8.1 g/day ; n = 18 ) , or 15 ml of safflower oil per day , containing the equivalent n-6 fatty acid ( 11.2 g/day linoleic acid , LA ; n = 17 ) ( control group ) . The intervention period lasted for 12 weeks . Results Plasma levels of adiponectin did not change after the increase in dietary intake of ALA in the flaxseed oil supplementation group , compared to the control group . No changes in body mass index , serum lipid concentrations , LDL density , or plasma TNF-α were found in the flaxseed oil versus the control group . Conclusions Dietary ALA has no effect on plasma adiponectin concentration in dyslipidemic men BACKGROUND Inflammation plays an important role in the pathogenesis of coronary artery disease . We examined whether dietary supplementation with alpha-linolenic acid ( ALA , 18:3n-3 ) affects the levels of inflammatory markers in dyslipidaemic patients . METHODS We recruited 76 male dyslipidaemic patients ( mean age=51+/-8 years ) following a typical Greek diet . They were r and omly assigned either to 15 ml of linseed oil ( rich in ALA ) per day ( n=50 ) or to 15 ml of safflower oil ( rich in linoleic acid ( LA , 18:2n-6 ) ) per day ( n=26 ) . The ratio of n-6:n-3 in linseed oil supplemented group was 1.3:1 and in safflower oil supplemented group 13.2:1 . Dietary intervention lasted for 3 months . Blood lipids and C-reactive protein ( CRP ) , serum amyloid A ( SAA ) , and interleukin-6 ( IL-6 ) levels were determined prior and after intervention . CRP and SAA were measured by nephelometry and IL-6 by immunoassay . RESULTS Dietary supplementation with ALA decreased significantly CRP , SAA and IL-6 levels . The median decrease of CRP was 38 % ( 1.24 vs. 0.93 mg/l , P=0.0008 ) , of SAA 23.1 % ( 3.24 vs. 2.39 mg/l , P=0.0001 ) and of IL-6 10.5 % ( 2.18 vs. 1.7 pg/ml , P=0.01 ) . The decrease of inflammatory markers was independent of lipid changes . Dietary supplementation with LA did not affect significantly CRP , SAA and IL-6 concentrations but decreased cholesterol levels . CONCLUSIONS Dietary supplementation with ALA for 3 months decreases significantly CRP , SAA and IL-6 levels  in dyslipidaemic patients . This anti-inflammatory effect may provide a possible additional mechanism for the beneficial effect of plant n-3 polyunsaturated fatty acids in primary and secondary prevention of coronary artery disease Objective : To 
    Output:
    
agent
However , subgroup and meta-regression analysis suggested that in subjects with a more profound increase of dietary LA intake , LA might increase the blood CRP level .
Other acute phase reactants including fibrinogen and plasminogen activator inhibitor-1 and adhesion molecules were not significantly changed when LA was increased in diet .
Our meta- analysis suggested that increasing dietary LA intake does not have a significant effect on the blood concentrations of inflammatory markers .
However , the extent of change in dietary LA intake might affect the effect of LA supplementation on CRP
***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: PUFA of the n−6 and n−3 series have beneficial effects on key risk factors of coronary heart disease ( CHD ) . Our earlier studies on the intake of FA and on the FA composition of plasma and platelet phospholipids suggested the need to improve the n−3 PUFA nutritional status in the Indian population . The present long-term study was conducted on 80 middle-aged Indian subjects ( 40 men and 40 women ) using the subjects ' own home-prepared diets to evaluate the effects of dietary n−3 PUFA on biochemical indices of CHD risk .  Substitution of Blend G ( equal proportions of groundnut and canola oils ) for groundnut oil or substitution of Blend S ( equal proportions of sunflower and canola oils ) for sunflower oil  increased α-linolenic acid ( ALNA ) fourfold and decreased the linoleic acid (LA)/ALNA ratio from 35 to 6 and 65 to 9 , respectively . Twelve subjects ( six men and six women ) who received Blend G were switched back to groundnut oil and were administered 0.3 g daily of long-chain ( LC ) n−3 PUFA from fish oil . At the end of the trial period for both blends in both sexes , plasma lipid and apolipoprotein levels had not changed , and ADP-induced aggregation had decreased . In plasma and platelet phospholipids , LA as well as LCn-3 PUFA had increased , suggesting competition between LA and ALNA for metabolism into the respective LC-PUFA . Fish oil supplementation  increased LCn-3 PUFA in plasma and platelet phospholipids , decreased ADP-induced platelet aggregation , and increased plasma cholesterol . On the basis of the increased LCn-3 PUFA in plasma phospholipids , it was calculated that 0.75 % energy ( en% ) ( 2.2 g ) ALNA ( from vegetable oils ) may be required to increase LCn-3 PUFA