***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 
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    Input: In a double-blind , placebo-controlled study we investigated the effects of dietary fish oil supplementation on arterial wall characteristics in 20 patients with non-insulin-dependent diabetes mellitus . Estimates reflecting compliance values in the large arteries and more peripheral vasculature , as measured by pulse-contour analysis , improved significantly after 6 weeks of fish oil therapy compared with values recorded at baseline and after 6 weeks ' administration of olive oil . The large-artery compliance estimate increased from 1.50 ( confidence interval [ CI ] , 1.31 to 1.69 ) mL/mm Hg at baseline to 1.68 ( CI , 1.52 to 1.84 ) mL/mm Hg after fish oil administration ( P < .01 ) . The oscillatory compliance value increased from 0.015 ( CI , 0.011 to 0.019 ) mL/mm Hg at baseline to 0.022 ( CI , 0.016 to 0.028 ) mL/mm Hg after fish oil ingestion ( P < .05 ) . No changes occurred in arterial blood pressure , cardiac output , stroke volume , or systemic vascular resistance with either intervention . The improved compliance estimates with fish oil ingestion occurred without altering fasting blood glucose and cholesterol concentrations . These results support the hypothesis that fish oils alter vascular reactivity and favorably influence arterial wall characteristics in patients with non-insulin-dependent diabetes mellitus . These direct vascular effects , expressed at the level of the vessel wall , may contribute to the cardioprotective actions of fish oil in humans Objective : Fish oil supplement has been proposed as a non-pharmacological strategy to correct the atherogenic lipid profile associated with type 2 diabetes mellitus . However , fish oil may have deleterious effects on lipid peroxidation and glycemic control . Design : In this study , 44 type 2 diabetic patients were r and omized to vitamin E st and ardized ( 53.6 mg/day ) supplementation ( capsules ) with 4 g daily of either fish oil ( n=23 ) or corn oil ( n=21 ) for 8 weeks preceded by a 4 week run-in period of corn oil supplementation . LDL was isolated by density gradient ultracentrifugation and oxidized in vitro with Cu2 + . As a marker of in vivo oxidation malondialdehyde concentration in LDL ( LDL-MDA ) was measured . Results : Fish oil reduced both mean lag time ( before , 57.8 ; after , 48.8 min , P<0.001 ) and mean propagation rate ( before , 0.018 ΔOD/min ; after , 0.015 ΔOD/min , P<0.001 ) , whereas corn oil had no influence on lag time and propagation rate . The changes in lag time and propagation rate differed significantly between fish oil and corn oil treatment . LDL-MDA changes differed borderline significantly between groups ( FO , 110.4 pmol/mg protein ; CO , 6.7 pmol/mg protein ; P=0.057 ) . Fish oil supplementation had no influence on glycemic control as assessed from HbA1c and fasting blood glucose . Conclusion : According to our findings , fish oil supplementation leads to increased in vivo oxidation and increased in vitro oxidation susceptibility of LDL particles . More studies are needed to clarify the clinical importance of this finding . Sponsorship : Financially supported by The Danish Heart Association and Dansk Droge A/S. Dansk Droge A/S generously provided the fish oil and corn oil capsules Summary This study was conducted to examine the effect of ω3 fatty acid supplementation on plasma lipid , cholesterol and lipoprotein fatty acid content of non-insulin-dependent diabetic individuals consuming a higher ( 0.65 , n = 10 ) or lower ( 0.44 , n = 18 ) ratio of dietary polyunsaturated to saturated fatty acid ( P/S ) . The participants were initially given an olive oil supplement ( placebo ) equivalent to 35 mg of 18:1 · kg body weight–1 · day–1 for 3 months . This was followed by two ω3 supplement periods in a r and omized crossover . In these 3-month periods , participants were given a linseed oil supplement equivalent to 35 mg of 18:3ω3 · kg body weight–1 · day–1 or a fish oil supplement equivalent to 35 mg of 20:5ω3 + 22:6ω3 · kg body weight–1 · day–1 . At the end of each supplement period , a blood sample was drawn from each participant for lipid , lipoprotein , insulin , glucagon and C-peptide analyses . At the end of each 3-month period a 7-day dietary record was completed to calculate dietary fat intake and P/S ratio . Results indicate that fish oil significantly reduced plasma triacylglycerol level ( p < 0.05 ) and increased 20:5ω3 and 22:6ω3 content of all lipoprotein lipid classes . Linolenic acid supplementation had no effect on plasma triacylglycerol level , but it increased 18:3ω3 content of lipoprotein cholesterol ester fractions ( p < 0.05 ) . A slight increase in 20:5ω3 , but not 22:6ω3 , content was noted in lipoprotein lipid classes as a result of 18:3ω3 supplementation . LDL and HDL cholesterol , insulin , glucagon and C-peptide levels were not affected by either ω3 supplement . It is concluded that a modest intake of ω3 fatty acids , such as could be obtained from consuming fish regularly , will reduce plasma triglyceride level without affecting LDL or HDL cholesterol levels . [ Diabetologia ( 1997 ) 40 : 45–52 The study assessed the efficacy of fish oil supplementation in counteracting the classic dyslipidemia of the atherogenic lipoprotein phenotype ( ALP ) . In addition , the impact of the common apolipoprotein E ( apoE ) polymorphism on the fasting and postpr and ial lipid profile and on responsiveness to the dietary intervention was established . Fifty-five ALP males ( aged 34 to 69 years , body mass index 22 to 35 kg/m(2 ) , triglyceride [ TG ] levels 1.5 to 4.0 mmol/L , high density lipoprotein cholesterol [ HDL-C ] < 1.1 mmol/l , and percent low density lipoprotein [LDL]-3 > 40 % total LDL ) completed a r and omized placebo-controlled crossover trial of fish oil ( 3.0 g eicosapentaenoic acid/docosahexaenoic acid per day ) and placebo ( olive oil ) capsules with the 6-week treatment arms separated by a 12-week washout period . In addition to fasting blood sample s , at the end of each intervention arm , a postpr and ial assessment of lipid metabolism was carried out . Fish oil supplementation result ed in a reduction in fasting TG level of 35 % ( P<0.001 ) , in postpr and ial TG response of 26 % ( TG area under the curve , P<0.001 ) , and in percent LDL-3 of 26 % ( P<0.05 ) . However , no change in HDL-C levels was evident ( P=0.752 ) . ANCOVA showed that baseline HDL-C levels were significantly lower in apoE4 carriers ( P=0.035 ) . The apoE genotype also had a striking impact on lipid responses to fish oil intervention .  Individuals with an apoE2 allele displayed a marked reduction in postpr and ial incremental TG response ( TG incremental area under the curve , P=0.023 ) and a trend toward an increase in lipoprotein lipase activity relative to non-E2 carriers . In apoE4 individuals , a significant increase in total cholesterol and a trend toward a reduction in HDL-C relative to the common homozygous E3/E3 profile was evident . Our data demonstrate the efficacy of fish oil fatty acids in counteracting the proatherogenic lipid profile of the ALP but also that the apoE genotype influences responsiveness to this dietary treatment BACKGROUND There is conflicting evidence on the benefits of foods rich in vitamin E ( alpha-tocopherol ) , n-3 polyunsaturated fatty acids ( PUFA ) , and their pharmacological substitutes . We investigated the effects of these substances as supplements in patients who had myocardial infa rct ion . METHODS From October , 1993 , to September , 1995 , 11,324 patients surviving recent ( < or = 3 months ) myocardial infa rct ion were r and omly assigned supplements of n-3 PUFA ( 1 g daily , n=2836 ) , vitamin E ( 300 mg daily , n=2830 ) , both ( n=2830 ) , or none ( control , n=2828 ) for 3.5 years . The primary combined efficacy endpoint was death , non-fatal myocardial infa rct ion , and stroke . Intention-to-treat analyses were done according to a factorial design ( two-way ) and by treatment group ( four-way ) . FINDINGS Treatment with n-3 PUFA , but not vitamin E , significantly lowered