Possible role of ceramide in defining structure and function of membrane glycolipids.

A possible role of ceramide in defining the carbohydrate structure of glycolipids and the expression of glycolipid function has been proposed, on the basis of our finding that the ceramide composition of "lacto-series" glycosphingolipid isolated from human erythrocytes shows a remarkable correlation with the terminal carbohydrate structure: (i) The ceramides of three glycosphingolipids with Lex (or x) determinant [Gal beta 1 leads to 4(Fuc alpha 1 leads to 3) GlcNAc] had almost exclusively 16:0 fatty acid; in contrast, the ceramide of its positional isomer H determinant had mainly 20--24:0 fatty acids. (ii) The ceramide of two glycosphingolipids with NeuAc alpha 2 leads to 6GAL structure was predominantly of 16:0 fatty acid, in contrast to that of its positional isomer NeuAc alpha 2 leads to 3Gal residue, in which the ceramide had 20--24:0 fatty acids. These results, together with our previous observation that ceramide composition of mouse lymphoma and myelocytic leukemia MI cells affects their antigenicity, suggest that ceramide structure may define the organization of glycosyltransferase for synthesis of the carbohydrate determinants and may affect the organization and orientation of the carbohydrate chain in membranes, eliciting or suppressing the reactivity to its ligand. Because these glycolipids with Lex and NeuAc alpha 2 leads to 6Gal structures are developmentally regulated and are highly expressed in certain tumors, ceramide composition may affect development, differentiation, and oncogenesis.     

Chronic treatment with pioglitazone does not protect obese patients with diabetes mellitus type II from free fatty acid-induced insulin resistance

CONTEXT: Thiazolidinediones increase peripheral insulin sensitivity and decrease plasma free fatty acids (FFA). However, their exact mechanism of action has not been fully elucidated. OBJECTIVE: We studied the protective effect of pioglitazone on FFA-induced insulin resistance and the effects on intramyocellular glycosphingolipids. DESIGN: We studied glucose metabolism in the basal state and during a hyperinsulinemic euglycemic clamp by using stable isotopes. Studies were performed at baseline and after 4 months of treatment with pioglitazone. Patients were then studied on a third occasion during infusion of a lipid emulsion to increase plasma FFA to pretreatment levels. All studies were combined with muscle biopsies to measure intramyocellular ceramide and glycosphingolipids. PATIENTS: Patients were obese with poorly controlled type 2 diabetes mellitus. INTERVENTION: Patients were treated with 30 mg pioglitazone once daily. Main Outcome Measure: The change in peripheral insulin sensitivity after treatment with pioglitazone and during the infusion of the lipid emulsion was the main outcome measure. RESULTS: Peripheral glucose uptake (Rd) increased significantly, but returned to baseline levels after increasing plasma FFA to pretreatment levels. Insulin-mediated suppression of FFA was increased significantly. Intramyocellular ceramide concentrations were higher during the hyperinsulinemic clamp after treatment with pioglitazone, but not in the basal state. The intramyocellular content of glycosphingolipids and plasma concentrations of ceramide and glycosphingolipids did not change. CONCLUSIONS: Pioglitazone increases Rd and insulin-mediated suppression of plasma FFA, but does not protect patients with type 2 diabetes mellitus from FFA-induced insulin resistance. This effect of pioglitazone is not attained via a decrease in intramyocellular concentrations of ceramide or glycosphingolipids.     

Phospholipase activity in human bile

To investigate the importance of bacterial infection in the formation of free fatty acids found in brown pigment gallstones, free fatty acids and phospholipase activity in hepatic bile, with or without the presence of bacterial infection, were compared. The concentration of free fatty acids in bile with bacterial infection [0.467 +/- 0.447 mg per ml (mean +/- S.D.)] was significantly higher than when bacterial infection was absent (0.073 +/- 0.041 mg per ml; p less than 0.01). However, there was no significant difference in the composition of free fatty acids in hepatic bile when bacterial infection was present. Biliary phospholipase activity was determined by counting [14C] palmitic acid released from [14C]dipalmitoyl phosphatidylcholine that was incubated with native bile. The biliary phospholipase activity was significantly higher when bacterial infection was present. Furthermore, a positive correlation (p less than 0.001) was found between the activity of biliary phospholipases and the concentration of free fatty acids in hepatic bile. Most bacterial strains isolated from bile were shown to have both phospholipase A1 and A2 activity. On the other hand, human pancreatic juice and human gallbladder epithelial cells contained mainly phospholipase A2. Since fatty acids in the gallstone are mainly palmitic acid and must have been cleaved from first position in the biliary phosphatidylcholine molecule, bacterial phospholipase A1 seems to play an important role in the formation of calcium palmitate found in brown pigment gallstones.     

