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American Journal of Clinical Nutrition, Vol. 70, No. 1, 21-27, July 1999
© 1999 American Society for Clinical Nutrition

Original Research Communications

Relation between the intake of milk fat and the occurrence of conjugated linoleic acid in human adipose tissue1,2,3

Jin Jiang, Alicja Wolk and Bengt Vessby

1 From the Department of Food Science, Swedish University of Agricultural Sciences, Uppsala; the Department of Medical Epidemiology, Karolinska Institute, Stockholm; and the Department of Geriatrics, University of Uppsala, Sweden.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Background: Conjugated linoleic acid (CLA) is a group of naturally occurring fatty acids mainly present in fats from ruminants. CLA has been shown to be a potential anticarcinogen.

Objective: In this study, the relation between bovine milk fat intake and the occurrence of CLA in human adipose tissue was investigated.

Design: One hundred twenty-three men weighed and recorded the foods they consumed for 1 wk. Afterward, recall interviews were conducted by telephone monthly for 7 consecutive months to inquire about food consumption during the previous 24 h. The entire dietary recording procedure was repeated once. The fatty acid composition of adipose tissue and serum was analyzed.

Results: The average amount of one isomer of CLA—9-cis,11-trans-octadecadienoic acid (9c,11t-18:2)—as a percentage of total fatty acids was found to be 0.50% in adipose tissue and 0.25% in serum. The amount of 9c,11t-18:2 in adipose tissue was significantly correlated with milk fat intake (r = 0.42). The percentage of 9c,11t-18:2 in both adipose tissue and in serum was strongly correlated with myristoleic acid (14:1).

Conclusion: The amount of 9c,11t-18:2 in human adipose tissue was significantly related to milk fat intake.

Key Words: Conjugated linoleic acid • humans • adipose tissue • fatty acids • milk fat intake • men • Sweden • 9-cis • 11-trans-octadecadienoic acid • 9c • 11t-18:2


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Conjugated linoleic acid (CLA) is a generic name for a mixture of isomers of linoleic acid (18:2) with conjugated double bonds at positions 9 and 11 or 10 and 12, and each double bond may be in the cis or trans configuration (1). CLA has attracted considerable attention because of its potential beneficial health effects. It has been reported that CLA inhibits the initiation of mouse skin carcinogenesis as well as mouse forestomach and rat mammary tumorigenesis (1–4). Shultz et al (5) found that physiologic concentrations of CLA are cytostatic and cytotoxic to human malignant melanoma, colorectal, and breast cancer cells in vitro. CLA has also been found to be effective in preventing the catabolic effects of immune stimulation (6, 7). More recently, CLA was suggested to have hypocholesterolemic and antiatherogenic effects (8, 9). The mechanisms responsible for these unique physiologic effects are not known. Of the individual isomers of CLA, 9-cis,11-trans-octadecadienoic acid (9c,11t-18:2), has been implicated as the most important in terms of biological activity because, apparently, this isomer is the only one incorporated into the phospholipid fraction of tissues of animals fed a mixture of CLA isomers (3, 4).

CLA is a group of naturally occurring fatty acids, mainly present in foods from ruminant sources. CLA is produced from polyunsaturated fatty acids (PUFAs) by rumen bacteria during biohydrogenation (10). Dairy products are the major dietary sources of CLA, of which 9c,11t-18:2 is the major isomer, representing 80–90% of total CLA in bovine milk (11, 12).

CLA has also been identified in human serum and in bile and duodenal juices (13–15). The effect of diet on plasma and serum CLA concentrations has been studied by supplying human subjects with a high-CLA diet. In 2 such studies, it was found that such a dietary modification increased plasma and serum concentrations of CLA (16, 17). However, little is known about the amount of CLA in human adipose tissue and whether this reflects dietary CLA intake. The purpose of this study was to determine the amount of CLA in adipose tissue and serum of humans and the relation between CLA concentrations and milk fat intake.


   SUBJECTS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Subjects
One hundred twenty-three men, randomly selected from Uppsala county in central Sweden, weighed and recorded the food they consumed for 1 wk. Afterward, recall interviews were conducted by telephone monthly for 7 consecutive months to inquire about food consumption during the previous 24 h. This procedure was repeated once; thus, two 1-wk dietary records were collected and 14 dietary interviews were completed for the subjects. The results of these 2 methods of dietary assessment—dietary records and 24-h recall interviews—were compared. All 123 men participated in the 24-h recall interviews; however, only 103 men completed the two 1-wk dietary records. Adipose tissue needle biopsy and blood samples were then collected and the following information was noted: age, height, and weight. The study was approved by the Ethical Committee of the Medical Faculty, Uppsala University, Sweden. All subjects signed an informed consent form before entering the study.

Dietary assessment
Before completing the self-administered dietary records, each participant obtained detailed instructions from a research dietitian about how to weigh and record all foods consumed. During telephone interviews, a standardized form for the 24-h dietary recall was used to collect the data. Dietary data from food records and telephone interviews were computerized by using the personal computer program MATS (18), which includes a listing of 1593 foods and dishes. Nutrients were calculated by using the Swedish Food Administration Food Database (19). This database provides information on the contents of 14 main fatty acids in different foods. Milk fat intake was estimated by summing the amounts of total fat from all dairy products and the milk fat from dishes containing dairy ingredients. Total energy and nutrient intakes for each subject were calculated as the mean daily intake derived from both the dietary records and 24-h recall interviews. The daily intake of CLA was estimated according to published data on the concentration of CLA in total fat in different foods (11, 20).

