1052 Am J Clin Nutr 1995;61:1052-7. Printed in USA. © 1995 American Society for Clinical Nutrition

Increasing the dietary polyunsaturated fat content alterswhole-body utilization of 16:0 and 1O:013

M Thomas Clandinin, Larry CH Wang, Ray V Rajotte, Margaret A French, YK Goh, and Elaine S Kielo

ABSTRACT Six healthy adult males were fed four differ-

ent diets to determine the effects of the quantity of fat (30% or40% of energy as fat) and type of fat (polyunsaturated orsaturated) on utilization of fatty acids. Each diet was fed for 15d. The ratio of dietary polyunsaturated to saturated fat (P:S)was formulated at either 0.2 or 1.0 at both fat intakes. Subjectsprovided breath tests to measure background ‘3C and responseto [1-’3C]10:0 and [1-’3C]16:0 fed with a test meal. Increasing

the P:S increased whole-body oxidation oflabeled 10:0 by 30%

after consumption of both low- and high-fat diets. When la-beled 16:0 was fed, the amount of ‘3C excreted in breath

increased by a factor of 2.4 after the low-fat diet with a high

P:S compared with the diet with a low P:S. The results suggest

that the amount and type of fat in the diet affect utilization ofindividual fatty acids in normal subjects. Am J Clin Nutr

i995;61 :1052-7.

KEY WORDS Absorption, isotope, fatty acid, diet

Introduction

The process of intestinal adaptation has been examined by

investigating alteration in villus morphology (1), nutrient trans-port (2), membrane composition (3), and desaturation of fattyacids (4). Changes in nutrient transport are associated with

alterations in brush border membrane (BBM) phospholipid

content and composition (5). Previous studies of normal ratshave shown that feeding a diet high in polyunsaturated fatincreased the transport rate of 16:0, 18:0, 18:1, 18:2, and 18:3

in the jejunum and ileum (6). However, transport of medium-chain fatty acids was unchanged by dietary manipulation (6).

The morphology of the villi in both rat jejunum and ileum is

affected by the ratio of polyunsaturated to saturated fat (P:S) in

the diet (7, 8). Villus surface area is significantly increased

with diets high in polyunsaturated fat (7). Because the uptake

of palmitic acid is thought to occur from the upper third of thevillus (9), increasing the P:S in the diet may be associated withthe increased rate of uptake of palmitic acid.

The current concept regarding energy utilization assumes

that dietary fat oxidation occurs at a rate controlled by mech-

anisms independent of the individual long-chain fatty acidcomposition of the diet. Human studies have suggested thatdifferent fat substrates are metabolized for energy with differ-ent efficiencies (10). These observations suggest that the rela-tive amounts of major dietary fatty acids consumed may affect

the net contribution of fat oxidation to total energy production,

shifting energy homeostasis and affecting whole-body fat par-titioning for adenosine triphosphate (AlP) synthesis or energy

storage.

In view of these animal and human studies, an experiment

with human subjects was conducted to determine whether thetotal amount of fat and the P:S of the fat consumed affects the

amount of 10:0 or 16:0 absorbed and utilized from a constanttest meal. Dietary medium-chain triglycerides (MCTs) are hy-

drolyzed more efficiently than are long-chain triglycerides

(LCFs) (11), reach the liver more rapidly than long-chain fatty

acids, and undergo rapid /3-oxidation and production of carbondioxide. Thus, one objective of the present study was to deter-

mine whether high or low intakes of fat in isoenergetic dietsdecrease whole-body oxidation of saturated fatty acids that are

dependent (16:0) or independent (10:0) of carnitine-mediated

transport into the mitochondria. The second objective was todetermine whether increased amounts of polyunsaturated fat in

isoenergetic diets increases whole-body oxidation of saturatedfatty acids, reflecting a shift in the contribution of fat oxidation

to total energy production.

