The effect of a salmon diet on blood clotting,platelet aggregation and fatty acids in normal adult men

This study was designed to measure the effect of dietary n−3 fatty acids (FA) on platelets and blood lipids. Healthy men (n=9), ages 31 to 65, were fed diets in which salmon was the source of n−3 fatty acids. They were confined in a nutrition suite at this Center for 100 days. Food intake and exercise levels were rigidly controlled. Initially they were placed on a stabilization diet for 20 days, then six men were fed the salmon diet for 40 days. The others remained on the stabilization diet. The two groups switched diets for the last 40 days of the study. Both diets were isocaloric [16% protein, 54% carbohydrate, and 30% fat by energy-% (En%)]. The salmon diet contained 7.5% of calories from n−6 FA and 2% from n−3 FA, primarily eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in a 40∶60 ratio, while the stabilization diet contained 7.5% of calories from n−6 FA and less than 0.3% n−3 FA, mainly 18∶3n−3. The bleeding time was unaffected by the diets in this study. The prothrombin time was shortened (11.6 sec.vs. 12.6 sec., p<0.01) for the subjects consuming the salmon diet as compared to that measured after 20 days of the stabilization diet. Mean platelet volume increased significantly during the period in which the volunteers consumed the salmon diet compared to the baseline diet (p<0.01), while the mean platelet levels decreased. Platelet aggregation (PA) was measured in platelet rich plasma before, during, and after the salmon diet using collagen, ADP, arachidonic acid (AA), and thrombin agonists. The PA threshold for ADP was significantly increased for the subjects on the salmon diet (p<0.05). No change in the PA threshold was detected for collagen or thrombin. The PA threshold for AA was unchanged also, but the platelets in subjects consuming the salmon diet had a prolonged time to maximum aggregation (p<0.01) with this reagent compared to platelets from men on the stabilization diet. Plasma, red cell, and platelet total FA composition was determined by capillary GLC. While the men consumed the salmon diets, there were marked increases (3 to 10-fold) in the EPA and DHA levels in all blood components with concomitant decreases in linoleic acid and AA levels. Thus, a salmon diet, high in n−3 FA, did not influence the bleeding times, but it decreased the sensitivity of platelets to ADP and AA, increased the mean platelet size, decreased the platelet count, and changed the FA composition of the plasma, RBC and platelet membrane lipids.     

Effect of modified dairy fat on postprandial and fasting plasma lipids and lipoproteins in healthy young men

Fatty acid profile of milk fat can be modified by cow feeding strategies. Our aim was postprandially and after 4 wk to compare the effect of a modified milk fat (M diet) [with 16% of the cholesterolemic saturated fatty acid (C12–16) replaced by mainly oleic and stearic acids] with the effect of D diet, including a conventional Danish milk fat on plasma lipids and lipoproteins. A side effect of the cow feeding regime was a 5% (w/w) increase in trans fatty acid in M diet. Eighteen subjects were fed for two periods of 4 wk strictly controlled isoenergetic test diets with 40% of energy from total fat and the same content of dietary cholesterol in a randomized study with cross-over design. Contrary to expectations, fasting low density lipoprotein (LDL) cholesterol concentration did not differ after the experimental periods. However, M diet resulted in a higher fasting total triacylglycerol concentration compared to D diet (P=0.009). Postprandial samples were taken at two different occasions (i) at day 21, after breakfast and lunch and (ii) on the last day of the study 2, 4, 6, and 8 h after a fat load. Postprandial plasma triacylglycerol and chylomicron triacylglycerol showed higher peak values after D diet than M diet (interaction effect, diet × times P<0.05). In conclusion, M diet did not lower LDL cholesterol compared to D diet. Thus any cholesterol-lowering effect of oleic and stearic acids may have been obscured by the high content of cholesterol-raising saturated fatty acids in milk fat. A higher content of the trans fatty acids in M diet might have counteracted the cholesterol neutral/decreasing effect and increased plasma triacylglycerol.     

