Total Plasma Free Fatty Acid Research Articles

Plasma Fatty Acid Composition Was Associated with Apelin Gene Expression in Human Adipose Tissues.

Background Apelin is an adipokine with an intermediatory role in obesity and insulin resistance, which can be modified by dietary intake. Aims In this study, we aimed to determine the association of the plasma fatty acid composition with apelin plasma concentration and gene expression in visceral (VAT) and subcutaneous (SAT) adipose tissues. Methods In this cross-sectional study, we recruited 179 patients aged 19-75 years who were candidates for elective surgery. Through the surgery, SAT and VAT were collected to measure apelin gene expression. Anthropometric measurements, fasting blood samples, and dietary intakes were collected before surgery. Free fatty acids (FFAs) in fasting whole plasma were measured using gas chromatography with flame ionization detection. Linear regression models were used to estimate standardized β (STZ β) showing the association of individual and total FFAs with apelin gene expression after adjustment for potential confounding variables. Results In multivariable analysis, we observed a significant positive association of total plasma free fatty acids (FFAs) (STZ β = 0.241, P = 0.006), saturated fatty acid (SFA) (STZ β = 0.336, P < 0.001), and monounsaturated fatty acid (MUFA) (STZ β = 0.313, P < 0.001) concentrations with apelin gene expression from VAT after controlling for age, sex, body mass index, homeostatic model assessment for insulin resistance (HOMA-IR), physical activity, and energy intake. In the SFA family, there was a direct association with plasma concentration of myristic acid (STZ β = 0.372, P < 0.001), pentadecanoic acid (STZ β = 0.252, P = 0.002), and heptadecanoic acid (STZ β = 0.407, P < 0.001) with apelin mRNA expression in VAT. There was no significant association between FFAs and apelin plasma concentration and SAT mRNA levels. Conclusions In conclusion, circulating plasma FFAs, SFA, and MUFA had a positive association with apelin gene expression in VAT. It seems that plasma fatty acid composition may regulate apelin gene expression in VAT.

Effect of augmented glycation in mobilization of plasma free fatty acids in type 2 diabetes mellitus

Background and aimsType 2 Diabetes Mellitus (T2DM) is known to be associated with an increase in total plasma free fatty acid (FFA) concentration. The present study was conducted to determine the changes in plasma fatty acids at different levels of glycation in type 2 diabetes mellitus. MethodsThe study involved 50 subjects having different levels of glycation (HbA1c 4.9–15.0%) and further categorized in 5 groups [group 1 (HbA1c <6%), group 2 (HbA1c 6–7%), group 3 (HbA1c 7.1–9%), group 4 (HbA1c (9.1–12%) and group 5 (HbA1c >12%)] with 10 subjects in each group. ResultsA total of 19 free fatty acids were detected by gas chromatography-mass spectrometry (GC-MS) analysis in the plasma samples. The levels of lauric acid (C12:0) and stearic acid (C18:0) were significantly raised at an advanced stage of glycation (HbA1c 9.1–15%). Long-chain fatty acids, pentadecanoic acid (C15:0) and palmitic acid (C16:0) levels were elevated in hyperglycemia as compared to normoglycaemic subjects (HbA1c <6%). Moreover, levels of mono and polyunsaturated fatty acids, oleic acid (C18:1) and linoleic acid (C18:2, w6) were significantly decreased in patients with increased levels of glycation (HbA1c 6–15%). Conclusion: GC-MS is a novel way to study the plasma fatty acid profiling and findings of this study suggest that monitoring alterations in plasma FFA profile may be of prognostic value.

The Impact of Glucose-Based or Lipid-Based Total Parenteral Nutrition on the Free Fatty Acids Profile in Critically Ill Patients.