Subjects and methods

Subjects and diet

Procedures used in this experiment were approved by theEthics Review Committee for Human Experimentation of the

Faculty of Medicine, University of Alberta. Six free-living

males aged 26.2 ± 1.6 y (range 21-31 y) gave informed written

consent to participate in this study. Subjects were 174.0 ± 2.7cm (1 ± SEM) in height and weighed 63.8 ± 2.7 kg, with a

mean (± SEM) energy intake of 1 1.6 ± 0.8 MJ. Subjects werescreened for chronic disease, cigarette smoking, and atypical

sleeping and activity patterns. Subjects consumed three isoen-

I From the Nutrition and Metabolism Research Group, Departments of

Agricultural, Food and Nutritional Science, Medicine, and Zoology, and

the Surgical Medical Research Institute, University of Alberta, Edmonton,

Alberta, Canada.

2 Supported by the Natural Sciences and Engineering Research Council

of Canada.

3 Address reprint requests to MT Clandinin, Nutrition and Metabolism

Research Group, Department of Agricultural, Food and Nutritional

Science, 4-10 Agriculture Forestry Building, University of Alberta, Edm-

onton, Alberta, Canada T6G 2P5.

Received March 29, 1994.

Accepted for publication November 28, 1994.

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DIET FAT ALTERS UTILIZATION OF 16:0 AND 10:0 1053

ergetic meals per day consisting of normal foods. The diet

provided an energy intake equal to each subject’s estimated

requirements. Energy requirements were estimated by using

the Mayo Clinic Nomogram (12) to determine basal metabolic

rate (BMR) and by multiplying this figure by 1.7 for normal

activity (13). An additional energy increment was included if

the subject participated in extra activity. Subjects wereweighed daily, before breakfast, and energy intake was ad-

justed slightly if a sustained weight loss or gain was observed.

The study consisted of four test periods of 15 d each. During

each test period subjects were provided with a different diet

treatment. The four diets were as follows: high-fat, low P:S;

high-fat, high P:S; low-fat, low P:S; and low-fat, high P:S. The

diets were formulated based on published food-composition

tables (14-19) to contain 14.2%, 45.4%, and 40.4% of energy

as protein, carbohydrate, and fat, respectively, for the high-fat

diets, which are typical values for the North American diet. The

low-fat diet contained 14.8%, 55.2%, and 30% of energy asprotein, carbohydrate, and fat, respectively, which is the

amount of fat recommended by health professionals (Table 1).Each fat intake was further divided into a low-P:S diet (0.2) ora high-P:S diet (1.0), resulting in four diet treatments. MCTs

are found in dairy products with a ratio of 10:0 to 16:0 of ‘�‘0.1.To provide a similar isotopic dilution in each diet treatment

when labeled 10:0 was administered, the ratio of 10:0 to 16:0

was formulated at 0.17 for all diets. MCT oil was added to the

diet to attain this ratio in all diets fed.

Within each diet treatment three menus designated as cycles

1, 2, and 3 were used. The cycle 1 menu was always consumed1 d before and on all test days. All meals were prepared in the

metabolic kitchen and consumed at fixed times. Breakfast and

lunch were eaten under supervision and supper was provided

on a take-out basis. Subjects were instructed to consume only

the foods provided to them. Only decaffeinated coffee, tea, andenergy-free beverages were allowed as supplemental foods.

Fat and energy analysis of diet

On days 9, 10, and 13 of each test period duplicates of the

meal consumed by each subject were prepared and homoge-nized with water for laboratory analysis of nutrient content.

Two aliquots were stored at -20 #{176}Cfor subsequent determi-

nation of ‘3C, total fat, energy, and fatty acid contents of the

diets fed (Table 1). Thus the isotopic dilution of the test

substrates was constant and known. Fat extraction (20), sapon-

ification, and transesterification with potassium hydroxide and

boron trifluoride methanol reagent (21) were carried out. Fattyacid methyl esters were analyzed by gas-liquid chromatogra-

phy (Vista 6010 GLC and Vista 402 data system; VarianInstruments, Georgetown, Ontario) as described previously(22). Mean triacylglycerol content was determined based on

mean fatty acid chain length. Fatty acid methyl esters were

identified by comparison of retention data with that of authen-

tic standards (23) and quantitated by peak area comparison

with internal standards (10). Bomb calorimetry (model 1241;

Parr Instrument Company, Moline, IL) was performed on ali-

quots of meal homogenates freeze-dried to constant weight.

Atwater factors were applied to obtain metabolizable energyvalues (24).

