The amounts of ALA and LA in the diet, but not their ratio, determine ALA conversion.

To estimate in vivo ␣ -linolenic acid (ALA; C18: 3n-3) conversion, 29 healthy subjects consumed for 28 days a diet providing 7% of energy from linoleic acid (C18:2n-6) and 0.4% from ALA. On day 19, subjects received a single bolus of 30 mg of uniformly labeled [ 13 C]ALA and for the next 8 days 10 mg twice daily. Fasting plasma phospholipid concentrations of 12 C-and 13 C-labeled ALA, eicosapentaenoic acid (EPA; C20:5n-3), docosapentaenoic acid (DPA; C22:5n-3), and docosahexaenoic acid (DHA; C22:6n-3) were determined on days 19, 21, 23, 26, 27, and 28. To estimate hepatic conversion of n-3 fatty acids, a tracer model was developed based on the averaged 13 C data of the participants. A similar tracee model was solved using the averaged 12 C values, the kinetic parameters derived from the tracer model, and mean ALA consumption. ALA incorporation into plasma phospholipids was estimated by solving both models simultaneously. It was found that nearly 7% of dietary ALA was incorporated into plasma phospholipids. From this pool, 99.8% was converted into EPA and 1% was converted into DPA and subsequently into DHA. The limited incorporation of dietary ALA into the hepatic phospholipid pool contributes to the low hepatic conversion of ALA into EPA. A low conversion of ALA-derived EPA into DPA might be an additional obstacle for DHA synthesis. -Goyens, P. L. L., M. E. Spilker, P. L. Zock, M. B. Katan, and R. P. Mensink. Compartmental modeling to quantify ␣ -linolenic acid conversion after longer term intake of multiple tracer boluses. J.

Alpha-linolenic acid [ALA, 18:3(n-3)] and linoleic acid [LA, 18:2(n-6)] have comparable effects on serum lipid and lipoprotein concentrations, but their effects on lipoprotein subclass distributions and particle sizes are unknown. It is also not known whether these effects are changed by the ALA:LA ratio in the diet. To address these questions, healthy subjects (n = 54) consumed a control diet providing 7% of energy (En%) as LA and 0.4 En% as ALA during a 4-wk run-in period. For the following 6 wk of intervention, each diet was consumed by 18 subjects: the control diet, a low-LA diet (3 En% LA, 0.4 En% ALA), or a high-ALA diet (7 En% LA, 1.1 En% ALA). The ALA:LA ratio for the control diet was 1:19 and was 1:7 for the other 2 diets. Compared with the control group, LDL cholesterol decreased significantly in the ALA group (-0.32 mmol/L, P = 0.024), as did total cholesterol, apolipoprotein (apo) B, and the total:HDL cholesterol ratio. None of the dietary interventions affected HDL cholesterol, apo A-1, or triacylglycerol concentrations. The decrease in total VLDL particle concentrations in the low-LA group was due mainly to a decrease in medium VLDL (-16 nmol/L, P = 0.018) and in the high-ALA group to a decrease in small VLDL (-14 nmol/L, P = 0.044). We conclude that the ALA:LA ratio does not affect the serum lipoprotein profile. Compared with the control and LA diets, ALA lowered LDL cholesterol concentrations, possibly caused by the decrease in small VLDL.

Objective: To compare the effects of alpha-linolenic acid (ALA, C18:3n-3) to those of eicosapentaenoic acid (EPA, C20:5n-3) plus docosahexaenoic acid (DHA, C22:6n-3) on cardiovascular risk markers in healthy elderly subjects. Design: A randomized double-blind nutritional intervention study. Setting: Department of Human Biology, Maastricht University, the Netherlands. Subjects: Thirty-seven mildly hypercholesterolemic subjects, 14 men and 23 women aged between 60 and 78 years. Interventions: During a run-in period of 3 weeks, subjects consumed an oleic acid-rich diet. The following 6 weeks, 10 subjects remained on the control diet, 13 subjects consumed an ALA-rich diet (6.8 g/day) and 14 subjects an EPA/DHA-rich diet (1.05 g EPA/day þ 0.55 g DHA/day). Results: Both n-3 fatty acid diets did not change concentrations of total-cholesterol, LDL-cholesterol, HDL-cholesterol, triacylglycerol and apoA-1 when compared with the oleic acid-rich diet. However, after the EPA/DHA-rich diet, LDL-cholesterol increased by 0.39 mmol/l (P ¼ 0.0323, 95% CI (0.030, 0.780 mmol/l)) when compared with the ALA-rich diet. Intake of EPA/ DHA also increased apoB concentrations by 14 mg/dl (P ¼ 0.0031, 95% CI (4, 23 mg/dl)) and 12 mg/dl (P ¼ 0.005, 95% CI (3, 21 mg/dl)) versus the oleic acid and ALA-rich diet, respectively. Except for an EPA/DHA-induced increase in tissue factor pathway inhibitor (TFPI) of 14.6% (P ¼ 0.0184 versus ALA diet, 95% CI (1.5, 18.3%)), changes in markers of hemostasis and endothelial integrity did not reach statistical significance following consumption of the two n-3 fatty acid diets. Conclusions: In healthy elderly subjects, ALA might affect concentrations of LDL-cholesterol and apoB more favorably than EPA/DHA, whereas EPA/DHA seems to affect TFPI more beneficially.

Recently, we observed that impairments exist in skeletal muscle free fatty acid (FFA) utilization during exercise in obese subjects with Type II diabetes. The main objective of the present study was to investigate whether plasma FFA oxidation is impaired during exercise in non-obese Type II diabetic patients. Stable isotope tracers of palmitate and glucose were infused for 2 h at rest and 1h of bicycle exercise at 40% peak oxygen consumption ( V*O(2)max) in volunteers with Type II diabetes and a healthy control group. At rest, plasma FFA oxidation was not significantly different between subjects with Type II diabetes and control subjects (2.13+/-0.51 versus 1.93+/-0.54 micromol.kg(-1).min(-1) respectively). During exercise, Type II diabetic patients and control subjects had similar rates of total fat [Type II diabetes, 9.62+/-1.84 micromol.kg(-1).min(-1); control, 12.08+/-4.59 micromol.kg(-1).min(-1); not significant (NS)] and glucose oxidation (Type II diabetes, 44.24+/-10.36 micromol.kg(-1).min(-1); control, 57.37+/-14.54 micromol.kg(-1).min(-1); NS). No aberrations were present in plasma FFA uptake [rate of disappearance ( Rd ); Type II diabetes, 11.78+/-4.82; control, 10.84+/-3.39; NS] and oxidation rates (Type II diabetes 8.10+/-1.44; control 8.00+/-3.12, NS) in Type II diabetic patients; triacylglycerol-derived fatty acid oxidation was 2.6-fold lower in Type II diabetic patients than in control subjects, but this difference was not statistically significant. Muscle glycogen oxidation was lower in diabetes patients than in control subjects (Type II diabetes, 25.16+/-13.82 micromol.kg(-1).min(-1); control, 42.04+/-10.58 micromol.kg(-1).min(-1); P<0.05) and plasma glucose contributed more to energy expenditure in Type II diabetes (26+/-3% in diabetic versus 15+/-2% in control, P <0.05). We conclude that plasma FFA oxidation is not impaired during exercise in non-obese Type II diabetic patients. The data confirm that Type II diabetes is a heterogeneous disease, and that the adaptation at the substrate level differs between obese and non-obese patients and may contribute to differences in the final appearance of the various phenotypes.