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Biomedical subjects

A J Sinclair

Publications and source records attributed to A J Sinclair.

At least 91 records · Page 5Linked to original sources
PubMed1996

Platelet and aorta arachidonic and eicosapentaenoic acid levels and in vitro eicosanoid production in rats fed high-fat diets.

There is a significant interest in the interrelationship between long-chain n-3 and n-6 fatty acids due to their ability to modulate eicosanoid production. In general, the intake of arachidonic acid (AA) results in enhanced eicosanoid production, whereas n-3 polyunsaturated fatty acids (PUFA) decrease the production of eicosanoids from AA. The purpose of this study was to investigate whether the effects of dietary AA on eicosanoid production in the rat were correlated with the AA and EPA levels in platelets and aorta (eicosanoid-producing tissues). Four groups of male Sprague-Dawley rats were fed a high-fat diet enriched with eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) (approximately 100 mg/day of EPA + DHA) for 24 d. During the last 10 d, the four groups were orally supplemented with 0, 30, 60, and 90 mg/day of ethyl arachidonate. A further group of rats was fed a control diet (without long-chain n-3 PUFA) for 24 d. In vitro aorta prostacyclin (PGI2) production, serum thromboxane A2 (TxA2) production and plasma, and platelet and aorta phospholipid (PL) fatty acids were measured. Enriching the diet with n-3 PUFA resulted in significant reductions in tissue AA levels and an increase in the n-3 PUFA, particularly EPA. On this diet, the AA to EPA ratio was 1:1 in platelet PL, and it was 2:1 in the aorta PL. There were significant decreases in the in vitro PGI2 and TxA2 production compared with the control animals. The inclusion of AA in the diet resulted in marked increases in AA levels in the platelet and aorta PL with corresponding decreases in EPA. The lowest dose of AA (30 mg/rat) reversed the effects of 100 mg/day of n-3 PUFA on AA levels in platelet and aortic PL and on in vitro aorta PGI2 and serum TxA2 production. The dietary AA caused a differential (twofold) increase in TxA2 relative to PGI2 for all three levels of AA supplementation. There were greater changes in the levels of AA and/or EPA in platelet PL compared with the aorta PL, which might have accounted for the differential effects of these PUFA on thromboxane production compared with PGI2 production in this study.

Animal Feed↗
PubMed1996

Arachidonic acid to eicosapentaenoic acid ratio in blood correlates positively with clinical symptoms of depression.

In this study of 20 moderately to severely depressed patients, diagnosed using current research diagnostic criteria and excluding known bipolar affective disorder and reactive depression, we investigated relationships between severity of depression and levels and ratios of n-3 and n-6 long-chain polyunsaturated fatty acids (PUFA) in plasma and erythrocyte phospholipids (PL). Severity of depression was measured using the 21-item Hamilton depression rating scale (HRS) and a second linear rating scale (LRS) of severity of depressive symptoms that omitted anxiety symptoms. There was a significant correlation between the ratio of erythrocyte PL arachidonic acid (AA) to eicosapentaenoic acid (EPA) and severity of depression as rated by the HRS (P < 0.05) and the LRS for depression (P < 0.01). There was also a significant negative correlation between erythrocyte EPA and the LRS (P < 0.05). The AA/EPA ratio in plasma PL and the ratio of erythrocyte long-chain (C20 and C22 carbon) n-6 to long-chain n-3 PUFA were also significantly correlated with the LRS (P < 0.05). These findings do not appear to be simply explained by differences in dietary intake of EPA. We cannot determine whether the high ratios of AA/EPA in both plasma and erythrocyte PL are the result of depression or whether tissue PUFA change predate the depressive symptoms. We suggest, however, that our findings provide a basis for studying the effect of the nutritional supplementation of depressed subjects, aimed at reducing the AA/EPA ratio in tissues and severity of depression.

Adult↗
PubMed1996

Body fat distribution and non-insulin-dependent diabetes: comparison of a fiber-rich, high-carbohydrate, low-fat (23%) diet and a 35% fat diet high in monounsaturated fat.