Experimental procedures

Each subject participated in all four test periods. The order inwhich the subjects received the diet treatments was systemat-

ically randomized. The first 9 d of each test period served as astabilization period during which time there would be a turn-over of at least two generations of mucosal cells (25). Duringdays 9, 10, and i3 of each test period, subjects were confined

to the metabolic laboratory and they provided 6-mm breath

samples hourly from 0730 to 1630 for analysis of breath ‘3C02

enrichment. Analysis of breath carbon dioxide enrichment onday 9 permitted examination of ‘3C contribution from the testdiet. On days 10 and 13 of each test period either

[1-’3Cjpalmitic acid or [1-’3C]decanoic acid was ingested incapsule form at the breakfast meal by the subjects. The order of

ingestion of each labeled fatty acid was systematically random-

ized. The enriched fatty acids were obtained from MSD Iso-

topes (Merck Sharpe, and Dohme, Canada Limited, Montreal).

The [1-’3C]16:0 was 99% chemically pure and contained 99.5atom % [1-’3C]. The labeled decanoic acid was 99% pure and

contained 95.2 atom % [1-’3C]. The labels were fed based onprior analysis of chemical and isotopic purity of the fatty acidsat a dose of 15 mg [1-’3C]16:0/kg body wt and 3 mg [1-’3C]i0:

0/kg body wt to provide a dose of 0.86 and 0.24 mg ‘3C/kgbody wt, respectively.

Breath collection

Hourly breath samples were collected from the reclining

subject for 6 mm between 0730 and 1630 on the test days. Thesubject breathed through a mouthpiece and Rudolph valve(Roxon Medi-Tech Ltd, Montreal) into a 100-L latex bag. The

TABLE 1Major fatty acid composition of meals based on laboratory analysis’

Fatty acid (% by wt) 10:0 16:0 18:0 18:lw-9 l8:2o-6

High-fat diets

Low P:S (ii = 45) 4.9 ± 0.3 27.5 ± 0.3 8.9 ± 0.3 24.6 ± 0.9 8.4 ± 0.2

High P:S (a = 45) 3.9 ± 0.2 22.5 ± 0.3 6.9 ± 0.2 22.3 ± 0.8 26.1 ± 0.4

Low-fat diets

Low P:S (n = 54) 4.9 ± 0.2 28.1 ± 0.4 9.4 ± 0.3 25.0 ± 0.8 6.8 ± 0.6

High P:S (�i = 54) 4.0 ± 0.2 22.0 ± 0.4 7.6 ± 0.2 23.2 ± 0.7 21.5 ± 1.7

‘ I ± SEM. Meals were formulated by using food-composition tables. High-fat diets were formulated to contain the following nutrients (per MI/meal):

8.46 g protein, 27.12 g carbohydrates, and 10.75 g fat. Low-fat diets were formulated to contain the following nutrients (per 4.19 MJ/meal): 8.79 g protein,

32.97 g carbohydrate, and 7.96 g fat. The high-fat meals provided 42 ± 0.08% of energy as fat and 5.27 ± 0.084 Mi of energy. The low-fat diet provided

29 ± 0.80% of energy as fat and 4.75 ± 0.096 MI of energy. The P:S of the high-P:S diet was 0.85 ± 0.02 and that of the low-P:S diet was 0.2 ± 0.01.

The ratio of 10:0 to 16:0 in the diet was constant at 0.17. P:S, ratio of polyunsaturated to saturated fat.

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of Standards and Technology # 20) demonstrated the analytical

precision (CV) of this instrument to be 0.0036%. The CV of

replicate determinations (n = 12) was 0.0069% for purified

carbon dioxide from combusted unlabeled palmitic acid. Du-

plicate analyses were performed for each breath sample col-

lected. Results were expressed as 6’3C (‘3C:12C, difference in

parts per thousand) against the standard Pee Dee Belemnite

(PDB), ie, %. Background 13C values were then subtracted

from each sample time on a day when a substrate was fed to

yield atom percent excess (APE) values due to oxidation of the

substrate only (27). Values at the initial time point for each

substrate test day were used as the zero reference point. Sub-

sequent points were adjusted accordingly and used to compare

profiles based on similar intakes of ‘3C label and dietary intake

of the test fatty acid in the breakfast meal. The percentage of

administered dose excreted in the breath per hour was calcu-

lated as indicated previously (10), including a correction factor

of 1.25 to adjust for uptake of label into the bicarbonate pool

(28). The ‘3C enrichment of all four diet treatments and the

different menu cycles within each diet treatment were mea-

sured by combusting a 10-mg aliquot of the freeze-dried meal

sample in a semimicro bomb (Parr Instrument Company) pres-

sured to 0.81 MPa of oxygen. The resultant carbon dioxide was

purified on a vacuum line as described previously (29) and the

13C abundance measured.