to about the same extent as 0.1 en% ( 0.3 g ) LCn-3 PUFA ( from fish oils ) . Since both n−6 and n−3 PUFA play a critical role in fetal growth and development and in the programming of diet-related chronic diseases in adults , an improvement in the n−3 PUFA nutritional status in cereal-based diets through long-term use of cooking oils containing 25–40 % LA and 4 % ALNA may contribute to the prevention of CHD in Indians High linoleic acid ( LA ) intakes have been suggested to reduce alpha-linolenic acid [ ALA , 18:3(n-3 ) ] metabolism to eicosapentaenoic acid [ EPA , 20:5(n-3 ) ] and docosahexaenoic acid [ DHA , 22:6(n-3 ) ] , and favor high arachidonic acid [ ARA , 20:4(n-6 ) ] . We used a r and omized cross-over study with men ( n = 22 ) to compare the effect of replacing vegetable oils high in LA with oils low in LA in foods , while maintaining constant ALA , for 4 wk each , on plasma ( n-3 ) fatty acids . Nonvegetable sources of fat , except fish and seafoods , were unrestricted . We determined plasma phospholipid fatty acids at wk 0 , 2 , 4 , 6 , and 8 , and triglycerides , cholesterol , serum CRP , and IL-6 , and platelet aggregation at wk 0 , 4 , and 8 .  LA and ALA intakes were 3.8 + /- 0.12 % and 1.0 + /- 0.05 % , and 10.5 + /- 0.53 % and 1.1 + /- 0.06 % energy with LA : ALA ratios of 4:0 and 10:1 during the low and high LA diets , respectively . The plasma phospholipid LA was higher and EPA was lower during the high than during the low LA diet period ( P < 0.001 ) , but DHA declined over the 8-wk period ( r = -0.425 , P < 0.001 ) . The plasma phospholipid ARA : EPA ratios were ( mean + /- SEM ) 20.7 + /- 1.52 and 12.9 + /- 1.01 after 4 wk consuming the high or low LA diets , respectively ( P < 0.001 ) ; LA was inversely associated with EPA ( r = -0.729 , P < 0.001 ) but positively associated with ARA : EPA ( r = 0.432 , P < 0.001 ) . LA intake did not influence ALA , ARA , DPA , DHA , or total , LDL or HDL cholesterol , CRP or IL-6 , or platelet aggregation . In conclusion , high LA intakes decrease plasma phospholipid EPA and increase the ARA : EPA ratio , but do not favor higher ARA Dietary alpha-linolenic acid ( ALA ) can be converted to long-chain ( n-3 ) PUFA in humans and may potentially reproduce the beneficial effects of eicosapentaenoic ( EPA ) and docosahexaenoic ( DHA ) acids on risk factors for coronary heart disease ( CHD ) . This study compared the effects of increased intakes of ALA with those of dietary EPA and DHA on blood coagulation and fibrinolytic factors in fasting subjects . A placebo-controlled , parallel study was conducted in 150 moderately hyperlipidemic subjects , age 25 - 72 y. Subjects were r and omly assigned to one of five interventions and consumed a total intake of 0.8 or 1.7g/d EPA+DHA , 4.5 or 9.5g/d ALA or control ( linoleic acid ; LA ) for 6 mo . Fatty acids were incorporated into 25 g of fat spread , which replaced the subject 's normal spread and three capsules . Long-term supplementation with either dietary EPA+DHA or estimated biologically equivalent amounts of ALA did not affect factors VIIa , VIIc , VIIag , XIIa , XIIag , fibrinogen concentrations , plasminogen activator inhibitor-1 or tissue plasminogen activator activity compared with the control . ( n-3 ) PUFA of plant or marine origin do not differ from one another or from LA in their effect on a range of blood coagulation and fibrinolytic factors Both ( n-3 ) long-chain PUFA ( LCPUFA ) and linoleic acid [ LA , 18:2(n-6 ) ] improve cardiovascular disease ( CVD ) risk factors , but a high-LA intake may weaken the effect of ( n-3 ) LCPUFA . In a controlled , double-blind , 2 x 2-factorial 8-wk intervention , we investigated whether fish oil combined with a high- or low-LA intake affects overall CVD risk profile .  Healthy men ( n = 64 ) were r and omized to 5 mL/d fish oil capsules ( FO ) [ mean intake 3.1 g/d ( n-3 ) LCPUFA ] or olive oil capsules ( control ) and to oils and spreads with either a high ( S/B ) or a low ( R/K ) LA content , result ing in a 7.3 g/d higher LA intake in the S/B groups than in the R/K groups . Diet , ( n-3 ) LCPUFA in peripheral blood mononuclear cells , blood pressure ( BP ) , heart rate ( HR ) , and plasma CVD risk markers were measured before and after the intervention . FO lowered fasting plasma triacylglycerol ( TAG ) ( P < 0.001 ) by 51 % and 19 % in the FO+R/K-group and FO+S/B-group , respectively , which was also reflected in postpr and ial TAG measured after the intervention ( P < 0.01 ) . Although a fat x FO interaction was found for monocyte chemoattractant protein-1 , neither the FO nor fat intervention affected fasting plasma cholesterol , glucose , insulin , fibrinogen , C-reactive protein , interleukin-6 , vascular cell adhesion molecule-1 , P-selectin , oxidized LDL , cluster of differentiation antigen 40 lig and ( CD40L ) , adiponectin , or fasting or postpr and ial BP or HR after adjustment for body weight changes . In conclusion , neither fish oil supplementation nor the LA intake had immediate pronounced effects on the overall CVD risk profile  in healthy men , but fish oil lowered plasma TAG in healthy subjects with initially low concentrations Excess ectopic fat storage is linked to type 2 diabetes . The importance of dietary fat composition for ectopic fat storage in humans is unknown . We investigated liver fat accumulation and body composition during overfeeding saturated fatty acids ( SFAs ) or polyunsaturated fatty acids ( PUFAs ) . LIPOGAIN was a double-blind , parallel-group , r and omized trial . Thirty-nine young and normal-weight individuals were overfed muffins high in SFAs ( palm oil ) or n-6 PUFAs ( sunflower oil ) for 7 weeks .  Liver fat , visceral adipose tissue ( VAT ) , abdominal subcutaneous adipose tissue ( SAT ) , total adipose tissue , pancreatic fat , and lean tissue were assessed by magnetic resonance imaging . Transcriptomics were performed in SAT . Both groups gained similar weight . SFAs , however , markedly increased liver fat compared with PUFAs and caused a twofold larger increase in VAT than PUFAs . Conversely , PUFAs caused a nearly threefold larger increase in lean tissue than SFAs . Increase in liver fat directly correlated with changes in plasma SFAs and inversely with PUFAs . Genes involved in regulating energy dissipation , insulin resistance , body composition , and fat-cell differentiation in SAT were differentially regulated between diets , and associated with increased PUFAs in SAT . In conclusion , overeating SFAs promotes hepatic and visceral fat storage , whereas excess energy from PUFAs may instead promote lean tissue in healthy humans Background Dietary alpha-linolenic acid ( ALA ) has been associated with reduced risk of development of atherosclerosis . Adiponectin is a hormone specifically secreted by adipocytes and considered to have anti-atherogenic properties . Aim of the study We examined the effect of increased dietary intake of ALA on plasma concentration of adiponectin . Methods Thirty-five non-diabetic , dyslipidemic men , 38–71 years old , were r and omly allocated to take either 15 ml of flaxseed oil rich in ALA ( 8.1 g/day ; n = 18 ) , or 15 ml of safflower oil per day , containing the equivalent n-6 fatty acid ( 11.2 g/day linoleic acid , LA ; n = 17 ) ( control group ) . The intervention period lasted for 12 weeks . Results Plasma levels of adiponectin did not change after the increase in dietary intake of ALA in the flaxseed oil supplementation group , compared to the control group . No changes in body mass index , serum lipid concentrations , LDL density , or plasma TNF-α were found in the flaxseed oil versus the control group . Conclusions Dietary ALA has no effect on plasma adiponectin concentration in dyslipidemic men BACKGROUND Inflammation plays an important role in the pathogenesis of coronary artery disease . We examined whether dietary supplementation with alpha-linolenic acid ( ALA , 18:3n-3 ) affects the levels of inflammatory markers in dyslipidaemic patients . METHODS We recruited 76 male dyslipidaemic patients ( mean age=51+/-8 years ) following a typical Greek diet . They were r and omly assigned either to 15 ml of linseed oil ( rich in ALA ) per day ( n=50 ) or to 15 ml of safflower oil ( rich in linoleic acid ( LA , 18:2n-6 ) ) per day ( n=26 ) . The ratio of n-6:n-3 in linseed oil supplemented group was 1.3:1 and in safflower oil supplemented group 13.2:1 . Dietary intervention lasted for 3 months . Blood lipids and C-reactive protein ( CRP ) , serum amyloid A ( SAA ) , and interleukin-6 ( IL-6 ) levels were determined prior and after intervention . CRP and SAA were measured by nephelometry and IL-6 by immunoassay . RESULTS Dietary supplementation with ALA decreased significantly CRP , SAA and IL-6 levels . The median decrease of CRP was 38 % ( 1.24 vs. 0.93 mg/l , P=0.0008 ) , of SAA 23.1 % ( 3.24 vs. 2.39 mg/l , P=0.0001 ) and of IL-6 10.5 % ( 2.18 vs. 1.7 pg/ml , P=0.01 ) . The decrease of inflammatory markers was independent of lipid changes . Dietary supplementation with LA did not affect significantly CRP , SAA and IL-6 concentrations but decreased cholesterol levels . CONCLUSIONS Dietary supplementation with ALA for 3 months decreases significantly CRP , SAA and IL-6 levels  in dyslipidaemic patients . This anti-inflammatory effect may provide a possible additional mechanism for the beneficial effect of plant n-3 polyunsaturated fatty acids in primary and secondary prevention of coronary artery disease Objective : To 
    Output:
    