Rat adult offspring serum lipoproteins are altered by maternal consumption of a liquid diet

Palatable liquid diets for the administration of ethanol (EtOH) to animals have proven to be a major advance for the study of the effects of EtOH consumption under conditions of isocaloric nutrition of the control animals. Using a liquid diet, the original aim of the reported studies was to examine the effect of maternal EtOH consumption during pregnancy on the lipoprotein (Lp) profiles of the adult offspring measured by means of nuclear magnetic resonance spectroscopy. However, initial data suggested that compared to a maternal chow diet, the basal maternal liquid diet (without EtOH) had a significant effect on specific serum Lp of the adult offspring. The adult off-spring of mothers who had consumed a basal liquid diet with-out EtOH exhibited significant increases in their plasma triglycerides (TG) and cholesterol content compared to adult offspring whose mothers consumed a chow diet. Further, there were significant increases in the offspring's VLDL and low density Lp (LDL) subfractions' particle number, regardless of whether the maternal liquid diet was ad libitum-fed, pair-fed, or EtOH-containing. The increase in offspring plasma TG was due to increases in specific VLDL subfraction particle numbers and not to increased TG content per particle. Similarly, the increase in plasma cholesterol was the result of elevated level of the very small LDL particles but not to an increased amount of cholesterol per LDL particle. These findings should be further examined in light of the widespread use of liquid diets in, research to administer EtOH, especially for studies of fetal alcohol syndrome.     

Effects of three dietary fats on plasma lipids and lipoproteins in fasting and post-prandial humans after a short-term diet

The effects of 3 dietary fats (olive oil, canbra oil and butter) on the fatty acids of blood lipids and on serum lipoproteins were compared in 6 healthy adult outpatients, after a 6-day normocaloric diet including 35% of the studied fat. Important, although incomplete, changes appeared in the fatty acid composition of the various serum lipids and in the composition and distribution of serum lipoproteins. These changes probably result from the degree of saturation of the fat ingested. Moreover, differences were observed among individual subjects. Genetic differences, which are important in clinical practice, are stressed in connection with risks of vascular diseases and hyperlipidemia and affect intestinal fat absorption and lipoprotein metabolism.     

Heterogeneity of molecular weight and apolipoproteins in low density lipoproteins of healthy human males

The molecular weights of five low density lipoprotein (LDL) subfractions from four normal healthy males were determined by analytic ultracentrifuge sedimentation equilibria. Protein content of each subfraction was determined by elemental CHN analysis, and weights of apoprotein peptides were calculated. Molecular weights in subfractions of increasing density were 2.92±0.26, 2.94±0.12, 2.68±0.09, 2.68±0,28 and 2.23 ±0,22 million Da, and protein weight percentages were 21.05, 21.04, 22.05, 23.10 and 29.10, in subfractions, 1,2,3,4 and 5, respectively. Total mean apoprotein weights for respective subfractions were 614±53,621±45, 588±9,637±83 and 645 ±62 KDa. In addition to a single apoprotein B-100 (apo B-100) peptide with a mean carbohydrate content of 7.1% and a molecular weight of 550 KDa per LDL particle, there may be one or more apoprotein E peptides of 34 KDa and/or apoprotein C-III of 9 KDa. In addition, subfractions 4 and 5 may contain 3–7% apolipoprotein (a). There is considerable heterogeneity among LDL subfractions as well as within the same fraction from different individuals. This heterogeneity may relate to differences in origin, metabolism and/or atherogenicity as a result of their content of apoproteins other than apo B-100. Presented in part at the 78th AOCS Annual Meeting held in New Orleans, LA, May 1987; received best presentation award     

The urinary excretion of thiobarbituric acid reactive substances and malondialdehyde by normal adult males after consuming a diet containing salmon

In this study we investigated the output of thiobarbituric acid reactive substances (TBARS) and malondialdehyde (MDA), as thiobarbituric acid (TBA)-MDA adduct, in the urine from subjects eating a diet in which the only source of n−3 long-chain, polyunsaturated fatty acids was fresh salmon. Nine healthy men, ages 30–65, were confined in the United States Department of Agriculture Western Human Nutrition Research Center, San Francisco, CA, for 100 d; food intake and exercise levels were controlled. All subjects were placed on a stabilization diet (StD) for 20 d, then six were fed the salmon diet for 40 d. The others remained on the StD. The groups switched diets for the last 40 d. Both diets were isocaloric (16% protein, 54% CHO and 30% fat by energy %). The salmon diet contained 7.5% of calories from n−6 fatty acids (FAs) and 2% from n−3 FAs, primarily eicosapentaenoic acid and docosahexaenoic acid in a 50∶60 ratio, while the StD contained 7.5% from n−6 FAs and <0.3% n−3 FAs (with presumably no significant amounts of C₂₀ or C₂₂ n−3 FAs). Twenty-four hour urinary output was collected, and 2% 3−d pool samples prepared for analysis of urinary TBARS and the TBA-MDA adduct. The total urinary output of each individual varied considerably, and on a daily basis the concentration of autoxidation products in an individual's urine varied also. However, the mean daily output (in μmoles TBA-MDA equivalents/day) at the end of the salmon diet feeding period was significantly greater (7.05±1.33 TBARS,P<0.05; and 7.07±1.73 TBA-MDA adduct,P<0.01) compared to when the subjects were eating the StD (5.65±1.09 TBARS and 4.65±0.76 TBA-MDA adduct). When the TBARS and TBA-MDA adduct values were normalized relative to creatinine output (in nmoles TBA-MDA equivalents/μmole creatinine), the data achieved even greater statistical significance. The mean output of the group eating the salmon diet was 0.478±0.076 for TBARS (P<0.01) and 0.476±0.082 for the TBA-MDA adduct (P<0.001)vs. 0.345±0.059 for TBARS and 0.283±0.041 for the TBA-MDA adduct when the subjects were consuming the StD. Thus, the consumption of cooked fish may increase one's exposure to MDA and other autoxidation products, compounds that may be carcinogenic or mutagenic.     