Introduction: Our study aim was to assess how the macronutrient intake during total parenteral nutrition (TPN) modulates plasma total free fatty acids (FFAs) levels and individual fatty acids in critically ill patients. Method: Adult patients aged 18–80, admitted to the intensive care unit (ICU), who were indicated for TPN, with an expected duration of more than three days, were included in the study. Isoenergetic and isonitrogenous TPN solutions were given with a major non-protein energy source, which was glucose (group G) or glucose and lipid emulsions (Smof lipid; group L). Blood samples were collected on days 0, 1, 3, 6, 9, 14, and 28. Results: A significant decrease (p < 0.001) in total FFAs occurred in both groups with a bigger decrease in group G (p < 0.001) from day 0 (0.41 ± 0.19 mmol∙L−1) to day 28 (0.10 ± 0.07 mmol∙L−1). Increased palmitooleic acid and decreased linoleic and docosahexaenoic acids, with a trend of increased mead acid to arachidonic acid ratio, on day 28 were observed in group G in comparison with group L. Group G had an insignificant increase in leptin with no differences in the concentrations of vitamin E, triacylglycerides, and plasminogen activator inhibitor-1. Conclusion: Decreased plasma FFA in critically ill patients who receive TPN may result from increased insulin sensitivity with a better effect in group G, owing to higher insulin and glucose dosing and no lipid emulsions. It is advisable to include a lipid emulsion at the latest from three weeks of TPN to prevent essential fatty acid deficiency.

Changes in Plasma Free Fatty Acids Associated with Type-2 Diabetes.

Type 2 diabetes mellitus (T2DM) is associated with increased total plasma free fatty acid (FFA) concentrations and an elevated risk of cardiovascular disease. The exact mechanisms by which the plasma FFA profile of subjects with T2DM changes is unclear, but it is thought that dietary fats and changes to lipid metabolism are likely to contribute. Therefore, establishing the changes in concentrations of specific FFAs in an individual’s plasma is important. Each type of FFA has different effects on physiological processes, including the regulation of lipolysis and lipogenesis in adipose tissue, inflammation, endocrine signalling and the composition and properties of cellular membranes. Alterations in such processes due to altered plasma FFA concentrations/profiles can potentially result in the development of insulin resistance and coagulatory defects. Finally, fibrates and statins, lipid-regulating drugs prescribed to subjects with T2DM, are also thought to exert part of their beneficial effects by impacting on plasma FFA concentrations. Thus, it is also interesting to consider their effects on the concentration of FFAs in plasma. Collectively, we review how FFAs are altered in T2DM and explore the likely downstream physiological and pathological implications of such changes.

Increased oxidative stress in patients with amyotrophic lateral sclerosis and the effect of edaravone administration

Objectives and methods: Compared to age-matched healthy controls (n = 55), patients with amyotrophic lateral sclerosis (ALS) (n = 26) showed increased oxidative stress as indicated by a significantly increased percentage of oxidized coenzyme Q10 (%CoQ10) in total plasma coenzyme Q10, a significantly decreased level of plasma uric acid, and a significantly decreased percentage of polyunsaturated fatty acids in total plasma free fatty acids (FFA). Therefore, the efficacy of edaravone, a radical scavenger, in these ALS patients was examined.Results and discussion: Among 26 ALS patients, 17 received edaravone (30 mg/day, one to four times a week) for at least 3 months, and 13 continued for 6 months. Changes in revised ALS functional rating scale (ALSFRS-R) were significantly smaller in these patients than in edaravone-untreated ALS patients (n = 19). Edaravone administration significantly reduced excursions of more than one standard deviation from the mean for plasma FFA levels and the contents of palmitoleic and oleic acids, plasma markers of tissue oxidative damage, in the satisfactory progress group (ΔALSFRS-R ≥ 0) as compared to the ingravescent group (ΔALSFRS-R < −5). Edaravone treatment increased plasma uric acid, suggesting that it is an effective scavenger of peroxynitrite. However, edaravone administration did not decrease %CoQ10. Therefore, combined treatment with agents such as coenzyme Q10 may further reduce oxidative stress in ALS patients.

