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Articles

Total Fat Intake Modifies Plasma Fatty Acid Composition in Humans¹

Susan K. Raatz^*2, Douglas Bibus, William Thomas^** and Penny Kris-Etherton

^* General Clinical Research Center, Hormel Institute and ^** Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis, Minnesota 55455 and Nutrition Department, Pennsylvania State University, University Park, Pennsylvania 16802

²To whom correspondence should be addressed at MMC 504, 420 Delaware St. S.E., University of Minnesota, Minneapolis, MN 55455. E-mail: raatz{at}mail.ahc.umn.edu

	ABSTRACT

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Plasma fatty acid composition reflects dietary fatty acids. Whether the total fat content of the diet alters the fatty acid composition of plasma phospholipid, cholesteryl ester, triacylglycerol and free fatty acids is unknown. To evaluate the effects of low versus high fat diets on plasma fatty acids, a 12-wk, randomized, crossover, controlled feeding trial was conducted in healthy men and women with isoenergic low fat (20% energy) and high fat (45% energy) diets containing constant proportions of fatty acids. Ten subjects consumed one experimental diet for 28 d, their usual diet for 4 wk and the alternate experimental diet for 28 d. Endpoint measures of plasma fatty acids were determined at the end of each experimental period. The effects of the two diets were compared within subjects by analysis of variance. Plasma fatty acids (%) varied in response to total dietary fat with significantly greater total polyunsaturated fat, (n-6) and 18:2(n-6) levels in phospholipids and cholesteryl esters after high fat dietary consumption. The low fat diet was associated with significantly greater total (n-3) fatty acids, 20:5(n-3) and 22:6(n-3) levels in plasma phospholipid fatty acids and cholesteryl esters. Consumption of a low fat diet alters fatty acid patterns in a manner similar to that observed with feeding of (n-3) long-chain fatty acids. This change is likely related to decreased competition for the enzymes of elongation and desaturation, with reduced total intake of 18:2(n-6) favoring elongation and desaturation of available (n-3) fatty acids.

KEY WORDS: • (n-3) fatty acids • (n-6) fatty acids • phospholipids • free fatty acids • triacylglycerol • cholesteryl ester

	INTRODUCTION

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Many studies have demonstrated that the levels of specific fatty acids in plasma are reflective of fatty acids consumed in the diet (Dougherty et al. 1987 , Judd et al. 1989 , Lopez et al. 1991 , Ma et al.1995 , Manku et al. 1983 ). These investigations have primarily focused on the fatty acid composition of the diet rather than examining the total fat content of the diet. Dietary recommendations have been made to decrease total fat intake, but little is known about the effects of decreasing total fat intake on plasma fatty acids. In this investigation, the effects of low versus high fat diets containing a constant fatty acid distribution was evaluated by measuring the plasma fatty acid distribution of phospholipid, cholesterol ester, triacylglycerol and free fatty acids.

Plasma phospholipid fatty acids are believed to reflect short-term (weeks to months) dietary fat intake (Holman 1986 , Kwon et al. 1991 , Riboli et al. 1987 ). Tissue membrane phospholipids maintain a consistent pattern of fatty acid composition yet, within a limited range, exhibit responsiveness to changes in the availability of circulating fatty acids (Lands 1991 , Spector 1992 ). The fatty acid composition of tissue lipids is maintained by the flux of fatty acids into and out of various glycolipids (Lands 1995 ), with relatively rapid turnover occurring between plasma phospholipids and tissue membranes. The fatty acid composition of the phospholipid fraction of plasma is closely related to the fatty acid composition of erythrocyte and platelet membrane phospholipids (Holman 1986 ). Therefore, plasma phospholipid fatty acids have the potential to function as a surrogate measure of the potential effects of diet on a whole range of cell membrane lipids.

The majority of cholesterol in blood is esterified into free fatty acids in the form of cholesteryl esters (Mayes 1993 ). Cholesteryl esters are carried in the core of plasma lipoproteins, because they are insoluble in an aqueous environment. Cholesteryl esters, like triacylglycerols, form lipid droplets in cells as storage sites of cholesterol and fatty acids. Free fatty acids and triglycerides are the major forms of lipids found in circulation (Mayes 1993 ).

Circulating fatty acids provide substrate for energy production, for incorporation into lipid-containing structures and for storage lipid. The present study was conducted to evaluate whether modifications in the level of total dietary fat would alter the fatty acid content of circulating lipids.