Effect of a new fermented soy milk product on serum lipid levels in normocholesterolemic adult men

This study was undertaken to verify the effect of a daily intake of a new fermented soy milk produced with Enterococcus faecium and Lactobacillus jugurti on the serum lipid levels in normocholesterolemic middle-aged men. The study was randomized, double-blind and placebo-controlled and was performed for a period of 6 weeks. Forty-four normocholesterolemic healthy, male volunteers, aged 40-55 years old were randomly separated in two groups: The F-group received 200 ml of the fermented product daily and the P-group received 200 ml of placebo (chemically fermented). The blood samples were drawn initially and after 3 and 6 weeks and serum values for total cholesterol, HDL-cholesterol and triglyceride were determined. The LDL-cholesterol value was estimated. No significant changes in the fermented group (F) were observed for total cholesterol, LDL-cholesterol or triglyceride levels, while the HDL-cholesterol level was significantly higher (p < or = 0.05) after 6 weeks. The total cholesterol and LDL-cholesterol levels were significantly higher (p < or = 0.05) in the placebo group (P), but no changes were found for the HDL-cholesterol and triglyceride levels during the experimental period. In conclusion, the intake of 200 ml/day of the fermented soy milk, produced with E. faecium and L. jugurti, for 6 weeks, did not affect the serum total cholesterol and LDL-cholesterol, and led an increase of 10% in the HDL-cholesterol level.     

Experimental nephrotic syndrome in the rat induced by puromycin aminonucleoside: Hepatic synthesis of lipoproteins and apolipoproteins

Hepatic synthesis of lipoproteins and apolipoproteins was investigated in male Wistar rats with severe nephrotic syndrome induced by puromycin aminonucleoside by incubating liver slices with a mixture of¹⁴C-amino acids. Labeled lipoproteins were separated by preparative ultracentrifugation from the incubation medium after the addition of carrier plasma. The incorporation of¹⁴C-amino acids into very low density lipoproteins (VLDL) (1.006 g/ml), low density lipoproteins (LDL) (1.006–1.063 g/ml) and high density lipoproteins (HDL) (1.063–1.210 g/ml) was increased in nephrotic liver 6.1-, 5.7- and 5.0-fold, respectively. The measurement of radioactivity associated to apolipoproteins isolated by SDS-PAGE documented an increased incorporation into apolipoprotein E (apoE) of nephrotic VLDL (33.1% vs 20% of the total radioactivity incorporated into VLDL apoproteins) and a markedly increased incorporation into apolipoprotein A-I (apoA-I) of nephrotic HDL (44.3% vs 16.3% of the total radioactivity incorporated into HDL apoproteins). In nephrotic liver, the total incorporation of amino acids into apolipoproteins (apoVLDL+apoLDL+apoHDL) was increased 12.6 times for apoA-I, 6.4 times for apoB, 5.0 times for apoE, 4.2 times for apoC+apoA-II and 2.5 times for apoA-IV. We suggest that, in nephrotic liver: (a) the synthesis of VLDL, LDL and HDL is increased, and (b) the total synthesis of apoA-I is selectively increased when compared to that of the other apolipoproteins. Preliminary reports of this work were presented at the Annual Meeting of the European Society for the Study of the Liver (Düsseldorf, September 13–15, 1979); at the 5th International Symposium on Atherosclerosis (Houston, November 6–9, 1979) and at the Annual Meeting of the Italian Society for the Study of the Liver (Rome, December 14–15, 1979).     