Plasma free fatty acids do not provide the link between obesity and insulin resistance or β-cell dysfunction: results of the Reading, Imperial, Surrey, Cambridge, Kings (RISCK) study.

To investigate the relationship between adiposity and plasma free fatty acid levels and the influence of total plasma free fatty acid level on insulin sensitivity and β-cell function. An insulin sensitivity index, acute insulin response to glucose and a disposition index, derived from i.v. glucose tolerance minimal model analysis and total fasting plasma free fatty acid levels were available for 533 participants in the Reading, Imperial, Surrey, Cambridge, Kings study. Bivariate correlations were made between insulin sensitivity index, acute insulin response to glucose and disposition index and both adiposity measures (BMI, waist circumference and body fat mass) and total plasma free fatty acid levels. Multivariate linear regression analysis was performed, controlling for age, sex, ethnicity and adiposity. After adjustment, all adiposity measures were inversely associated with insulin sensitivity index (BMI: β=-0.357; waist circumference: β=-0.380; body fat mass: β= -0.375) and disposition index (BMI: β=-0.215; waist circumference: β=-0.248; body fat mass: β=-0.221) and positively associated with acute insulin response to glucose [BMI: β=0.200; waist circumference: β=0.195; body fat mass β=0.209 (P values <0.001)]. Adiposity explained 13, 4 and 5% of the variation in insulin sensitivity index, acute insulin response to glucose and disposition index, respectively. After adjustment, no adiposity measure was associated with free fatty acid level, but total plasma free fatty acid level was inversely associated with insulin sensitivity index (β=-0.133), acute insulin response to glucose (β=-0.148) and disposition index [β=-0.218 (P values <0.01)]. Plasma free fatty acid concentration accounted for 1.5, 2 and 4% of the variation in insulin sensitivity index, acute insulin response to glucose and disposition index, respectively. Plasma free fatty acid levels have a modest negative association with insulin sensitivity, β-cell secretion and disposition index but no association with adiposity measures. It is unlikely that plasma free fatty acids are the primary mediators of obesity-related insulin resistance or β-cell dysfunction.

Contribution of very low-density lipoprotein triglyceride fatty acids to postabsorptive free fatty acid flux in obese humans

ObjectiveIn the fasting state, plasma free fatty acids (FFA) are thought to derive almost exclusively from adipose tissue lipolysis. However, there are mixed reports as to whether the spillover of fatty acids (FA) from very low-density lipoprotein triglyceride (VLDL–TG) hydrolysis contributes significantly to the plasma FFA pool. Because substantial VLDL–TG fatty acid spillover into the plasma FFA pool would profoundly impact the interpretation of isotope dilution measures of FFA flux, we investigated the contribution of VLDL–TG spillover to plasma FFA appearance. Materials/MethodsEighteen obese adults (15 women) participated in these studies. Each volunteer received a primed, continuous infusion of their own ex-vivo labeled ([1-14C]triolein) VLDL–TG and a continuous infusion of [U-13C]oleate (8nmol·kg fat free mass−1·min−1) to measure VLDL–TG and FFA rate of appearance (Ra), respectively. The presence of 14C-oleate in the plasma FFA–oleate pool was used to calculate the contribution of spillover from VLDL–TG–oleate to the plasma FFA–oleate Ra. ResultsThe spillover rate of VLDL–TG–oleate into plasma FFA–oleate was 6±2μmol/min (7%±2% of [14C]oleate from VLDL–TG) and FFA–oleate flux was 240±61μmol/min. Thus, only 3%±1% of total plasma FFA–oleate appearance could be accounted for by VLDL–TG spillover. ConclusionThe contribution of VLDL–TG spillover to the total plasma FFA pool is negligible and will not materially affect the interpretation of FFA flux measures as an index of adipose tissue lipolysis.