bag was then evacuated at 8 L/min. Part of the samplewas passed through an infrared detector (model LB-2; Sensor-

medics Corporation, Anaheim, CA) at 0.5 L/min to measure

the percentage of carbon dioxide in the breath sample. Carbondioxide analyzer output was monitored on a chart recorder to

calculate the total volume of air collected. A reference standard

was used to calibrate the carbon dioxide analyzer several times

daily. The sample outlet from the carbon dioxide analyzer was

connected to a 100-cm long spiral trap containing 10 mL 1 mol

NaOH/L. The respiratory sample was bubbled through the

sodium hydroxide solution for 3 mm, trapping all carbondioxide. The resulting sodium hydroxide solution was with-

drawn into an evacuated tube and frozen at -26 #{176}Cfor further

analysis. Respiratory carbon dioxide was regenerated undervacuum by mixing the sodium hydroxide solution with phos-

phoric acid (85% wt:vol) in a Rittenburg tube. The tube was

maintained at 25 #{176}Cuntil the reaction was complete (�20 mm),

frozen in liquid nitrogen, immersed in an acetone-liquid nitro-

gen slush bath, and then attached to the mass spectrometer.

Mass spectrometry

13CO2 abundance analysis was performed with a dual-inletisotope ratio mass spectrometer (MAT 25 1 ; Finnigan, Bremen,Germany). ‘3C abundances were corrected for 170 and pressure

drift (26). Multiple 13C abundance analyses (n = 6) of carbon

dioxide liberated from a limestone standard (National Institute

c’J0

x

. C,,

tFat, P:S = 0.2 8 IFat, P:S = 0.2

6

4

2

00800 1 000 1200 1400 1600 1 800 0600 0800 1000 1200 1400 1600 1800

Cd01�

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I Fat, P : S = 1.08 -tFat,P:S=1.0

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- - I0600 0800 1 000 1 200 1400 1600 1 800 0600 0800 1 000 1200

Time of DayFIGURE 1. Typical response [atom percent excess (APE) ‘3C02 in breath] of one subject fed four different diets with 30% or 40% of energy as total

fat and with a ratio of polyunsaturated to saturated fat (P:S) of 0.2 or 1.0 vs time. The subject was given either [1-’3C]10:0 (0) or [1-’3C]16:0 (#{149})after

a stabilization period on each diet. Values are normalized to correct for different dosages of the two substrates. Error bars from duplicate enrichment

measurements fall within the data points.

1400 1600 1800

Time of Day

1054 CLANDININ El AL

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C10:0

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.High Fat

3.0

2.5

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DIET FAT ALTERS UTILIZATION OF 16:0 AND 10:0 1055

I C16:O

4 5 6 7 8 9

Hours after Administration of Dose

FIGURE 2. Mean (± SEM) mmol ‘3C excreted per hour in breath

carbon dioxide for six subjects fed a high-P:S diet compared with a

low-P:S diet with 30% of energy as fat or 40% of energy as fat. Whole-

body absorption and oxidation of both 10:0 and 16:0 increased after the

high-P:S and low-fat diet (*P < 0.05 between the low- and high-fat diets).

P:S, ratio of polyunsaturated to saturated fat.

Statistics

Differences in response to the four diet treatments were

tested by analysis of variance (ANOVA) using SAS software

(SAS Institute, Inc, Cary, NC).

Results

Subjects were allowed a few days interlude between each

diet treatment, which resulted in total compliance with com-pletion of the test meals over the 10-wk study period. The mean

weight variance over the total study was minimal for the six

subjects. Body weight fluctuation over the study was 0.22 kg(SEM).

