linoleic-acid and Hypertriglyceridemia

Intravenous lipid emulsions (IVLEs) are an essential component of parenteral nutrition. With the recent incorporation of new lipid emulsions into the Canadian and American market, the clinician responsible for prescribing these lipids should be educated regarding the different fatty acid (FA) profiles of these lipids, as well as their metabolic and functional effects.. New IVLEs contain a mix of soybean oil and olive oil, or a mix of soybean oil, coconut oil, olive oil and fish oil. These new lipid emulsions provide less essential fatty acids (FAs) (linoleic and alpha linolenic acids) than in pure soybean oil, yet incorporation of fish oil into an IVLE may decrease the amount of essential FAs required. Fish oil is a treatment for hypertriglyceridemia, and therefore, IVLEs that include fish oil may decrease serum triglycerides. Historical perspective is that fish oil can be associated with increased bleeding time. Evidence suggests that there is no association between fish oil and increased bleeding in patients, even those who are using anticoagulants. New IVLEs provide less vitamin K than soybean oil alone. Patients, or the parenteral nutrition solutions that include these new IVLEs should be supplemented with vitamin K.. Canadian and American Guidelines for IVLEs were based on soybean oil. Current practice should be tailored to which IVLE is being prescribed.

Topics: alpha-Linolenic Acid; Blood Coagulation; Canada; Coconut Oil; Fat Emulsions, Intravenous; Fish Oils; Humans; Hypertriglyceridemia; Linoleic Acid; Olive Oil; Parenteral Nutrition; Soybean Oil; United States; Vitamin K

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 randomized 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, resulting 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 postprandial 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 ligand (CD40L), adiponectin, or fasting or postprandial 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.

Topics: Adult; Biomarkers; Cardiovascular Diseases; Diet; Dietary Supplements; Double-Blind Method; Fish Oils; Humans; Hypertriglyceridemia; Linoleic Acid; Male; Risk Factors; Triglycerides

To study the effect of omega-3 polyunsaturated fatty acid supplementation on lipid profile in hypertriglyceridaemic patients.. General practice.. Prospective, double blind study of 12 weeks' duration.. Eight patients received fish oil (1800 mg C20: 5 omega-3 eicosapentaenoic acid (EPA) and 1200 mg C22:6 omega-3 docosahexaenoic acid (DHA). Nine patients received corn oil (3000 mg C18: 2 omega-6 linoleic acid daily).. Lipid profile analysis showed a decrease in triglyceride levels after fish oil supplementation. An unexpected and unexplained finding was the rise in total cholesterol and LDH cholesterol with corn oil supplementation.. Fish oil causes a decrease in triglyceride levels in hypertriglyceridaemic patients.

Topics: Adult; Cholesterol; Cholesterol, LDL; Double-Blind Method; Female; Fish Oils; Humans; Hypertriglyceridemia; Linoleic Acid; Linoleic Acids; Male; Middle Aged; Prospective Studies; Triglycerides

There is a strong coincidence of obesity and a chronic state of modest inflammation. Secretion of pro-inflammatory cytokines from adipocytes and immune cells represents a key mechanism in this process and is affected by fatty acids.. A study cohort of 100 overnight fasted healthy volunteers underwent an oral lipid tolerance test (OLTT) by ingestion of 160ml of a protein- and sugar-free lipid emulsion of defined composition. Venal blood was drawn at 0h (fasting) and at 2, 4, and 6h after lipid ingestion. Subjects were characterized by anthropometric and standard laboratory parameters. Serum concentrations of CCL2, IP-10, chemerin, and RANTES were measured by enzyme-linked immunosorbent assay (ELISA). Murine 3T3-L1 adipocytes were stimulated with free fatty acids (FA) and with sex steroids and concentrations of CCL2 and chemerin in cell culture supernatants were measured by ELISA.. A significant reduction of circulating CCL2, IP-10, and chemerin concentrations was observed as a consequence of triglyceride ingestion whereas RANTES levels were increased. CCL2 serum concentrations were positively correlated with resistin and visfatin levels and with LDL/HDL ratio and negatively with adiponectin. There were significant differences in chemerin and RANTES serum concentrations in female and male subjects. CCL2 secretion from 3T3-L1 adipocytes was inhibited by treatment with linoleic (LA) and oleic acid (OA) whereas chemerin secretion was induced. Chemerin release from 3T3-L1 adipocytes was inhibited by testosterone.. Oral lipid loading is linked to reduced circulating pro-inflammatory chemokines CCL2, IP-10, and chemerin and to increased RANTES levels, suggesting that dietary lipids affect immune function.