	METHODS

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Study participants.

A randomized, crossover design was used to compare the effects on plasma phospholipid, cholesteryl ester, triacylglycerol and free fatty acid composition in 10 healthy subjects fed controlled high versus low intakes of dietary fat. Health status was determined by responses to a medical questionnaire to eliminate subjects with past or current medical problems. None of the participants were taking any medications, either prescription or over-the-counter. Subjects selected for inclusion in the trial included healthy men (n = 4) and women (n = 6) between the ages of 22 and 65 y who were within 20% of ideal body weight. After the initial health screening, routine anthropometry, blood and urine analyses were performed to detect any previously undiagnosed conditions. The screening measures included a complete blood cell count, plasma cholesterol, triacylglycerol, glucose, aspartate aminotransferase, alkaline phosphatase, bilirubin, creatinine, urea nitrogen and a routine urinalysis. These analyses were conducted in the Biochemistry Laboratory, Fairview University Medical Center. One man had a previously undiagnosed thalassemia trait that was considered to be of no consequence in relation to the current trial, and he was included in the study group. The average age (mean ± SEM) of the subjects participating in the study was 38 ± 5 y. Body mass index (mean ± SEM) was 23.8 ± 0.2 kg/m².

Of the 10 subjects selected for participation, all completed every aspect of the study.

Approval for this study was obtained from the University of Minnesota Committee for the Use of Human Subjects in Research. Informed consent was obtained from all study participants.

Experimental protocol.

All 10 subjects were fed both a controlled high fat diet (45% of energy) and a controlled low fat diet (20% of energy) for 28 d. Diet order was randomly determined. After completion of the first experimental diet, subjects returned to their habitual diet for a washout period of 21–28 d. All subjects then crossed over to the alternate experimental diet that they consumed for 28 d during diet period two. Endpoint measures were determined at baseline and at the end of each 28-d feeding period.

Diets.

The two experimental diets were formulated with food items commonly available. The nutrient composition of the test diets was calculated with the Nutritionist V nutrient analysis software (1999) . The nutrient data for all food items used in the menus were from the U.S. Department of Agriculture standard reference database or manufacturer’s data as included in Nutritionist V. Isoenergic high and low fat diets were designed to provide a varying fat content but constant percentages of fatty acids (Table 1 ). The fat contents of the two diets were 20 and 45% of total energy, respectively, and the fatty acid distribution was 1:1:1 for polyunsaturated (PUFA)³ /monounsaturated/saturated fatty acids. The cholesterol content of the diets was constant at a level of 100 g/239 kJ (1000 Kcal). The high and low fat diets provided a (n-6)/(n-3) ratio of 12.3 and 11.1, respectively. Carbohydrate provided 40 and 65% of total energy in the high fat and low fat diets, respectively. The primary source of additional carbohydrate in the low fat diet was sugar, with the low fat diet containing 163.7 g of total sugars and 80.3 g of sucrose; the high fat diet contained 79.6 g of total sugar and 33.4 g sucrose. Both diets were isoenergic and provided 15% of the total energy as dietary protein. Table 2 presents a sample of the menu items used in the diets.

An energy level designed to promote weight maintenance was estimated for each subject. Energy intake levels required for weight maintenance were determined by multiplying the estimated basal energy expenditure (Harris and Benedict 1919 ) by an activity factor. The activity factors, which ranged from 1.6 to 1.95, were estimated based on the reported physical activity level of each subject. The energy intake (mean ± SEM) of the group was 636.5 ± 26.55 kJ (minimum 525.8, maximum 764.8 kJ). Daily weights were obtained to determine whether energy levels needed to be modified to promote stability of body weight. None of the subjects required modification of their energy intakes throughout the trial.

All meals were prepared in the Metabolic Kitchen of the General Clinical Research Center, University of Minnesota. Subjects were asked to consume one meal each day on the General Clinical Research Center (typically dinner); the remainder of the foods were packaged for consumption elsewhere. Subjects were required to consume all foods provided and to eat no other foods than those provided. Compliance with the research diet was evaluated by asking the subjects whether they had consumed all foods and whether any additional items were eaten, and by monitoring body weight on the prescribed energy levels.

Blood collection.