Comparison of changes in erythrocyte and platelet phospholipid and fatty acid composition and protein oxidation in chronic obstructive pulmonary disease and asthma

OBJECTIVE: To analyse and compare the phospholipid and fatty acid composition of total lipids and the occurrence of lipid peroxidation and protein oxidation directly in erythrocytes or platelets from chronic obstructive pulmonary disease (COPD) and asthma patients. PATIENTS: Fifteen consecutive outpatients with COPD (all smokers) and asthma (non-smokers) recruited during a moderate-to-severe (COPD) or moderate (asthma) exacerbation. Fifteen subjects with smoking habits similar to those of COPD patients were studied as a control group. METHODS: Phospholipid and total fatty acid compositions were analysed by two-dimensional thin layer chromatography or gas chromatography-mass spectrometry, respectively. The lipid fluorescence of lipid extracts was measured by spectrofluorimetry. Protein carbonyl contents and profiles were measured by immunoblot detection. RESULTS: No differences were found either in erythrocyte or platelet cholesterol or phospholipid levels. Only a decrease in the content of phosphatidylserine + phosphatidylinositol (P<0.003) was detected in platelets from the asthma patients. In erythrocytes, the fatty acid profile changed in both lung pathologies, especially as regards polyunsaturated fatty acids (decreases in arachidonic and 22:4 fatty acid contents). Other observed changes were: COPD, an increase in palmitic fatty acid; asthma, an increase in oleic and decreases in eicosapentaenoic and 22:6 + 24:1 fatty acids. In platelets, the fatty acid profiles revealed many differences between both lung pathologies: COPD, a decrease in 18:1 and increases in 20:5 and 22:5 + 24:0; asthma, a decrease in 20:4 and increase in 22:6 + 24:1. In COPD vs. asthma patients, fatty acid changes were mainly detected in platelets, especially in 18-carbon species, with decreases in stearic and 18:1 fatty acids in the COPD patients. Protein oxidation levels were increased in both lung pathologies in both erythrocytes and platelets. CONCLUSIONS: COPD and asthma are associated with common or specific changes in the lipid composition of erythrocytes and/or platelets. The data point to lipid peroxidation and protein oxidation phenomena in both types of blood cell, although platelets would be more susceptible to stress.     

Sphingolipids, insulin resistance, and metabolic disease: new insights from in vivo manipulation of sphingolipid metabolism

Obesity and dyslipidemia are risk factors for metabolic disorders including diabetes and cardiovascular disease. Sphingolipids such as ceramide and glucosylceramides, while being a relatively minor component of the lipid milieu in most tissues, may be among the most pathogenic lipids in the onset of the sequelae associated with excess adiposity. Circulating factors associated with obesity (e.g., saturated fatty acids, inflammatory cytokines) selectively induce enzymes that promote sphingolipid synthesis, and lipidomic profiling reveals relationships between tissue sphingolipid levels and certain metabolic diseases. Moreover, studies in cultured cells and isolated tissues implicate sphingolipids in certain cellular events associated with diabetes and cardiovascular disease, including insulin resistance, pancreatic beta-cell failure, cardiomyopathy, and vascular dysfunction. However, definitive evidence that sphingolipids contribute to insulin resistance, diabetes, and atherosclerosis has come only recently, as researchers have found that pharmacological inhibition or genetic ablation of enzymes controlling sphingolipid synthesis in rodents ameliorates each of these conditions. Herein we will review the role of ceramide and other sphingolipid metabolites in insulin resistance, beta-cell failure, cardiomyopathy, and vascular dysfunction, focusing on these in vivo studies that identify enzymes controlling sphingolipid metabolism as therapeutic targets for combating metabolic disease.     