Effects of diet and type IIa hyperlipoproteinemia upon structure of triacylglycerols and phosphatidyl cholines from human plasma lipoproteins

Four normal and two individuals with Type IIa hyperlipoproteinemia were placed on the National Heart and Lung Institute Type IIa diet (low cholesterol, smaller than 300 mg/day, high polyunsaturated, low saturated fat diet) for 1 week and on a normal diet the following week. Plasma samples were obtained and the triacylglycerols, phospholipids, and cholesterol contents of plasma and of very low density lipoproteins, low density lipoproteins, and high density lipoproteins determined. Triacyglycerol fatty acid composition was determined and stereospecific analyses of triacglycerols and phosphatidyl cholines performed. Structural determinations were limited to one normal and one Type IIa individual. In normal and Type IIa individuals, chylomicrons contained twice the amount of 18:0 as did the very low density lipoproteins, low density lipoproteins, or high density lipoproteins. The structure of the triacyglycerols from the very low density lipoproteins and low density lipoproteins was asymmetric with at least 50M% 16:0 in the sn-1 position and mostly 18:1 in positions sn-2 and 3. There was a marked difference in the distribution of 18:2 in low density lipoproteins of the normal and Type IIa individuals. The control contained equal amounts of 18:2 in the sn-1 and sn-3 positions, whereas IIa low density lipoprotein was asymmetric with 26% of the 18:2 in position sn-1 and 3% in the sn-3 position. Very low density lipoprotein was asymmetric with regard to 18:2 in control and IIa samples with an average of 5% of the 18:2 in position sn-1 and 40% in position sn-3. The phosphatidyl cholines contained predominantly 16:0 and 18:0 in position sn-1, whereas the acids in position sn-2 were unsaturated with very little difference between lipoprotein classes. Neither the short dietary periods nor source of plasma affected the structure of the phosphatidyl cholines.     

Effect of betaine supplementation on plasma nitrate/nitrite in exercise-trained men

Background  

Betaine, beetroot juice, and supplemental nitrate have recently been reported to improve certain aspects of exercise performance, which may be mechanistically linked to increased nitric oxide. The purpose of the present study was to investigate the effect of betaine supplementation on plasma nitrate/nitrite, a surrogate marker or nitric oxide, in exercise-trained men.     

Inadequate physician knowledge of the effects of diet on blood lipids and lipoproteins.

Background  

To assess the nutrition knowledge of physicians on the basic effects of diet on blood lipids and lipoproteins.     

Effects of stearic acid on plasma lipid and lipoproteins in humans

More than 40 years ago, saturated FA with 12, 14, and 16 carbon atoms (lauric acid, myristic acid, and palmitic acid) were demonstrated to be “hypercholesterolemic saturated FA.” It was further concluded that the serum total cholesterol level would hardly be changed by isocaloric replacement of stearic acid (18∶0) by oleic acid (cis-18∶1n−9) or carbohydrates. These earlier studies did not address the effects of the various FA on the serum lipoprotein profile. Later studies found that the hypercholesterolemic saturated FA increase serum total cholesterol levels by raising concentrations of both the atherogenic LDL and the antiatherogenic HDL. Consequently, the ratio of total to HDL cholesterol will hardly change when carbohydrates replace these saturated FA. Compared with other saturated FA, stearic acid lowers LDL cholesterol. Studies on the effects on HDL cholesterol are less conclusive. In some, the effects on HDL cholesterol were comparable to those of palmitic acid, oleic acid, and linoleic acid, whereas in others a decrease was observed. This may suggest that in this respect the source of stearic acid is of importance, which needs however further study. From all these studies, however, it can be concluded that stearic acid may decrease the ratio of total to HDL cholesterol slightly when compared with palmitic or myristic acid. Without doubt, the effects of stearic acid are more favorable than those of trans monounsaturated FA.     

鲑鱼来源的聚脱氧核苷酸分子量分布对其生物学活性的影响

目的分析鲑鱼来源的聚脱氧核苷酸分子量分布对其生物学活性的影响。方法采用乙醇分级沉淀去纤苷类似物(defibrotide analogue,DFA),收集三步分级沉淀样品,脱水烘干,即H、M、L组分,体积排阻高效液相色谱(HPLC)法测定其分子量分布,S-2251底物法检测各分级组分对纤溶酶活性的影响,经典魏氏法检测各分级组分对红细胞沉降率的影响。结果获得H、M、L组分分别为0.46、1.03和0.38 g,80%H、M及L组分聚脱氧核苷酸链长分布分别为60~100、30~50及小于25 nt。DFA及H、M组分均可提高纤溶酶活性,与各组分分子量、浓度呈正相关,但L组分促纤溶活性不明显。与对照组相比,DFA及各分级组分均可引起红细胞沉降率显著升高,并呈剂量-效应关系,差异有统计学意义(P0.05)。结论分子量分布是影响DFA活性的关键因素,为天然来源的聚脱氧核苷酸活性产物的筛选提供了参考。     