The analyzed fat content of meals in each diet treatment was

close to the values formulated from food-composition tables

and was consistent for diets with a low and high P:S (Table 1).The analyzed P:S and ratio of 10:0 to 16:0 of the diets was

close to that calculated and was consistent within each diet

treatment. The ‘3C enrichment of the different menu cycles

within the different diet treatments averaged -24.23 ± 0.2%(SEM) (n = 40). The mean ‘3C enrichment of the breakfast

meal for cycle 1, which was always fed on test days, was

-23.85 ± 0.2%. Therefore, the meals and especially the break-

fast meal on test days were consistent in ‘3C content.

After [1-’3C]palmitic acid was fed, excess respiratory ‘3C

was detected in breath carbon dioxide within ‘�2.5 h (Figure1). ‘3C excretion peaked during the afternoon or reached a

plateau. When [1-’3Cjdecanoic acid was fed, ‘3C02 was de-

tected within 1.5 h and peaked within 4 h of feeding. ‘3CO2

content of breath 24 h after ingestion of the labeled substrate

indicated that expired ‘3CO2 was within 5% of the backgroundvalue. Therefore, a minimum of 72 h between ingestion of

labeled substrates was sufficient time for the ‘3C content of thebreath to return to the background amount. No significantdifference was found between the order the diet was fed and the

order of label administered.

The APE of 13CO2 expired after ingestion of labeled palmiticand decanoic acids over time is illustrated for one subject fedeach of the four diets (Figure 1). Responses were calculated permilligram of labeled fatty acid fed per kilogram body weight

for each fatty acid. Subsequent calculations were normalizedfor the amount of dietary (including isotope) 10:0 or 16:0ingested in the breakfast meal. The response (area under the

curve over 9 h) observed for labeled decanoic acid was ‘�50times that of labeled palmitic acid. The ratio of 10:0 to 16:0

area was the least for the low-fat, high-P:S diet but was not

significant compared with the other three diet treatments.The amount of ‘3C in the breath carbon dioxide was aver-

aged for the six subjects at each sampling time for each diet

period. The response ratio is defined as the normalized average_______ mmol ‘3C excreted after the high-P:S diet compared with thatMean observed after the low-P:S diet at each fat intake (Figure 2). If

there was no effect of diet treatment, the response ratio wouldbe expected to vary around 1 .0. However, when the substratefed was labeled 10:0, an increase in the P:S from 0.2 to 1.0increased the average response ratio to 1 .3 when the normal-

ized pooled subjects were fed both the low- and high-fat diets,an increase of 30%. Responses to the low- and high-fat diets

FIGURE 3. Mean (± SEM) half-life of disappearance of ‘3C in respi-

ratory carbon dioxide. After consumption of the low-fat diet, ‘3C tended to

disappear more rapidly from respiratory carbon dioxide when subjects

were fed a high-P:S diet. *� < 0.08. P:S, ratio of polyunsaturated to

saturated fat.

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ci)

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V

0

1056 CLANDININ El AL

We thank Grace Hubert and Arlene Parrott for their assistance in food

preparation.

0P:S0.2 1.0 0.2 1.0 P:S 0.2 1.0 0.2 1.0

L�r�JL�r�J H�JL��r�J

Fat 40% 30% Fat 40% 30%

FIGURE 4. Mean (± SEM) oxidation rate of 10:0 and 16:0 of six

subjects over a 9-h test period. After consumption of the high-P:S diet the

absorption-oxidation rate observed for 10:0 decreased when the overall fat

content of the diet decreased (*P < 0.05) with a simultaneous increase

observed for the absorption-oxidation rate of 16:0. P:S, ratio of polyunsat-

urated to saturated fat.

were indistinguishable statistically. When labeled 16:0 was fedwith a low-fat diet, the pooled response ratio increased to 2.4

when the amount of polyunsaturated fat in the diet was in-

creased. Feeding a high-P:S diet increased the response ratio by

140%. Therefore, an increase in the amount of polyunsaturated

fat while low amounts of fat in the diet were maintained

increased the whole-body oxidation of medium- and, to a

greater extent, long-chain fatty acids.