The effects of a fiber-rich, high-carbohydrate, low-fat (HCLF) diet and a modified-fat (MF) diet high in monounsaturated fat on body fat distribution were examined by dual-energy X-ray absorptiometry (DXA) in 16 subjects with non-insulin-dependent diabetes (NIDDM) during a randomized crossover study. Subjects lost similar amounts of body fat consuming the HCLF and MF diets (-0.83 +/- 0.37 and -0.87 +/- 0.40 kg, respectively) despite a marked difference in total fat consumption. With the MF diet, the ratio of upper- to lower-body fat (UF:LF) remained unchanged because fat was lost proportionately from the upper and lower body. In contrast, with the HCLF diet, a disproportionate loss of lower-body fat caused the UF:LF to increase. The effects of diet on regional body fat loss were significant (P < 0.05, two-factor repeated-measures ANOVA).

Absorptiometry, Photon↗
PubMed1996

Short-term diets rich in arachidonic acid influence plasma phospholipid polyunsaturated fatty acid levels and prostacyclin and thromboxane production in humans.

Two small-scale dietary intervention studies were conducted to examine the effect of diets rich in arachidonic acid (AA) and n-3 long-chain polyunsaturated fatty acids (n-3 LCP), on the in vivo production of prostacyclin (PGI2) and thromboxane (TXA2). The first was a pilot study and contained insufficient numbers for statistical analyses. It involved a 7-d intervention with 10 subjects divided into three groups, consuming diets rich in AA (500 mg/d), rich in AA and docosahexaenoic acid (DHA) (500 mg/d of each), or rich in DHA and eicosapentaenoic acid (EPA) (approximately 1500 mg/d of n-3 LCP). Plasma phospholipid (PL) levels of AA increased in all subjects in groups 1 (n = 4) and 2 (n = 3). DHA levels increased in all subjects in Groups 2 and 3 (n = 3), and EPA levels increased in all subjects from Group 3 but fell in all subjects from Group 1. The in vivo production of PGI2, measured as its urinary metabolite, was increased in two subjects in Group 1 and one subject in Group 2, with all other subjects showing little change. Urinary TXA2 metabolite increased in all subjects from Group 1. The second study was conducted in seven subjects, who consumed a low fat diet for 2 wk: the 1st wk was a vegetarian diet (no LCP) followed by a 2nd wk where the subjects were required to consume 500 g (raw weight) of kangaroo meat daily (305 mg/d AA, 325 mg/d n-3 LCP). The meat diet was associated with a marked rise in the serum PL levels of AA, EPA and docosapentaenoic acid 22:5(n-3) and with a significant increase in the urinary output of the prostacyclin metabolite, but no effect on TXA2 production, as measured by its urinary metabolite level. The results of these studies have shown that diets that contain both AA and n-3 LCP are associated with an increase in PGI2 production, without affecting TXA2 production. Further studies with purified LCP are warranted.

Adult↗
PubMed1996

Dietary fish oil prevents reperfusion Ins(1,4,5)P3 release in rat heart: possible antiarrhythmic mechanism.

Dietary enrichment with fish oil-derived n-3 polyunsaturated fatty acids has been shown to suppress the arrhythmias that occur during postischemic reperfusion. We have recently implicated a rapid release of D-myo-inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] during postischemic reperfusion in the generation of these arrhythmias. The effects of dietary supplementation with fish oil on both cardiac Ins(1,4,5)P3 and arrhythmogenic responses to reperfusion were therefore investigated in perfused rat hearts. Comparisons were made with control and n-6 polyunsaturated or saturated fat-supplemented diets. In control hearts, reperfusion increased Ins(1,4,5)P3 levels [from 9 +/- 2 at 20 min ischemia to 26 +/- 3 counts per minute (cpm)/mg protein with 2 min of reperfusion] and produced a high incidence of ventricular tachycardia (92% VT) and ventricular fibrillation (85% VF). Dietary fish oil supplementation, which increased composition of n-3 fatty acids in myocardial membrane phospholipids, prevented the reperfusion-induced rise in Ins(1,4,5)P3 (11 +/- 1 at 20 min ischemia and 12 +/- 2 cpm/mg protein after 2-min reperfusion) and significantly suppressed reperfusion arrhythmias (38% VT, 13% VF; P < 0.01 vs. control group). Thus the inhibition of reperfusion-induced rises in Ins(1,4,5)P3 by n-3 polyunsaturated fatty acids after dietary fish oil supplementation provides a possible mechanism for the inhibitory effect of n-3 fatty acids on reperfusion-induced arrhythmias.