Topics: Adipocytes; Adolescent; Adult; Animals; Cell Line; Chemokine CCL2; Chemokine CCL5; Chemokine CXCL10; Chemokines; Cohort Studies; Dietary Fats; Fatty Acids, Nonesterified; Female; Healthy Volunteers; Humans; Hypertriglyceridemia; Inflammation; Intercellular Signaling Peptides and Proteins; Linoleic Acid; Male; Mice; Middle Aged; Oleic Acid; Sex Characteristics; Triglycerides; Young Adult

Susceptibility of lipoprotein to oxidation is usually studied using purified lipoproteins. However, for large clinical studies or routine clinical assessment, a rapid less time-consuming method is desirable. Therefore, we studied copper-mediated oxidation of the macromolecule fraction of plasma in comparison with oxidation directly in whole unfractionated plasma in a group of hyperlipidemic individuals.. Lag phase rate (LR), propagation phase rate (PR), lag time (LT), and maximal extent of oxidation were determined for copper-mediated oxidation in plasma from 16 hyperlipidemic individuals. Oxidation parameters obtained for whole plasma (WP) and macromolecules were subjected to correlation analysis with plasma lipid concentrations and with the oleic acid/linoleic acid ratio (18:1/18:2) in phospholipids (PL), triglycerides (TG), and cholesterol esters (CE).. Total cholesterol (TC) concentration was significantly correlated with lag rate (negative, p<0.05), lag time (positive, p<0.01), and with maximal extent of oxidation (positive, p<0.05) for plasma macromolecules (PM). Triglyceride concentration was not significantly correlated with lag rate, lag time, or propagation rate for plasma macromolecules. Triglyceride concentration was positively correlated with the maximal extent of oxidation (p<0.01) for plasma macromolecules. In the cholesterol ester fraction, the 18:1/18:2 ratio was significantly correlated (positive, p<0.05) with lag time. Phospholipid 18:1/18:2 ratio did not correlate with oxidative parameters. This ratio in triglycerides correlated better, but statistical significance was not obtained. Parameters obtained with whole plasma did not significantly correlate with lipid values.. Oxidation parameters obtained for plasma macromolecules correlated with lipid parameters known to be associated with oxidative susceptibility of lipoproteins and were unaffected by soluble antioxidants found in whole plasma or serum. Therefore, plasma macromolecules were superior to whole plasma for assessing lipoprotein susceptibility to oxidation. This approach will facilitate larger clinical trials by saving the time and labor involved in lipoprotein isolation.

Topics: Chemical Fractionation; Copper; Humans; Hypertriglyceridemia; Kinetics; Linoleic Acid; Lipids; Lipoproteins; Macromolecular Substances; Methods; Oleic Acid; Oxidation-Reduction

Susceptibility of lipoprotein to oxidation is usually studied using purified lipoproteins. However, for large clinical studies or routine clinical assessment, a rapid, less time-consuming method that minimizes hydroperoxide accumulation in lipoprotein during preparation is desirable. Methods using whole plasma are complicated by the presence of an anticoagulant that may affect oxidation and the presence of antioxidants in the plasma aqueous phase. Lipoproteins in serum are relatively unprotected from initiation of oxidation.. We studied copper-mediated oxidation of a macromolecule fraction of plasma prepared by simple molecular sieve chromatography.. LDL was more susceptible to oxidation than plasma macromolecules. The lag times approached zero as the copper concentration increased. The propagation rate was linear for PM vs. the copper concentration while LDL became saturated at 10-20 micromol/l. The interassay CVs for the lag phase rate, lag time, PR and maximal DeltaA(max) were 23%, 7.7%, 4.9%, and 3.3%, respectively.. This procedure should be applicable to large numbers of individuals in investigations regarding the effects of drugs and diets on lipid composition and oxidative susceptibility.