Blood was collected from fasting participants via venipuncture. A 10-mL sample of whole blood was collected from each subject on d 28 of each diet period. The samples were collected in EDTA-anticoagulated tubes and refrigerated immediately. Within 2 h of collection, the samples were centrifuged at 3000 x g for 10 min. Plasma was separated into two 2.0-mL aliquots and frozen at -20°C until transfer to -80°C for long-term storage.

Plasma fatty acid analysis.

When all plasma samples were collected, they were transferred to the Hormel Institute, University of Minnesota (Austin, MN) for analysis of plasma phospholipid, cholesteryl ester, triacylglycerol and free fatty acids. Fatty acid analysis was performed by gas chromatography at the same time by a single technician. Lipids were extracted from the plasma using chloroform/methanol (2:1 vol) according to the method of Folch et al. (1957 ). A known amount of standard (17:0) was added to each sample before extraction to quantify recovery and plasma lipid concentration. Phospholipids were separated from neutral lipids by thin layer chromatography. Fatty acid methyl esters (FAME) of the aforementioned lipid classes were formed through transesterification with boron trifluoride (12%) in excess methanol (Supelco, Bellefonte, PA).

The fatty acid composition of all lipid fractions were determined by capillary gas chromatography. The methyl ester samples were evaporated under nitrogen and resuspended in heptane containing methyl-tridecanoic acid (NuChek Prep, Elysian, MN) as an internal standard. FAME were separated with a capillary gas chromatograph with a bonded phase, fused silica capillary column (FFAP-007, 50-m x 0.25-mm internal diameter, 0.25-nm film; Quadrex, New Haven, CT). The gas chromatograph was temperature programmed from 170° to 220°C at a rate of 5°C/min after a 5-min initial time. The identities of sample methyl ester peaks were determined by comparison of authentic FAME (NuChek Prep).

Statistical methods.

The effects of the two diets were compared within subjects by balanced analysis of variance. All statistical analyses were performed with Minitab, Release 12.1 for Windows (1998; Minitab Inc., State College, PA).

	RESULTS

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Effect of test diet on plasma phospholipid fatty acids.

After the consumption of the high fat diet compared with the low fat diet, significantly greater percentages of total PUFA, total (n-6) fatty acids, and 18:2(n-6) were observed (Table 3 ). Although the 18:2(n-6) content of phospholipid fatty acids was greater in response to high fat feeding, there was a corresponding lower level of 20:4(n-6). These differences were accompanied by lower percentages of total saturated fatty acids and 16:0 after consumption of the high fat diet. Total (n-3) fatty acids in the phospholipids were greater after consumption of the low fat diet. The 20:5(n-3), 22:5(n-3) and 22:6(n-3) levels were all significantly increased in subjects when they consumed the low fat diet compared to consumption of the high fat diet.

Consumption of the high fat diet was associated with significantly greater proportions of total PUFA, total (n-6) and 18:2(n-6) fatty acids in plasma cholesteryl esters (Table 3) . The low fat diet resulted in a significantly greater levels of 20:5(n-3), 22:6(n-3) and total (n-3) fatty acids, as well as 16:0, 18:1(n-9) and total monounsaturated fatty acids.

Effect of test diet on plasma triacylglycerol fatty acids.

In triacylglycerols, fatty acid proportions did not differ between diet periods (Table 3) . Plasma triglyceride concentrations were 1.57 ± 0.32 and 0.91 ± 0.18 mmol/L after the consumption of low fat and high fat diets, respectively (P = 0.002). The greater plasma triglyceride concentration after low fat diet consumption is consistent with the consumption of a high carbohydrate, low fat diet, whereas the unchanged composition of fatty acids reflects the constant fatty acid content of the experimental diets.

Effect of test diet on plasma free fatty acids.

More subtle modifications in response to total dietary fat intake were observed in plasma free fatty acids. Proportions of total PUFA, 18:2(n-6), total (n-6) and 18:3(n-3) were greater after the consumption of the high fat diet (Table 3) . No significant differences were observed in any other fatty acids.