Adenosine Triphosphate↗
PubMed1996

Effect of dietary n-3 deficiency on the electroretinogram in the guinea pig.

Despite the abundance of n-3 polyunsaturated fatty acids, particularly docosahexaenoic acid (DHA), in the retina of all mammals, their role in vision remains unclear. However, the widely accepted notion that DHA is universally important in the retinal function was questioned in an earlier study (see text) involving guinea pigs, completely depleted of retinal DHA. The purpose of this study was to replicate this mammalian model of such deficiency and to determine any abnormalities in the electroretinogram. Guinea pigs were raised through three generations on 1 of 2 semipurified diets, containing different amounts of n-3 fatty acids, as determined by the supplementary oil which was the sole source of lipid in each diet. The added oils were safflower oil (n-6/n-3 = 72.0) or canola oil (n-6/n-3 = 2.5). Comprehensive electroretinographic assessment was conducted on guinea pigs, aged 6-9 weeks (safflower n = 13, canola n = 12), and retinae were extracted and the phospholipid fatty acid profile analyzed. Phospholipid fatty acid analysis revealed significant DHA deficiency (p < 0.001) in guinea pigs reared on the safflower oil diet (retinal DHA 2.5%) as compared with the canola oil group (retinal DHA 21.0%). Analysis of the electroretinogram showed significant reductions (p < 0.003) in both peak-to-peak and a-waves of safflower oil fed animals.

Animals↗
PubMed1995

Dietary manipulation of long-chain polyunsaturated fatty acids in the retina and brain of guinea pigs.

High levels of n-6 docosapentaenoic acid (22:5n-6) have been reported in the retina of guinea pigs fed commercially-prepared gain-based rations (commercial diet). In rats and monkeys, high levels of 22:5n-6 are an indicator of n-3 polyunsaturated fatty acid (PUFA) deficiency. We have examined the fatty acid composition of the retina and brain in guinea pigs fed a commercial diet or one of three semi-purified diets containing three different levels of n-3 PUFA. The diets comprised a diet deficient in n-3 PUFA (semi-purified diet containing safflower oil), two diets containing alpha-linolenic acid (standard commercial laboratory diet and semi-purified diet containing canola oil), and a diet containing alpha-linolenic acid, eicosapentaenoic acid, and docosahexaenoic acid (DHA) (semi-purified diet containing canola oil, safflower oil, and fish oil). Two groups of guinea pigs were given the diets from day 1 to 4 wk or day 1 to 8 wk, when they were sacrificed and the retinal tissues were extracted and analyzed for PUFA content by gas-liquid chromatography. Fatty acid analyses of the retinal phospholipids of the four-week-old animals revealed that the group fed DHA (from the fish oil) had the highest level of DHA (32%), compared with values of 19 and 13% for the groups fed canola oil diet and commercial diet, respectively, and 2% for the group fed the diet deficient in n-3 PUFA.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

The arachidonic acid content of the Australian diet is lower than previously estimated.

Linoleic acid [18:2(n-6)] is the most abundant polyunsaturated fatty acid in the Western diet and is considered to be the primary source of tissue arachidonic acid [20:4(n-6)]. Dietary 20:4(n-6) may also contribute to tissue 20:4(n-6) levels in humans, but the extent of this contribution is unclear. We believe that literature estimates of 20:4(n-6) intake of 200-1000 mg/d are too high, possibly because of incorrect values in food composition tables where high amounts of 20:4(n-6) are recorded in margarines, some vegetable products and animal fat. We assessed the 20:4(n-6) content of common Australian foods and found that the 20:4(n-6) levels (on a 100-g edible basis), were 891 mg and 390 mg, respectively, for duck and chicken egg yolks, 294 mg for liver, 153 mg for kidney, 75 mg for skinless turkey, 56 mg for lean pork, 49 mg for lean lamb, 31 mg for chicken breast, 56 mg for chicken legs and 35 mg for lean beef. Eicosapentaenoic acid [20:5(n-3)] levels were < 10 mg/100 g in chicken meat, turkey meat, emu meat and chicken eggs, whereas the values for 20:5(n-3) for beef, lamb, liver, kidney and duck egg yolk ranged from 11 to 138 mg/100 g food. Applying our current 20:4(n-6) measurements to previously determined food intakes of Australian adults determined in an Australiawide survey in 1983, we estimated the mean 20:4(n-6) intake for Australian adult males to be 130 mg/d and females 96 mg/d. Whether such intakes of dietary 20:4(n-6) make an important contribution to tissue 20:4(n-6) levels is uncertain.