Lipid fractions from liver inhibit specific binding of [3H]ouabain to dog heart

Ethyl acetate extracts of bovine liver contain organic material which inhibits specific binding of [³H]ouabain in a radioreceptor binding assay. Filtration of Sephadex LH-60 resolved active material in a cholesterol-rich fraction which was further purified on a silica gel column and by TLC and found by GLC/MS to be composed mainly of long-chain fatty acids and their methyl esters. Certain authentic saturated and unsaturated fatty acids were active in the binding assay: lauric, myristic and myristoleic acids being most active. Since the amount of active saturated acids in the extracts is too small to account for the total observed activity, the presence of active unsaturated fatty acids is indicated. Furthermore, another active unidentified substance was associated with the neutral lipid fraction which also contained cholesterol and methyl esters of palmitic and stearic acids as major identifiable components, and gave a concentration-displacement curve parallel to that of ouabain. Authentic cholesterol and methyl esters of both saturated and unsaturated fatty acids were inactive in the binding assay. Thus, inhibition of specific binding of [³H]ouabain by lipid extracts of liver appears to be due, in part, to certain fatty acids and, in addition, to a potent unidentified substance associated with neutral lipids.     

Metabolic effects of dietary stearic acid in mice: changes in the fatty acid composition of triglycerides and phospholipids in various tissues.

The fatty acid patterns of triglycerides and phospholipids extracted from adipose tissue, liver, heart, kidney, spleen, and lung of 3 groups of C57BL/6 mice were determined after feeding diets rich in palmitic acid (16:0) (high palmitic: 16:0 = 45.1% of total fatty acids), stearic acid (18:0) (high stearic: 18:0 = 42.9% of total fatty acids) and oleic acid (18:1) (high oleic: 18:1 = 79.7% of total fatty acids) for 9 months. Triglyceride content of adipose, liver, heart, kidney, lung and spleen tissues was significantly enriched in palmitic acid in mice fed the high palmitic diet (range among all tissues: 19.9% +/- 0.2% to 29.0% +/- 1.9% of total fatty acids) and in oleic acid in mice fed the high oleic diet (range 56.0% +/- 1.9% to 71.6% +/- 1.2%). The stearic acid content of organ triglycerides in mice fed the high stearic diet ranged from 3.7% +/- 0.3% to 10.8% +/- 1.2%; however, the content of oleic acid on this diet (range: 57.0% +/- 1.8% to 71.4% +/- 1.7%) was similar to the one observed in mice fed the high oleic diet. In all organs, phospholipids had a significantly higher percentage of stearic acid (range: 23.5% +/- 0.9% to 51.5% +/- 6.6%) than triglycerides, regardless of diet. To evaluate the production of oleate from stearate and palmitate, 2 groups of mice were fed the high palmitic and the high stearic diets for 1 week and then injected intravenously with [1-14C]palmitate and [1-14C]stearate and the amount of labelled oleate in liver triglycerides was measured.(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in individual plasma free fatty acids in obese females during fasting and refeeding

In order to determine whether the metabolism of individual free fatty acids is affected by fasting, plasma levels were measured daily in seven obese females during ten days of fasting and four days of refeeding. There was a gradual rise in free fatty acids throughout the fasting period with some variability during the last three days. Free fatty acids remained high during early refeeding followed by a decrease at the end of refeeding. Changes in concentration were most pronounced for oleic (18:1w9) and palmitic (16:0) acids which had the highest initial levels. Expressed as percent change from baseline, oleic, palmitic, and linoleic (18:2w6) acids had similar patterns, while changes were more dramatic for palmitoleic acid (16:1) and less so for stearic acid (18:0) than the others. When expressed as proportion of total free fatty acids, there was very little change in any individual free fatty acid despite the large fluctuations in actual plasma values. It appears that the five major free fatty acids in plasma undergo similar changes during fasting and refeeding, and the palmitic and oleic acids can serve as suitable tracers for metabolic studies.     

饲克山病病区粮大鼠游离脂肪酸变化及硒和维生素E的影响

以克山病病区粮饲养大鼠１０周，用ＨＰＬＣ法测定其血浆游离脂肪酸（ＦＦＡ）含量和组成。结果表明，病区粮组血浆ＦＦＡ、Ｃ（１８：３）、Ｃ（２０：４）、ＰＵＦＡ含量增高，而Ｃ（１６：０）含量降低；同时伴有ＧＳＨ－Ｐｘ、ＣＡＴ活力降低，ＬＰＯ、ＣＫ、ＬＤＨ、α－ＨＢＤＨ含量增高。饲料中补充Ｓｅ或ＶＥ对纠正上述变化有相似但又不尽相同的效果，以联合补充效果最佳．结果提示，Ｓｅ和ＶＥ不足影响ＦＦＡ含量和组成，可能参与克山病的病因和发病机制。     

Free fatty acid and triglyceride content of Mycobacterium avium cultured under different growth conditions