The Impact of Flaxseed Lignan Complex Consumption on Waist to Height and Hip Ratios, Body Weight, BMI, Insulin Resistance, Percent Pancreatic Beta-Cell Function, Free Fatty Acids, HDL2- HDL3- and Non-HDL-Cholesterol and Lp(a) in Older Human Type 2 Diabetics

The variables examined are a waist circumference-associated clinically significant cluster not yet examined for changes due to flaxseed lignan complex ( FLC) administration in people with type 2 diabetes. It was hypothesized that FLC relative to placebo would increase (or better manage) percent pancreatic beta-cell function and plasma HDL2-cholesterol concentration and decrease (or better manage) the waist:height ratio (WHTR), body weight, BMI, waist:hip ratio, insulin resistance, total plasma free fatty acid, Lp(a), HDL3- and non-HDL-cholesterol concentrations. The objective was to test this hypothesis. Sixteen (11 male, 5 female) people with type 2 diabetes (mean age 66 years, mean BMI 31.2 kg/m2) completed this double-blind, randomized, crossover placebo-controlled study. Patients consumed 4 capsules/day of FLC (600 mg secoisolariciresinol diglucoside/day) or placebo for 3 months followed by a 3-month washout period (no exposure to FLC or placebo) followed by 3 months on that (FLC or placebo) to which they had not been previously exposed in this study. All data is reported as mean (SEM). Only WHTR was better FLC managed (60.1 [2.8] [start] – 60.5 [2.8] [finish] [FLC] vs. 60.1 [2.7] [start] – 61.4 [2.7] [finish] [placebo]) (p=0.04) with no other significant differences due to FLC. Diet (including alcohol), smoking, medication (dose and type) and exercise patterns did not change over the course of the study. Better WHTR management has been suggested by some to be an even more powerful indicator of improved metabolic control in type 2 diabetics (compared to waist circumference). However, while it is concluded that FLC significantly better managed the WHTR, it did not affect significantly the other aforementioned dependent variables. The clinical significance, if any, of these findings awaits elucidation.

No attenuation of gastric distress or benefit to performance with adaptation to octanoate-rich esterified oils in female cyclists

We investigated the effects of modifying a normal dietary fatty-acid composition and the ingestion of high-fat exercise supplements on gastrointestinal distress, substrate oxidation, and endurance cycling performance. Five female cyclists completed a randomized triple-crossover comprising a 2-week diet high in octanoate-rich esterified oil (MCFA), or twice, long-chain fatty acids (LCFA). Following the diets, the participants performed 3 h of cycling at 50% peak power followed by ten maximal sprints while ingesting: a carbohydrate (CHO)+MCFA-rich oil emulsion after (a) the 2-week MCFA-rich dietary condition (MC-MC, Intervention), and (b) after one LCFA-rich dietary condition (LC-MC, Placebo), or (c) CHO only following a second LCFA-rich diet (LC-CHO, Control). Ingestion of the CHO+MCFA-rich oil emulsion during 3-h steady-state exercise substantially reduced endogenous-fat oxidation by 88% (90% confidence interval: 59 to 117%) and 74% (40 to 108%) in the MC-MC and LC-MC conditions, respectively, relative to LC-CHO, but there was no effect of MCFA adaptation. Adaptation (MC-MC) also had no clear effect on endogenous CHO (11%; −10 to 33%) or exogenous octanoic-acid oxidation rates (−2%; −20 to 16%), relative to the placebo (LC-MC). Ingestion/oxidation efficiency of octanoic acid was high (0.98), but the CHO+MCFA-rich oil emulsion caused mild to moderate gastrointestinal distress during exercise and there was no attenuating effect of MCFA adaptation evident, nor any clear benefit of the oil emulsion or adaptation to performance. Plasma triacylglycerol concentrations were lower by 17% (23 to −4%) and 15% (20 to −3%; reduction likely) in the LC-MC and MC-MC conditions, respectively, relative to LC-CHO. Total plasma free-fatty acid concentrations were 20% lower (39 to 3%) in the LC-MC condition, relative to LC-CHO. Plasma glycerol concentrations trended lower in the LC-MC and MC-MC conditions, but uncertainty meant these effects were qualified unclear. There was no clear effect of MCFA adaptation on total and 13C-enriched plasma octanoic acid concentrations, nor were there any detectable elongation products (13C-enriched fatty acids >8:0) seen in the plasma in either the MC-MC or LC-MC conditions. In conclusion, despite high efficiency of exogenous-MCFA oxidation, no clear benefit to prolonged endurance performance was observed with the ingestion of a CHO+MCFA-rich esterified oil emulsion or following adaptation to a MCFA-rich diet in female cyclists.