Adult↗
PubMed1995

Neuropsychological function in older subjects with non-insulin-dependent diabetes mellitus.

Neuropsychological function was compared in three well-matched groups of subjects: Group 1, 20 diabetic patients with hypertension, mean age 69.1 +/- 4.8 years, 14 males and 6 females; Group 2, 20 normotensive diabetic patients, mean age 69.0 +/- 6.2 years, 14 males and 6 females; Group 3, 20 healthy community controls, mean age 68.1 +/- 4.5 years, 13 males and 7 females. There were no significant differences between the groups in education or estimated IQ using the NART (National Adult Reading Test). Groups 1 and 2 did not differ significantly in duration of diabetes (mean 10.6 and 9.5 years, respectively), or mean glycosylated haemoglobin, HbA1 (mean 9.8 and 10.6%, respectively), or mean blood glucose before and after testing. On a battery neuropsychological tests, sensitive to cognitive impairment in older subjects, analysis of covariance using estimated IQ as the covariate showed no significant differences between the groups on tests of recall, with (Brown-Peterson Test) and without (Kendrick Object Learning Test) interference, forward and backward digit span, concentration (serial subtraction), verbal fluency, immediate and delayed prose recall, digit symbol substitution or psychomotor speed (Kendrick Digit Copying Test). These results provide no support for an association between cognitive deficits and Type 2 diabetes mellitus in older subjects or for the view that such deficits may also be mediated by hypertension.

Aged↗
PubMed1995

Expression of cyclin D2 in Epstein-Barr virus-positive Burkitt's lymphoma cell lines is related to methylation status of the gene.

The cyclin D2 gene is not expressed in resting primary B lymphocytes or in group I Burkitt's lymphoma (BL) cell lines that retain the characteristics of authentic BL cells. Expression of cyclin D2 is induced in primary B lymphocytes following infection with Epstein-Barr virus (EBV) or transfection of the EBV genes EBNA-LP and EBNA-2. However, attempts to induce cyclin D2 expression in BL cell lines by the enforced expression of EBV genes were unsuccessful. Since the demethylation agent 5-azacytidine has been shown to modulate viral gene expression in BL cells, we explored the possibility that methylation plays a significant role in the control of cyclin D2 expression. We show that 5-azacytidine treatment of the Mutu CI 179 BL cell line led to expression of cyclin D2 RNA and that expression correlated with differences in the methylation status of a CCGG restriction enzyme site near the transcription initiation region of the cyclin D2 gene. Thus, methylation appears to play a direct role in the regulation of the cyclin D2 locus in BL.

Antigens, Viral↗
PubMed1995

Host cell requirements for efficient infection of quiescent primary B lymphocytes by Epstein-Barr virus.

Quiescent primary B lymphocytes are efficiently immortalized by Epstein-Barr virus (EBV). This process requires both the delivery and expression of the viral genome and results in activation of the cell division cycle. Infection of B lymphocytes depends on a direct interaction between the viral glycoprotein gp340/220 and CD21, the C3dg complement receptor. This interaction is required for the adsorption of EBV. In addition, several lines of evidence suggest that the interaction of EBV with CD21 modulates the phenotype of cells. CD21 forms part of a multimeric signal transduction complex with CD19, TAPA-1, and Leu-13. In normal B lymphocytes, CD19 becomes tyrosine phosphorylated following stimulation of the antigen receptor and recruits the signal-transducing enzyme phosphatidylinositol 3-kinase kinase. Here, we investigated the involvement of signal transduction pathways in efficient infection. Protein synthesis is not required for events leading to the transcription of the viral genome, suggesting that the early stages of infection do not depend on the expression of novel cell genes and consistent with the Wp promoter being the first viral promoter used upon infection. Since the stimulation of cells with gp340/220 leads to an increase in the level of CD19 tyrosine phosphorylation, we investigated the potential contribution of both tyrosine and phosphatidylinositol 3-kinase kinases to efficient infection. Both kinases contribute to the posttranscriptional control of viral gene expression following infection, but neither is required for the entry or initial transcription of the virus. Thus, it appears that EBV exploits a host signal transduction pathway to efficiently infect primary cells.