the risk of the primary endpoint ( relative-risk decrease 10 % [ 95 % CI 1 - 18 ] by two-way analysis , 15 % [ 2 - 26 ] by four-way analysis ) . Benefit was attributable to a decrease in the risk of death ( 14 % [ 3 - 24 ] two-way , 20 % [ 6 - 33 ] four-way ) and cardiovascular death ( 17 % [ 3 - 29 ] two-way , 30 % [ 13 - 44 ] four-way ) . The effect of the combined treatment was similar to that for n-3 PUFA for the primary endpoint ( 14 % [ 1 - 26 ] ) and for fatal events ( 20 % [ 5 - 33 ] ) . INTERPRETATION Dietary supplementation with n-3 PUFA led to a clinical ly important and statistically significant benefit . Vitamin E had no benefit . Its effects on fatal cardiovascular events require further exploration Eicosapentaenoic acid ( EPA ) ethyl ester ( 1.8 g/d ) was administered to 16 diabetic patients ( 5 insulin-dependent and 11 noninsulin-dependent diabetics ) for 6 mon . EPA in total plasma fatty acids increased from 4.0±2.4 mol% ( mean±SD ) to 7.5±3.1 mol% ( p<0.001 ) . Albumin excretion , measured with spot urine , was significantly reduced from 65 to 36 mg/g creatinine ( geometric means , p<0.001 ) . Fasting blood sugar levels , glycohemoglobin , body weight and blood pressure did not change significantly during the study . There were also no significant changes in serum levels of creatinine , urea nitrogen , total cholesterol and triglycerides . Although no overt hemorrhage was observed in the patients , hematocrit was reduced from 42.6±2.8 % to 41.0±3.9 % ( p<0.02 ) . Ten other similar diabetic patients ( 4 insulin-dependent and 6 non-insulin-dependent diabetics ) were followed as a reference group , not concomitantly , for 6 mon with neither EPA ethyl ester nor placebo . The parameters mentioned above were not changed significantly in this group during 6 mon . EPA administration might retard the appearance of overt diabetic nephropathy The short-term effect of high fiber intake on fish-oil treatment in 15 free-living , non-insulin-dependent diabetic patients was evaluated by using a controlled , sequential study design . During an 8-wk fish-oil-treatment period when patients received 20 g fish oil/d , the usual daily fiber intake was increased with a 15-g pectin supplement at midpoint . Fish oil alone lowered triacylglycerol and very-low-density-lipoprotein-cholesterol concentrations by 41 % and 36 % , respectively ( both P < 0.01 by the end of the treatment period ) with unchanged mean total , low-density- , and high-density-lipoprotein-cholesterol concentrations . When the fiber intake was increased , however , total and low-density-lipoprotein-cholesterol concentrations decreased significantly ( P < 0.001 and < 0.05 , respectively ) with fish-oil treatment . The cholesterol ester fraction of plasma lipids was reduced by 34 % when compared with fish oil alone ( P < 0.05 ) . The plasma triacylglycerol fraction decreased further by 44 % ( P < 0.001 ) . Other beneficial effects observed included a 30 % decline in the fatty acid fraction ( P < 0.002 ) by end of the treatment period . Diabetic control was maintained during the 12-wk study . In conclusion , a high fiber intake may be beneficial in fish oil-treated diabetic patients Fish-oil supplementation decreases serum triacylglycerols but may worsen hyperglycemia in patients with non-insulin-dependent diabetes mellitus . The reason for the possible deterioration of glycemia is unclear . We examined whether inhibition of tri 
    Output:
    
No significant change in or total or HDL cholesterol , HbA1c , fasting glucose , fasting insulin or body weight was observed .
The increase in VLDL remained significant only in trials of longer duration and in hypertriglyceridemic patients .
The elevation in LDL cholesterol was non-significant in subgroup analyses .
No adverse effects of the intervention were reported .
Omega-3 PUFA supplementation in type 2 diabetes lowers triglycerides and VLDL cholesterol , but may raise LDL cholesterol ( although results were non-significant in subgroups ) and has no statistically significant effect on glycemic control or fasting insulin .