Dairy food consumption alters lipid responses in humans

Metabolic syndrome is associated with insulin resistance, alterations in glucose metabolism and dyslipidemia. During caloric restriction, calcium supplementation and dairy food intake augment weight and fat loss, yet the effects of calcium and dairy food on lipid metabolism particularly in those losing weight to reverse associated metabolic problems have not been studied. The objective of this study was to determine whether calcium, provided as a calcium carbonate supplement, or dairy foods in a calorie-restricted diet changed lipid responses compared to a calorie-restricted, low-calcium diet. The high-dairy group lost more total, trunk fat and intra-abdominal adipose tissue compared with the placebo and high calcium groups. Significant changes in lipid metabolism associated with insulin resistance were found, and yet were different between the dietary groups. Plasma total free fatty acids, including significant changes in 16:0, 18:0, 18:1n9 and 18:1n7 all increased in the placebo and high-calcium supplement groups but decreased significantly in the high-dairy group compared to baseline. Only the high-dairy group demonstrated significant decreased concentrations of FFA circulating in plasma during weight loss. These results imply that a component(s) in dairy products affects aspects of lipid metabolism discrete from the effects of calcium alone during caloric restriction

Acute in vivo elevation of intravascular triacylglycerol lipolysis impairs peripheral T cell activation in humans

Previous studies have shown suppressive effects of polyunsaturated fatty acids (PUFAs) on T cell proliferation, but the precise mechanism for this effect has not been fully investigated in vivo in humans. The objective was to determine whether this effect is the result of altered T cell membrane properties and impaired CD3- and CD28-mediated signaling in vivo in humans. Peripheral T cells were isolated from healthy subjects before and 2 h after an intravenous infusion of heparin plus a PUFA-rich lipid emulsion during a euglycemic hyperinsulinemic clamp to induce a 2.5-fold elevation in plasma linoleic acid concentration without significant change in plasma total free fatty acid concentrations. Intravenous infusion of heparin plus the lipid emulsion reduced peripheral T cell membrane fluidity and altered lipid raft organization, both of which were associated with reduced T cell proliferation after stimulation with CD3 plus CD28. Tyrosine phosphorylation of linker of activated T cells and activation of protein kinase B in T cells were also impaired without a reduction in T cell receptor expression. In addition, acute PUFA elevation was associated with a reduction in T cell membrane cholesterol exchange with the cellular milieu ex vivo. A selective increase in plasma linoleic acid concentration and in intravascular lipolysis has a suppressive effect on peripheral T cell CD28-dependent activation, and this effect is associated with changes in plasma membrane properties. Our results have important implications for nutritional therapy in patients at high risk of septic complications and may also be of relevance to postprandial lipid metabolism disorders such as insulin resistance and type 2 diabetes.

What does the measurement of whole-body fatty acid rate of appearance in plasma by using a fatty acid tracer really mean?