Adult↗
PubMed1995

Aspirin-induced conformational changes in platelet membrane in subjects with stroke.

Objectives of this case-control study were (1) to examine membrane conformational changes and dynamics in platelets of patients with stroke prior to and following short-term aspirin administration and (2) to investigate changes in platelet membrane fluidity which may be associated with the ageing process. The study population consisted of 10 patients with ischaemic stroke (age range 61-92, mean 76 years; 6 females and 4 males), 9 age- and sex-matched controls (age range 64-88, mean 73 years; 5 females and 4 males), and 8 healthy young controls (age range 22-39, mean 32 years; 4 females and 4 males). The patients were recruited from the medical and geriatric wards, whereas both young and old controls were recruited from hospital staff and the local community. Aspirin, at a dose of 150 mg/day, was administered to all three groups for 7 days. The order parameter S, which is an index of membrane fluidity and conformation, was measured by the techniques of spin labelling and electron spin resonance spectroscopy on platelets from venous blood samples from patients prior to (within 48 h of admission) and following 7 days of aspirin therapy and from venous blood samples from both young and old controls before and after 7 days of oral aspirin therapy. There was an age-related decrease in platelet membrane fluidity. There was no significant difference in the value of 'S' between patients with ischaemic stroke and old controls. Treatment with aspirin led to a significant decrease in membrane fluidity in both patients and old controls, but had no apparent effect on the platelet membrane fluidity of younger controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

EBNA-2 and EBNA-LP cooperate to cause G0 to G1 transition during immortalization of resting human B lymphocytes by Epstein-Barr virus.

Epstein-Barr virus (EBV) is unusual among DNA tumour viruses in that the virus particle is able to infect and immortalize resting cells with very high efficiency. Mutation of the viral genome has indicated that at least six viral genes (LMP-1 and EBNAs 1, 2, 3A, 3C and LP) are essential for immortalization. We demonstrate that the activation of a G1 cyclin, cyclin D2, is an early event following infection with EBV and that cyclin D2 activation is dependent on the expression of viral genes. The different levels of cyclin D2 transcripts in Burkitt's lymphoma cell lines expressing different subsets of EBV immortalizing genes suggest an involvement of EBNA-2 or EBNA-LP in cyclin D2 regulation. By exposing resting primary B cells to a purified preparation of the EBV surface glycoprotein gp340, we have been able to achieve efficient expression of plasmid DNAs introduced by electroporation. Vectors encoding two viral genes, EBNA-2 and EBNA-LP, are sufficient to activate the expression of cyclin D2 in this system. Thus, the progression of resting B lymphocytes into the G1 phase of the cell cycle can be reconstituted in the absence of virus by the cooperation of two of the six viral genes required for immortalization.

Antigens, Viral↗
PubMed1994

Reduced signal transduction through glucocorticoid receptor in Burkitt's lymphoma cell lines.

Signal transduction through the glucocorticoid receptor (GR) was shown to be significantly reduced in Epstein-Barr virus (EBV)-positive group I Burkitt's lymphoma (BL) cell lines compared to human B-lymphocytes immortalized by EBV (LCLs). On the basis of hormone binding assays, nuclear DNA binding activity, and transactivation assays the response was reduced 5- to 10-fold. Direct sequence analysis of the expressed glucocorticoid receptor mRNA in two BL cell lines indicated that the phenotype did not result from mutation of the GR gene. By preparing a high-titer polyclonal antiserum against the t-1 region of the human GR, we further showed that the deficient GR response in BLs is largely reflected in reduced GR steady-state protein levels in BL cells compared to LCLs. However, the level of GR mRNA varies less between the BL cell lines and the LCLs. The Cp promoter of EBV which normally drives expression of the EBNA gene family in EBV-immortalized LCLs contains a functional glucocorticoid response element. Transfection of GR expression constructs to group I BL cells converted the GR response to approximately LCL levels both with respect to hormone binding and glucocorticoid-dependent transcription of a glucocorticoid-dependent promoter. A modest activation of EBNA-2 expression was seen in some such cell lines, suggesting that the lower GR response contributes to the down-regulation of EBNA expression observed in BL.