Previous investigations demonstrated that Mycobacterium avium has a requirement for fatty acid, which can be fulfilled by palmitic (C16:0) or oleic (C18:1) acids, and that it incorporates the fatty acid into triglycerides that are later utilized. Mycobacterium avium was grown in continuous culture or batch-cultured in medium that contained palmitic acid as the fatty acid source, but lacked albumin. Cells were extracted and free fatty acids and triglycerides were obtained by preparative thin-layer chromatography. The triglycerides were further purified by column chromatography. The free fatty acids were methylated and analyzed by gas chromatography. Oleic acid represented 40 to 64% of the total free fatty acids, except for cells batch-cultured and limited for nitrogen. The latter cells contained about 27% oleic acid, and 24% of the free fatty acids were of sizes greater than C24:0. The amount of palmitic acid varied considerably, but it and oleic acid together usually accounted for 70% of the total free fatty acids. The overall fatty acid content of the triglycerides was similar to that of the free fatty acids. However, two size classes of triglycerides were found that approximated the sizes of tristearin (C54) and tricaprylin (C24), molecular weights of 892 and 471 daltons, respectively. It is concluded that these types of studies may eventually lead to more accurate identification of pathogenic mycobacteria by means of gas chromatographic analyses.     

Distinctive roles of unsaturated and saturated fatty acids in hyperlipidemic pancreatitis

AIM: To investigate how the saturated and unsaturated fatty acid composition influences the susceptibility of developing acute pancreatitis.METHODS: Primary pancreatic acinar cells were treated with low and high concentrations of different saturated and unsaturated fatty acids, and changes in the cytosolic Ca²⁺ signal and the expression of protein kinase C (PKC) were measured after treatment.RESULTS: Unsaturated fatty acids at high concentrations, including oleic acid, linoleic acid, palmitoleic acid, docosahexaenoic acid, and arachidonic acid, induced a persistent rise in cytosolic Ca²⁺ concentrations in acinar cells. Unsaturated fatty acids at low concentrations and saturated fatty acids, including palmitic acid, stearic acid, and triglycerides, at low and high concentrations were unable to induce a rise in Ca²⁺ concentrations in acinar cells. Unsaturated fatty acids at high concentrations but not saturated fatty acids induced intra-acinar cell trypsin activation and cell damage and increased PKC expression.CONCLUSION: At sufficiently high concentrations, unsaturated fatty acids were able to induce acinar cells injury and promote the development of pancreatitis. Unsaturated fatty acids may play a distinctive role in the pathogenesis of pancreatitis through the activation of PKC family members.     

Fatty acid composition of amastigote and trypomastigote forms of Trypanosoma cruzi

The fatty acid composition of total lipids from trypomastigote and amastigote forms of Trypanosoma cruzi and of Vero cells before and after parasite infection were analyzed by gas-liquid chromatography and mass spectrometry. Even-numbered, saturated, monoenoic and polyenoic acids ranging from C-12 to C-18 were characterized in both T. cruzi development stages. Significant changes in the fatty acid composition occurred during the T. cruzi life cycle. Oleic and linoleic acids were prominent in trypomastigote forms, whereas palmitic acid was the major fatty acid of amastigotes. Other differences include higher stearic acid and lower palmitoleic and linolenic acid levels as well as the absence of lauric acid in amastigotes as compared with trypomastigote forms. The fatty acid pattern of Vero cells before T. cruzi infection as compared with that after infection showed mostly qualitative differences. Linoleic and linolenic acids were observed only in T. cruzi infected cells.     

棕榈酸对雨蛙肽诱导的大鼠胰腺腺泡细胞炎症早期基因表达谱的影响

背景：高三酰甘油血症是急性胰腺炎的发病原因之一。血浆中增多的游离脂肪酸（FFA）可损伤多种细胞，导致细胞功能障碍，可能在高三酰甘油血症性急性胰腺炎的发生、发展中起重要作用。目的：探讨饮食中的主要FFA棕榈酸对雨蛙肽诱导的大鼠胰腺腺泡细胞炎症早期基因表达谱的影响。方法：以胶原酶消化法分离大鼠胰腺腺泡细胞，将细胞分为3组，雨蛙肽组加入终浓度为100nmol／L的雨蛙肽，雨蛙肽＋棕榈酸组加入相同剂量的雨蛙肽和终浓度为1mmol/L的棕榈酸，正常对照组不予处理。培养3h后提取细胞总RNA，应用含15000余条大鼠基因的大鼠Affymetrix 230A基因芯片检测基因表达谱的变化。结果：雨蛙肽＋棕榈酸组较雨蛙肽组出现30条上调基因和15条下调基因，其功能涉及细胞信号转导、转录、脂质代谢、蛋白修饰等不同层次。结论：棕榈酸可能通过影响大鼠炎症胰腺腺泡细胞多种结构和功能基因的表达而加重其损伤。     