We evaluated the validity of using a single fatty acid tracer to assess total plasma long-chain free fatty acid (FFA) kinetics and the relationship between the rate of appearance (R(a)) of fatty acids in plasma and the fatty acid composition of adipose tissue triglyceride (TG). A mixture of [(13)C]-labeled myristate, palmitate, stearate, oleate, and linoleate was infused in healthy men during basal conditions and during conditions that stimulate (epinephrine infusion) and inhibit (insulin infusion) lipolysis of adipose tissue TGs. Calculated total FFA, R(a) based on palmitate, oleate, or linoleate tracers, was within 15% of the measured sum of the individual fatty acid R(a) under all conditions, whereas stearate and myristate tracers consistently underestimated and overestimated total FFA R(a), respectively. The fatty acid R(a) profile closely matched the fatty acid profile of subcutaneous adipose tissue TGs during epinephrine infusion, but not during basal conditions and insulin infusion. Our data support the common practice of using labeled palmitate or oleate as fatty acid tracers for assessing total plasma FFA kinetics and suggest that a source of lipids other than adipose tissue TG release fatty acids into the systemic circulation.

Systemic fatty acid responses to transient focal cerebral ischemia: influence of neuroprotectant therapy with human albumin.

Human albumin therapy is highly neuroprotective in focal cerebral ischemia. Because albumin is the main carrier of free fatty acids (FFA) in plasma, we investigated the content and composition of plasma FFA in jugular vein (JV), femoral artery (FA) and femoral vein (FV) of rats given intravenous human albumin (1.25 g/kg) or saline vehicle (5 mL/kg) 1 h after a 2 h middle cerebral artery occlusion (MCAo) or sham surgery. Arachidonic acid was the only FFA significantly increased by MCAo in all plasma samples prior to albumin administration, remaining at the same level regardless of subsequent treatments. Albumin treatment induced in both MCAo- and sham-groups a 1.7-fold increase in total plasma FFA (mainly 16:0, 18:1, 18:2n-6) during 90-min reperfusion. MCAo selectively stimulated the albumin-mediated mobilization of n-3 polyunsaturated fatty acids (PUFA), with an early increase in 22:5n-3 and 22:6n-3 in the FA prior to detectable changes in the JV. In the MCAo-albumin group, the lower level of FFA in JV as compared with FA and FV suggests an albumin-mediated systemic mobilization and supply of FFA to the brain, which may favor the replenishment of PUFA lost from cellular membranes during ischemia and/or to serve as an alternative source of energy, thus contributing to albumin neuroprotection.

Changes in plasma free fatty acid concentrations in rheumatoid arthritis patients during fasting and their effects upon T-lymphocyte proliferation.

To measure whether changes in the concentrations of circulating free fatty acids (FFAs) after a 7 day fast in rheumatoid arthritis (RA) patients would inhibit in vitro T-lymphocyte proliferation. The concentration and composition of plasma FFAs were measured in nine RA patients at the conclusion of a 7 day fast. A FFA mixture was made up based on these findings (20% linoleic, 43% oleic, 10% stearic, 27% palmitic acid). Mitogen-induced lymphocyte proliferative responses were measured after co-culture of peripheral blood mononuclear cells (PBMC) from healthy individuals in the presence of increasing concentrations of this FFA mixture (from 0 to 2000 microM) and in the presence of FFA mixtures where the relative proportions of fatty acids varied. Both the concentration of the FFA mixture and the ratio between the unsaturated and saturated fatty acids significantly influenced in vitro lymphocyte proliferation (P<0.0001). Unexpectedly, the highest concentrations of the FFA mixture increased lymphocyte proliferation. At equimolar concentrations (600 microM), manipulating the amounts of oleic and linoleic fatty acids relative to stearic and palmitic fatty acids had a potent inhibitory effect upon lymphocyte proliferation. Fasting-associated increases in total plasma FFA concentrations do not inhibit, but rather enhance, in vitro lymphocyte proliferation. An inhibitory effect could only be achieved by manipulating the balance between the unsaturated and saturated fatty acids.