Triacylglycerol oxidation in pig lipoproteins after a diet rich in oxidized sunflower seed oil

The effects of two sunflower seed oil diets differing in oxidation levels (PV in oils 1 and 190 mequiv O₂/kg) on lipoprotein TAG and total lipid oxidation were investigated in growing pigs. For 2 wk, two groups of 10 pigs were fed either of the diets, after which blood samples were collected. A method based on RP-HPLC and electrospray ionization-MS was used for the analysis of oxidized TAG molecules in chylomicrons and VLDL. The baseline diene conjugation method was used for the estimation of in vivo levels of lipoprotein lipid oxidation. TAG molecules with a hydroxy, an epoxy, or a keto group attached to a FA, as well as TAG core aldehydes were detected in the samples. Typically, lipoprotein TAG and total lipids were more oxidized in the pigs fed on the oxidized oil compared with those fed on nonoxidized oil. Oxidation of dietary fat was thus reflected in the lipoprotein oxidation, which confirmed our earlier findings.     

L-carnitine effect on plasma lipoproteins of hyperlipidemic fat-loaded rats

The effect of oral L-carnitine administration to rats fed olive oil has been studied. Carnitine significantly decreased triglyceride, cholesterol and phospholipid levels. Particularly, the levels of chylomicron and very low density lipoproteins in the blood were lowered. Low density lipoprotein levels were not affected, and high density lipoproteins were found to be decreased by 20%. Because carnitine did not change the composition of chylomicron and very low density lipoproteins fraction or affect the gastrointestinal triglyceride residue (about 1/3 of the original load), an effect of carnitine on hepatic fatty acid handling is most likely. The lowering of plasma free fatty acid levels by carnitine administration is in favor of an effect of carnitine on fatty acid handling. The effect on the liver is illustrated by the study of acetoacetate formation in in vitro perfused livers from previously olive oil loaded±carnitine-treated rats. Carnitine pretreatment stimulated ketogenesis. It is speculated that carnitine administration, by promoting β-oxidation, lowers the production of very low density lipoproteins. This may be accomplished partly by an increase in the hepatic level of fatty acid binding protein, which also has been observed.     

Distribution of antithrombin III and glucosylceramide in human plasma lipoproteins and lipoprotein deficient plasma

We have investigated the distribution of antithrombin-III and glucosylceramide (Glc-Cer) in human plasma, plasma lipoproteins and lipoprotein-deficient plasma. Antithrom bin III activity was measured employing immunochemical and biological assays. Glc-Cer was quantified by gas liquid chromatography (GLC). Whole plasma contained 145 μg antithrombin III/ml plasma, all of which was associated with the lipoprotein-deficient plasma (d>1.25 g/ml). Whereas, most if not all the plasma GlcCer was associated with plasma low density lipoproteins (LDL) (d-1.022–1.055 g/ml) and high density lipoproteins (HDL) (d-1.063–1.25). GlcCer was not found in the lipoprotein-deficient plasma. We conclude that GlcCer on lipoproteins does not contribute to antithrombin III activity. Moreover, the absence of GlcCer in lipoprotein-deficient plasma does not impair antithrombin-III activity.     

The effect of exercise on plasma high density lipoproteins

The influence of vigorous activity in man on plasma lipids and lipoproteins is reviewed, with particular emphasis on high density lipoproteins. Both cross sectional and longitudinal (or training) studies have been reported, many of them of less than ideal design. Nonetheless, a consistent pattern emerges in which increased exercise levels lead to lower plasma concentrations of triglycerides and very low density lipoproteins, and of low density lipoproteins. High density lipoprotein levels increase. Sometimes, but not uniformly, plasma total cholesterol level falls as the result of these changes. The increase in plasma high density lipoprotein appears to be the result largely of an increase in the less dense HDL₂ subfraction. Plasma apolipoprotein A-I levels (but not apo-A-II levels) seem to increase concomitantly. The precise biochemical mechanism responsible for these changes has not been elucidated; but the recent finding of increased lipoprotein lipase activity in adipose tissue and muscle of endurance runners suggests that increased lipolytic rate of trigly ceride-rich lipoproteins may be an initial step in a sequence of events leading to higher plasma levels of HDL₂.