Pharmacological treatment of non-alcoholic steatohepatitis: The current evidence

¹²⁵I-protein-radioiodinated pure pancreatic juice samples from patients with adenocarcinoma of the pancreas, chronic pancreatitis, or intact pancreas were analysed by high-resolution SDS-polyacrylamide gel electrophoresis and subsequent autoradiography. Experiments resulted in the detection of a 180K protein, probably a glycoprotein, in the pure pancreatic juice from pancreatic carcinoma (93%) and chronic pancreatitis (73%) patients, which was completely absent from pancreatic juice from intact pancreas. Sephadex G-200-isolated 18UK protein was found to be different from carcinoembryonic antigen (CEA) when traced by a commercial CEA radioimmunoassay, but it seemed identical in pancreatic juice samples from patients with pancreatic carcinoma and chronic pancreatitis, at least with regard to isoelectric point. In brief, the present results suggest that 180K protein identification in pancreatic juice permits adenocarcinoma of the pancreas and chronic pancreatitis to be differentiated from normal conditions but that distinction between pancreatic carcinoma and chronic pancreatitis is unlikely.     

Fatty acid binding protein in kidney of normotensive and genetically hypertensive rats

Fatty acid binding protein was purified from renal medulla, and its binding activity and fatty acid composition were determined in spontaneously hypertensive stroke-prone rats (SHRSP). Wistar-Kyoto rats (WKY) were used as controls. Fatty acid binding activity was higher in 5-week-old prehypertensive SHRSP than in control WKY (0.155 +/- 0.006 vs 0.030 +/- 0.001 mol palmitic acid/mol protein). However, in 40-week-old rats, the activity was decreased only in SHRSP with established hypertension (0.035 +/- 0.002 vs 0.028 +/- 0.003 mol palmitic acid/mol protein WKY). Fatty acid compositions were similar among 5-week-old and 40-week-old control WKY and 5-week-old SHRSP (palmitic acid, 24%; stearic acid, 14%; oleic acid, 30%; linoleic acid, 29%; arachidonic acid, 3%), although the total amount of bound long-chain fatty acids was decreased in 5-week-old SHRSP, explaining the high fatty acid binding activity in this preparation. Fatty acid binding protein from 40-week-old SHRSP had an elevated proportion of endogenous arachidonic acid, with other fatty acids being relatively reduced (palmitic acid, 8%; stearic acid, 2%; oleic acid, 4%; linoleic acid, 10%; arachidonic acid, 76%), indicating increased arachidonic acid transport in the cytosol. These results show that genetically hypertensive rats had an alteration in fatty acid transport mediated by fatty acid binding protein; this alteration may be involved in the pathogenesis of hypertension.     

幽门螺杆菌脂多糖化学组成和SDS－PAGE特性的研究

应用气液色谱法对幽门螺杆菌脂多糖中的单糖和脂肪酸进行定性和定量分析。该菌脂多糖中主要含有甘露糖、葡萄糖、半乳糖、氨基葡萄糖和鼠李糖,所含的主要脂肪酸为３─羟基─豆蔻酸、棕榈酸、月桂酸和豆蔻酸,其单糖和脂肪酸组成与大肠杆菌脂多糖相似。由于幽门螺杆菌脂多糖和大肠杆菌脂多糖在化学组成上的相似性,使两者的ＳＤＳ─ＰＡＧＥ图谱基本相同。     

Fat storage in pancreas and in insulin-sensitive tissues in pathogenesis of type 2 diabetes

Obesity is associated with increased storage of lipids in nonadipose tissues like skeletal muscle, liver, and pancreatic beta cells. These lipids constitute a continuous source of long-chain fatty acyl CoA (LC-CoA) and derived metabolites like diacylglycerol and ceramide, acting as signalling molecules on protein kinases activities (in particular, the family of PKCs), ion channel, gene expression, and protein acylation. In skeletal muscle, the increase in LC-CoA and diacylglycerol translocates and activates specific protein kinase C (PKC) isoforms, which will phosphorylate IRS-1 on serine, preventing its phosphorylation on tyrosine and association with PI3 kinase. This interrupts the insulin signalling pathway leading to the stimulation of glucose transport. In pancreatic beta cells, short-term excess of fatty acids or LC-CoA activates PKC and also directly stimulates insulin exocytosis. Long-term exposure to free fatty acids (FFA) leads to an increased basal and blunted glucose-stimulated insulin secretion by affecting gene expression, increase in K(ATP) channel activity, and uncoupling of the mitochondria. In addition, the saturated FFA palmitate increases cell death by apoptosis via increase in ceramide synthesis.     