Circulating palmitate uptake and oxidation are not altered by glycogen depletion in contracting skeletal muscle

The extent to which muscle glycogen depletion affects plasma free fatty acid (FFA) metabolism in contracting skeletal muscle is not well characterized. To study this question, rats were glycogen depleted (GD) or supercompensated (SC) by swimming exercise and diet treatment 24 h before perfusion of their isolated hindquarters at rest and during electrically induced muscle contractions. After 20 min of equilibration with glucose (6 mM), palmitate (2,000 microM), and [1-14C]palmitate, palmitate uptake and oxidation were found to be similar between groups at rest and during electrical stimulation. Palmitate uptake increased by 55% during electrical stimulation and averaged 2.75 +/- 0.56 mumol.g-1.h-1. Resting palmitate oxidation averaged 0.14 +/- 0.03 mumol.g-1.h-1 and increased to 0.53 +/- 0.06 and 0.47 +/- 0.08 mumol.g-1.h-1 during electrical stimulation in GD and SC, respectively. Glucose uptake was significantly higher in GD than in SC at rest and during electrical stimulation and significantly increased in both groups during electrical stimulation to reach values of 11.8 +/- 1.2 and 7.6 +/- 1.4 mumol.g-1.h-1, respectively. Lactate release was lower in GD than in SC at rest and during electrical stimulation and was highest after 2 min of stimulation in both groups. Additional experiments at perfusate palmitate concentrations of 600-900 microM yielded similar results. These results show that, in contracting perfused skeletal muscle, muscle glycogen depletion increases glucose utilization but does not affect total plasma FFA oxidation, suggesting that regulation within pathways of carbohydrate metabolism takes precedence over regulation between pathways of lipid and carbohydrate metabolism.

Lipoprotein lipase in plasma after an oral fat load: relation to free fatty acids.

Lipoprotein lipase (LPL) releases fatty acids from triglyceride-rich lipoproteins for use in cellular metabolic reactions. How this hydrolysis, which occurs at the vascular endothelium, is regulated is poorly understood. A fatty acid feedback system has been proposed by which accumulation of fatty acids impedes LPL-catalyzed hydrolysis and dissociates the enzyme from its endothelial binding sites. We examined this hypothesis in humans who were subjected to an oral fat tolerance test of a mixed-meal type. Plasma triglycerides, free fatty acids, and LPL activity were measured before and repeatedly during a 12-h period after intake of the fat load. Since soybean oil with a high content of linoleic fatty acid was the source of triglycerides, a distinction could be made between endogenous free fatty acids (FFA) and FFA derived directly from lipolysis of postprandial triglyceride-rich lipoproteins. Mean LPL activity was almost doubled (P less than 0.01) 6 h after intake of the oral fat load. The rise in LPL activity was accompanied by an increase of plasma triglycerides and linoleic free fatty acids (18:2 FFA), but not of total plasma FFA, which instead displayed a heterogeneous pattern with essentially unchanged mean levels. The postprandial response of LPL activity largely paralleled the postprandial responses of 18:2 FFA and triglycerides. The highest degree of parallelism was seen between postprandial 18:2 FFA and LPL activity levels. Furthermore, the integrated response (area under the curve, AUC) for plasma measurements of LPL correlated with the AUC for 18:2 FFA (r = 0.40, P less than 0.05), but not with the AUC for plasma triglycerides (r = 0.21, ns). The high degree of parallelism and significant correlation between postprandial plasma LPL activity and 18:2 FFA support the hypothesis of fatty acid control of endothelial LPL during physiological conditions in humans.

Palmitic acid kinetics in fasting, traumatized patients.

The contribution of free fatty acid oxidation to the elevation in energy expenditure after trauma has not been well characterized. Six control subjects and six traumatized patients were fasted for 48 hours and given a primed continuous infusion of (1-14C)palmitate to measure plasma palmitate and total free fatty acid kinetics. Traumatized patients had greater urinary nitrogen losses (20.8 vs. 9.3 g N per day) and a significantly greater ratio of measured to predicted resting energy expenditure (+36% vs. -6%) compared with controls. Individual and total plasma free fatty acid concentrations were similar for the two groups. The turnover and oxidation of plasma palmitate and total free fatty acids were not changed by multiple trauma. These results demonstrated that plasma free fatty acids and palmitate do not contribute to increased energy expenditure following trauma.