	DISCUSSION

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The intake of dietary lipid has an influence on the fatty acids found in circulation and in tissue membranes (Dougherty et al. 1987 , Judd et al. 1989 ). Sinclair and co-workers (1994 ) observed significant increases in the proportions and concentrations of plasma phospholipid 20:3(n-6), 20:4(n-6), 20:5(n-3) and 22:5(n-3) and a slight decrease in the proportions and concentrations of 18:2(n-6) in subjects who were fed very low fat diets (10% energy) containing lean beef. When beef fat or olive oil was added to the low fat diets, no change was observed in the fatty acid profile of the phospholipids. The addition of safflower oil, however, led to significant increases in 20:4(n-6) and 22:5(n-3) levels but decreases in 18:3(n-3) and 20:5(n-3) levels, likely due to the high (n-6) content of the oil. This observation is consistent with the results of our study in which a low fat diet caused significant increases in total saturated, total (n-3), 20:4(n-6), 20:5(n-3), 22:5(n-3) and 22:6(n-3) fatty acid levels and significant decreases in total PUFA, total (n-6) and 18:2(n-6) fatty acid levels. Because the percentage of dietary fatty acids was held constant in this experiment, it is likely that the observed differences are related to the absolute increase in fat, particularly PUFA and specifically 18:2(n-6).

As the total available (n-6) fatty acid supply increases, there is increased production of all of the highly unsaturated (n-6) fatty acids: 20:3(n-6), 20:4(n-6), 22:4(n-6) and 22:5(n-6) (Lands 1991 ). After high fat diet consumption, the subjects examined herein responded with significantly increased total (n-6) and 18:2(n-6) levels in plasma phospholipids, whereas the response to a low fat diet included increased concentrations and proportions of total (n-3), 20:5(n-3) and 22:6(n-3). This difference in fatty acid levels after the consumption of similar proportions but varied content of fatty acids suggests competition among the lipid series [(n-3), (n-6), (n-7) and (n-9)] for the enzymes of elongation and desaturation (Brenner 1974 , Hwang et al. 1988 , Lands 1991 ). When the relative supply of (n-3) fatty acids is abundant, these fatty acids are preferentially desaturated and elongated relative to (n-6) fatty acids (Holman 1986 ). This is consistent with the findings of the current study.

A number of studies have shown that a diet high in (n-3) fatty acids increases plasma and erythrocyte membrane (n-3) fatty acid concentrations. Allard and co-workers (1997) fed volunteers either menhaden oil [6.26 g (n-3) fatty acids daily] or olive oil for a 6-wk period. In those subjects supplemented with (n-3) fatty acids, there was a significant increase in the 20:5(n-3) and 22:6(n-3) levels in plasma phospholipids. The consumption of fish, fish oil and docosahexaenoic oil resulted in increased (n-3) and decreased (n-6) compositions of plasma lipid fractions as well as in platelet and erythrocyte membrane fatty acids (Vidgren et al. 1997 ). In a similar study, Lovegrove et al. (1997 ) demonstrated that enriching commonly eaten food products with 20:5(n-3) and 22:6(n-3) significantly increased the levels of these fatty acids in plasma and phospholipids when fed for a 22-d period. Mantzioris and co-workers (1994) demonstrated that dietary supplementation with flaxseed oil significantly increases the 18:3(n-3) content of plasma phospholipid, cholesteryl ester and triglyceride fractions and caused a 2.5-fold increase in 20:5(n-3) in circulation. Collectively, the studies conducted to date demonstrate that plasma (n-3) fatty acids can be increased with dietary modification.

In summary, this study demonstrates that the plasma phospholipid, cholesteryl ester and free fatty acid compositions are responsive to total dietary fat content. Specifically, the consumption of a low fat diet promotes an increase in the level of total and highly unsaturated long-chain (n-3) fatty acids (>C20) and a decrease in the total (n-6) content of plasma phospholipid and cholesteryl ester fatty acids. The observed modifications in phospholipid and cholesteryl ester fatty acids in response to a low fat diet are similar to those observed when (n-3) fatty acids of plant or animal origin are fed. This may explain some of the beneficial effects of low fat diets.

	ACKNOWLEDGMENTS

 
We thank the volunteers for their participation; Joanne Slavin, Daniel Gallaher, Linda Brady, Timothy Walseth and John Bantle for their advice; and the staff of the Surgical Laboratory and the General Clinical Research Center of the University of Minnesota for their technical and clinical assistance in the performance of this work.

	FOOTNOTES

 
¹ This study was supported by the American Dietetic Association Foundation: Kraft General Foods Fellowship (1994) and by grant M01RR00400 from the Division of Research Resources, National Institutes of Health.

³ Abbreviations used: FAME, fatty acid methyl esters; PUFA, polyunsaturated fatty acids.

Manuscript received May 15, 2000. Initial review completed June 21, 2000. Revision accepted October 24, 2000.

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