Topics: Copper; Humans; Hypertriglyceridemia; Kinetics; Linoleic Acid; Lipids; Lipoproteins; Macromolecular Substances; Methods; Oleic Acid; Oxidation-Reduction

To evaluate the mechanisms of suppression of postprandial hypertriglyceridemia by fish oil rich in docosahexaenoic acid, the effect on the intestinal absorption of triglyceride, activities of lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) and metabolism of chylomicrons (CM) and CM remnants were compared with that of safflower oil in Sprague-Dawley rats in a series of studies. The feeding of fish oil for 3 wk suppressed postprandial hypertriglyceridemia (study 1). Dietary fish oil did not alter the rate of lymphatic absorption of triglyceride (study 2). The activities of LPL and HTGL were measured at 5 h after the beginning of feeding, when serum triglyceride concentrations were highest in both dietary groups. The activities of LPL in adipose tissue and heart were greater (P < 0.05) and those of HTGL were lower (P < 0.05) in the rats fed fish oil (study 3). In contrast, there were no differences in the activities of LPL and HTGL in postheparin plasma between the fish and safflower oil groups (study 4). The clearance rates of CM and CM remnants were measured by injecting intravenously CM collected from rats fed safflower or fish oils with [14C]triolein and [3H]cholesterol (study 5). Dietary oil did not influence the half-lives of CM or CM remnants. The secretion of triglyceride from the liver of rats injected with Triton WR-1339 was lower (P < 0.05) in the rats fed docosahexaenoic acid, a major component of fish oil, than those fed linoleic acid, a major component of safflower oil (study 6). These observations strongly support the hypothesis that in rats, the principal cause of the suppression of postprandial hypertriglyceridemia by fish oil is the depression of triglyceride secretion from the liver.

Topics: Absorption; Animals; Chylomicrons; Docosahexaenoic Acids; Fish Oils; Hypertriglyceridemia; Linoleic Acid; Lipase; Lipoprotein Lipase; Liver; Male; Postprandial Period; Rats; Rats, Sprague-Dawley; Safflower Oil; Triglycerides

We have shown previously that the impaired insulin action in hereditary hypertriglyceridemic (hHTg) rat is accompanied by a specific fatty acid (FA) profile in the insulin target tissues, possibly due to a desaturation defect. Thus, the aim of this study was to measure the enzymatic activity and gene expression of delta-6 desaturase in liver of hHTg rats and the tissue FA composition in relation to insulin action.. Glucose, triglycerides and insulin in plasma were measured using commercially available enzymatic sets. The hepatic delta-6 desaturase activity in hHTg rats was determined radiometrically in a microsomal fraction using the 1-14C-linoleic acid as substrate. delta-6 Desaturase gene expression was measured by the Northern blot technique using a specific cDNA probe. Tissue FA profile was determined by gas chromatography in the total lipid fraction extracted to chloroform. The glucose turnover rate was measured in conscious freely moving animals with the aid of euglycemic hyperinsulinic clamp method.. Tissue triglycerides showed a high accumulation in skeletal muscle of hHTg rats. In the liver of these animals, a defect in delta-6 desaturase enzymatic activity was found, while the gene expression for delta-6 desaturase was not changed. Such decreased delta-6 desaturase activity in the liver was linked to a decrease of delta-6 desaturase index as calculated from the liver FA composition. Also the concentration of arachidonic acid (a final metabolite in the biosynthesis of polyunsaturated fatty acids of the n-6 series) was significantly decreased in hHTg rat liver. These changes in FA metabolism were accompanied by a decreased glucose infusion rate (a measure of in vivo insulin action) required to maintain euglycemia at hyperinsulinemia in hHTg rats, and correlated with the hepatic delta-6 desaturase activity.. 1. hHTg rats showed a reduced activity of the delta-6 desaturase in liver without any changes in gene expression for this enzyme; 2. such impairment is accompanied by a lower delta-6 desaturase index (18:2n-6/18:3n-6) found in the liver of these animals and by specific FA profiles in the tissues, particularly regarding the amount of long-chain PUFAs and 18:2n-6 metabolites; and (4) these alterations seem to be related to the impaired insulin action of hHTg rats.

Topics: Animals; Blood Glucose; Blotting, Northern; Fatty Acid Desaturases; Fatty Acids; gamma-Linolenic Acid; Gene Expression; Glucose Clamp Technique; Hypertriglyceridemia; Insulin; Linoleic Acid; Linoleoyl-CoA Desaturase; Liver; Male; Microsomes, Liver; Muscle, Skeletal; Rats; Rats, Wistar; RNA, Messenger; Triglycerides

Topics: Carbon Isotopes; Fatty Acids; Glycerides; Heart Diseases; Hyperlipidemias; Hypertriglyceridemia; Linoleic Acid; Lipid Metabolism; Lipids; Lipoproteins; Myocardial Infarction; Palmitates; Palmitic Acid; Tritium