Trauma metabolism and the heart: Uptake of substrates and effects of insulin early after cardiac operations

In a controlled, randomized study the myocardial uptake/release of individual free fatty acids, glucose, lactate, pyruvate, alanine, and glycerol was studied 1 hour after completion of coronary operations. The effects of insulin were evaluated by means of a hyperinsulinemic "clamp" technique. No significant uptake of free fatty acids was found despite markedly elevated arterial concentrations (mean +/- standard error of the mean, 2.01 +/- 0.19 mmol.L-1), oleic acid, together with palmitic and linoleic acid, constituting 80% of the total plasma free fatty acid level. Insulin treatment (1 unit.kg bw-1.hr-1) prevented a further increase of the plasma free fatty acid level, observed concomitantly in the control group. Insulin affected all individual free fatty acids similarly. Changes in plasma free fatty acid levels occurring during the study and the corresponding myocardial uptake correlated (rS = 0.50 to 0.81). No significant uptake or release of glucose, lactate pyruvate, and glycerol occurred, whereas a myocardial release of alanine was seen. The heart and the concomitant leg uptake/release of glucose (rS = 0.40, p less than 0.05) and lactate (rS = 0.67, p less than 0.01) correlated. A substantial uptake of glucose was achieved and a more positive myocardial balance was obtained for alanine, lactate, and pyruvate with insulin. The changes in heart and the concomitant leg uptake/release correlated (glucose, rS = 0.62, p less than 0.01; lactate, rS = 0.64, p less than 0.01; pyruvate, rS = 0.71, p less than 0.01). It is concluded that the myocardial uptake of substrates during the first hours after coronary surgery is markedly abnormal with no uptake of free fatty acids or carbohydrates. These changes can be explained to some extent by the insulin resistance of trauma metabolism and can be modified by insulin treatment.

High arachidonic acid levels in the cord blood of infants of mothers on vegetarian diets

1. Maternal and umbilical cord plasma samples were collected from forty-seven Asian women, twenty-eight life-long vegetarians and seventeen non-vegetarians, during delivery of their babies. The concentrations and fatty acid profiles of the plasma free fatty acid and triacylglycerol fractions were determined. 2. There were no significant differences between the levels of free fatty acid and triacylglycerol in either maternal or cord plasma from vegetarian compared with non-vegetarian Asian women. The fatty acid profiles of the lipid fractions in the two groups were similar. Total plasma free fatty acid levels in the maternal circulation correlated with umbilical cord levels. 3. The levels of linoleic acid in the maternal plasma free fatty acid fraction of the Asian women were much higher than previous reports on mixed populations of European women. In the Asian women arachidonic acid concentrations in both maternal and umbilical circulations were over four times higher than those reported for women unselected for race and diet.

Evaluation of free fatty acid kinetics during TPN feeding of healthy rats

Free fatty acid (FFA) kinetics were evaluated in TPN-fed healthy rats using a single fatty acid tracer. Rats were divided into three groups according to the nonprotein energetic substrate infused: glucose (A), monoacetoacetin-glucose (B), and lipid emulsion-glucose (C). Fat kinetics were measured by continuous infusion of [1- 14C]palmitate. Total FFA and individual FFA concentrations were measured and turnover and oxidation were determined for the total pool of FFA and for palmitate. Groups A and B were similar in all parameters. Group C had increased total and individual FFA concentrations. Group C appeared to have decreased total plasma FFA turnover and unchanged oxidation compared to groups A and B. Palmitate appeared to have a 400% increase in oxidation and a 50% increase in turnover for rats in Group C when compared to Groups A and B. It is concluded that a single tracer does not accurately reflect plasma FFA during TPN using lipid emulsion.