Effect of predigested fat on intestinal stimulation of plasma cholecystokinin and gall bladder motility in coeliac disease.

Cholecystokinin (CCK) release and gall bladder emptying in response to a fatty meal are completely abolished in coeliac disease. To determine the effect of lipid digestion on CCK release and gall bladder motility, six patients with untreated coeliac disease and a flat jejunal mucosa were studied on two separate days. After an overnight fast, the plasma CCK concentration and gall bladder volume were measured before and at regular intervals after the intraduodenal instillation of 60 ml corn oil (triglycerides) incubated with 40 ml saline or with 40 ml bile and pancreatic juice. The mean (SEM) concentration of free fatty acids in the aqueous phase of corn oil after incubation with bile and pancreatic juice (predigested corn oil) was 78 (35) mM compared with 0.1 (0.1) mM in the aqueous phase of corn oil incubated with saline (undigested corn oil). Integrated plasma CCK in response to predigested corn oil was significantly greater than that in response to undigested corn oil (101 (18) pM. 80 min v-2 (9) pM.80 min; p < 0.005). Similarly, integrated gall bladder contraction in response to predigested corn oil was significantly larger than that after undigested corn oil (817 (210) ml. 80 min v-225 (243) ml. 80 min; p < 0.05). In contrast to undigested corn oil, corn oil that has been predigested with bile and pancreatic juice induces plasma CCK secretion and gall bladder contraction in patients with untreated coeliac disease, presumably by generating and rendering soluble lipolytic products.     

Asynchronous secretion of newly synthesized pancreatic proteins in the rat

The secretion of newly synthesized pancreatic proteins was studied in conscious rats with cannulated pancreatic ducts. Labeled amino acids (3H-leucine and 14C-amino acid mixture) were injected intravenously. The proteins of the pancreatic juice were separated by gel electrophoresis, and the radioactivity in each band was determined. An early secretion of labeled trypsinogen and chymotrypsinogen was found, whereas amylase and lipase were secreted after a certain lag period. In vitro pulse chase experiments showed that amylase was synthesized in the acinar cell but did not move with the same efficacy to the zymogen granules and into the pancreatic juice as proteases.     

Effect of dietary elaidic versus vaccenic acid on blood and liver lipids in the hamster.

Male hamsters (30 per group) were fed five different semi-purified diets ad libitum. The diets, containing 30% of energy (en%) as fat, differed in their dietary fat composition (specified fatty acids exchanged at 10 en%) and were fed for 4 weeks. The five fatty acids compared in mixed triglycerides were elaidic acid (C18:1 9t), vaccenic acid (C18:1 11t), their cis-counterpart oleic acid (C18:1 9c), medium-chain fatty acids (MCFA; C8:0 and C10:0), and palmitic acid (C16:0). Compared with oleic acid, dietary MCFA and palmitic acid tended to increase blood cholesterol levels in the hamsters. The effect of elaidic and vaccenic acid on blood cholesterol did not differ from that of oleic acid. When elaidic acid and vaccenic acids were compared directly, the ratio of LDL/HDL-cholesterol in plasma was significantly higher in hamsters fed vaccenic acid than in those fed elaidic acid, and elaidic acid was incorporated at low levels, but more efficiently than vaccenic acid at the sn-2 position of platelet phospholipids. Biological consequences of this low incorporation are considered unlikely as levels of arachidonic acid (C20:4 n-6) and docosohexaenoic acid (C22:6 n-3) in the platelet phospholipids of all dietary groups did not differ. With respect to the effect on the LDL/HDL-cholesterol ratio, elaidic acid may be preferable to vaccenic acid. We conclude that this animal study does not provide evidence for the suggestion, based on epidemiological observations, that elaidic acid would be more detrimental to cardiovascular risk than vaccenic acid.