The half-lives of ‘3C in breath carbon dioxide were calcu-lated by linear regression of the logarithmic disappearance of

‘3C from breath carbon dioxide when subjects were fed labeled

10:0. The mean (± SEM) half-life of ‘3C in breath carbondioxide after each diet treatment was calculated (Figure 3). At

the high-fat level no significant difference in half-life wasobserved for either P:S ratio. After diets containing low

amounts of fat, the half-life for elimination of ‘3CO2 from the

breath tended to be shorter when a high-P:S diet was fed (P <

0.08). Thus, it is concluded that consumption of a low-fat,

high-P:S diet results in ‘3C disappearing from the breath faster,

with the 13C from 10:0 being oxidized faster.

For each diet treatment the oxidation rates over 9 h for the

labeled 10:0 and 16:0 feeding days were calculated from the

area under the curve interpolating between data points (Figure

4). The oxidation of labeled 16:0 over 9 h after consumption of

a high-P:S, high-fat diet was 7.2% of the original dose. When

subjects consumed the high-P:S diet, the mean oxidation of

10:0 was significantly greater (P < 0.05) after consumption of

the high-fat diet. Concurrently, there is an increase in the

oxidation of 16:0 when the subjects were consuming the high-

P:S, high-fat diet compared with the low-fat diet.

Discussion

In this study normal subjects were stabilized to four diets

with different amounts of fat and P-S ratios for 15 d. No

significant weight gain or loss was observed over the entire diet

period of nearly 3 mo, such as that observed in a study with

fish-oil supplementation by lulleken et al (30), in which an

average of 4 kg was lost on low-fat diets fed for several weeks.

The variation in weight observed in this study was comparable

with other human feeding studies using similar feeding regi-

mens (29, 31). Use of the technique of daily weighing and

correction of energy intake for any trend in weight change

ensured that subjects stayed in energy balance so that any

change in whole-body oxidation with different diets was due toa change in energy utilization.

Relative whole-body oxidation of long-chain fatty acids in-

creased significantly when lower amounts of dietary fat were

fed in conjunction with a diet high in polyunsaturated fat

compared with one high in saturated fat. A study by Jones and

Schoeller (31) found that after ingestion of high-fat diets, total

fat oxidation increased after ingestion of a high-P:S diet com-

pared with a low-P:S diet, but not breakdown of individual

fatty acid oxidation was reported.

The half-life of ‘3CO2 in the breath, when labeled 10:0 was

administered, tended to be shorter when a low-fat, high-P:S

diet was fed compared with a low-P:S diet. It is difficult to

propose at what stage of metabolism the change in kinetics

with dietary fat occurred. When subjects were fed the low-P:S

diet, an increase in the proportion of fat in the meal shortened

the half-life of breath ‘3CO2. This may be accounted for by

faster gastric emptying time and shorter mouth-to-cecum tran-

sit time observed by Cunningham et al (32), who implied that

a test meal would be absorbed more efficiently by a subject fed

a high-fat diet. When labeled 10:0 was fed with low-P:S dietsthere was a trend for the oxidation rate over 9 h to be greater

with the higher fat intake than with the low fat intake, which

supports the observations by Cunningham et al (32). It should

be stressed that our diets were isoenergetic whereas Cunning-

ham et al’s diets were not, and thus a change in total energy

may have played a significant role in the observations reported

by Cunningham et al (32).

When subjects were fed a high-P:S, high-fat diet, the ob-

served oxidation for labeled 16:0 over 9 h was 7.2% of the

original dose. This compares favorably with a 16:0 oxidation of

6.6% over 6 h observed by Watkins et al (33) in normal

subjects fed a high-fat, high-P:S lipid emulsion. The oxidation

rates observed after consumption of high-P:S diets suggest that

a change from a high-fat to a low-fat diet results in an increase

in whole-body oxidation of ‘3C from long-chain fatty acids,

such as palmitic acid, at the expense of other substrates, in this

case decanoic acid. These results indicate that a shift in dietary

fat consumption (from a diet with a low P:S to one with a high

P:S) alters the differential utilization of individual dietary fats.

This change in the partitioning of fats absorbed from the diet

for energy utilization would also be expected to alter conver-

sion of nonfat substrates to fat for storage, thus altering mech-

anisms for the net conservation of energy. U

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DIET FAT ALTERS UTILIZATION OF 16:0 AND 10:0 1057

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