Antigens, Viral↗
PubMed1994

The effect of linoleic, arachidonic and eicosapentaenoic acid supplementation on prostacyclin production in rats.

We examined the effect of dietary supplementation of linoleic acid (LA), arachidonic acid (AA) or eicosapentaenoic acid (EPA) to rats fed a diet low in linoleic acid on in vitro and in vivo production of prostacyclin. Male Sprague Dawley rats were fed a high-fat diet (50% energy as fat, 1.5% linoleic acid) for two weeks. Three of the groups were then supplemented orally with either 90 mg/d of LA, AA or EPA, all as the ethyl esters, for a further two weeks while remaining on the high-fat diet. Forty-eight hour urine samples were collected at the end of the second and fourth weeks. In vivo prostacyclin production was determined by a stable isotope dilution, gas chromatography/mass spectrometry assay for the major urinary metabolite of prostacyclins (2,3-dinor-6-keto-PGF1 alpha or PGI2-M and delta 17-2,3-dinor-6-keto-PGF1 alpha or PGI3-M). In vitro prostacyclin production was determined by radioimmunoassay of the stable metabolite (6-keto-PGF 1 alpha) following incubation of arterial tissue. Oral supplementation with AA resulted in a rise in plasma and aorta 20:4n-6, and increased in vitro prostacyclin and urinary PGI2-M production. EPA supplementation resulted in a rise in plasma and aorta 20:5n-3 and 22:5n-3, and a decline in plasma 20:4n-6, but not in the aorta. In the EPA-supplemented group, the in vitro prostacyclin and the urinary PGI3-M increased, but urinary PGI2-M decreased. The increase in in vitro prostacyclin production in the EPA-supplemented rats was unexpected and without obvious explanation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

The effect of dietary fat level and quality on plasma lipoprotein lipids and plasma fatty acids in normocholesterolemic subjects.

This study examined the effect on the plasma lipids and plasma phospholipid and cholesteryl ester fatty acids of changing froma typical western diet to a very low fat (VLF) vegetarian diet containing one egg/day. The effect of the addition of saturated, monounsaturated or polyunsaturated fat (PUFA) to the VLF diet was also examined. Three groups of 10 subjects (6 women, 4 men) were fed the VLF diet (10% energy as fat) for two weeks, and then in the next two weeks the dietary fat in each group was increased by 10% energy/week using butter, olive oil or safflower oil. The fat replaced dietary carbohydrate. The VLF diet reduced both the low density lipoprotein (LDL)- and high density lipoprotein (HDL)-cholesterol levels; addition of the monounsaturated fats and PUFA increased the HDL-cholesterol levels, whereas butter increased the cholesterol levels in both the LDL- and HDL-fractions. The VLF diet led to significant reductions in the proportion of linoleic acid (18:2 omega 6) and eicosapentaenoic acid (20:5 omega 3) and to increases in palmitoleic (16:1), eicosatrienoic (20:3 omega 6) and arachidonic acids (20:4 omega 6) in both phospholipids and cholesteryl esters. Addition of butter reversed the changes seen on the VLF diet, with the exception of 16:1, which remained elevated. Addition of olive oil resulted in a significant rise in the proportion of 18:1 and significant decreases in all omega 3 PUFA except 22:6 compared with the usual diet. The addition of safflower oil resulted in significant increases in 18:2 and 20:4 omega 6 and significant decreases in 18:1, 20:5 omega 3 and 22:5 omega 3. These results indicate that the reduction of saturated fat content of the diet (< 6% dietary energy), either by reducing the total fat content of the diet or by exchanging saturated fat with unsaturated fat, reduced the total plasma cholesterol levels by approximately 12% in normocholesterolemic subjects. Although the VLF vegetarian diet reduced both LDL- and HDL-cholesterol levels, the long-term effects of VLF diets are unlikely to be deleterious since populations which habitually consume these diets have low rates of coronary heart disease. The addition of safflower oil or olive oil to a VLF diet produced favorable changes in the lipoprotein lipid profile compared with the addition of butter. The VLF diets and diets rich in butter, olive oil or safflower oil had different effects on the 20 carbon eicosanoid precursor fatty acids in the plasma.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