Blood sampling and adipose tissue biopsy
Blood samples were drawn from an antecubital vein under standardized conditions after a 12-h overnight fast. After the blood was coagulated for 2 h at room temperature, serum was separated by low-speed centrifugation (2000 x g for 10 min at 20°C) and stored at 4°C until analyzed for serum lipids, which was done within 24 h. Triacylglycerol and cholesterol concentrations were measured in serum enzymatically by using the IL Test Triacylglycerol Enzymatic-Colorimetric Method 181709-00 and IL Test Cholesterol Triander's method 181618-80, respectively, with a Monarch apparatus (Instrumentation Laboratory, Lexington, MA). Biopsies from subcutaneous adipose tissue were obtained by fine-needle biopsy of the upper-outer quadrant of the buttock as described by Beynen and Katan (21). The tissue samples were stored at -70°C until analyzed.

Lipid extraction and analyses
Aspirated adipose tissue samples weighing 20–40 mg were homogenized and extracted with 15 mL chloroform:methanol (2:1, by vol) according to the method of Folch et al (22). For fatty acid analysis, 4 mL of the chloroform phase was dehydrated with anhydrous sodium sulfate and the solution was transferred into a screw-capped test tube. After the solvent was evaporated, the residue was dissolved in 1 mL chloroform. The total amounts of lipid were then quantified with a microbalance (Mettler MT/UMT; Mettler-Toledo AG, Grifensee, Switzerland).

The methyl esters of the extracted lipid were prepared by adding 2 mL 0.01 mol NaOH/L in dry methanol and heating in a continuously shaken glycerol bath for 15 min at 60°C. Afterward, 3 mL BF3 in methanol (20%) was added and the mixtures were heated for 15 min at 60°C. The test tube was then removed from the glycerol bath and cooled under cold, running water. After 2 mL 20% NaCl and 1 mL hexane were added, the mixture was mixed vigorously and centrifuged at 2500 x g for 5 min at 20°C. The hexane phase was collected and the fatty acid methyl esters were redissolved in 400 µL hexane for gas chromatographic quantification.

The methyl esters of CLA were analyzed with an HP5890 series II gas chromatograph (Hewlett-Packard Co, Rolling Meadows, IL) fitted with a flame ionization detector. The chromatogram was integrated by using computer software (JCL6000; Jones Chromatography Ltd, Mid Glam, United Kingdom). Samples were injected through the split injection port (split ratio, 40:1) onto a CP Sil 88 fused silica capillary column (50 m x 0.22 mm, 0.2-mm file thickness; Chrompack, Middelburg, Netherlands). The nitrogen carrier gas flow was 2 mL/min and the injector and detector temperatures were 250°C. The oven temperature was programmed at 120°C for 3 min, increased from 120 to 180°C at a rate of 5°C/min, and then held at 180°C for 25 min. Individual fatty acids were identified by comparing relative retention times with individual fatty acid standards (Larodan Fine Chemical AB, Malmö, Sweden). Heneicosanoic acid methyl ester (Larodan Fine Chemical AB) was used as an internal standard for quantification. Analytic results for CLA and other fatty acids were expressed as percentages of total fatty acids. Lipid from the corresponding serum samples (n = 123) was extracted, methylated, and analyzed by gas chromatography by using the same methods used for adipose tissue analysis.

Data analysis
Spearman correlation was used to analyze the relations between dietary intake and the amounts of specific fatty acids in adipose tissue and serum. Significant relations between fatty acids were plotted by using linear regression analysis. The analyses were performed by using the SAS statistical package (23).


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Characteristics of subjects
The average age of the subjects was 62 y (range: 46–72 y) and subjects had a mean (±SD) BMI (in kg/m2) of 26.4 ± 3.2. Of the 123 subjects, 12 had a BMI >30 and 1 was grossly obese with a BMI of 41.3. Fifteen of the men had hypertriglyceridemia and 23 had hypercholesterolemia. None of the men had any acute illness in the 3 mo before the study. The data were analyzed for the whole group of men as well as for a subgroup who were normolipidemic with a BMI <30. Because the results were not significantly different between these 2 groups, we present the data for the whole group.

The average daily intake of selected nutrients is shown in Table 1Go. Mean intakes of total energy and nutrients were not significantly different between the 2 dietary recording methods. The average daily milk fat intake estimated in this study group was {approx}25 g. The intakes of 10 major fatty acids were also estimated; palmitic acid (16:0), stearic acid (18:0), cis-oleic acid (c-18:1), and 18:2 accounted for >80% of the total fat intake. The estimated intake of CLA was {approx}160 mg/d, which included CLA from both milk fat and the fat of ruminant meat products (11, 20).


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  		TABLE 1. Daily intake of energy and selected nutrients1,
 
Adipose tissue fatty acid composition
The mean percentage compositions of the major fatty acids as well as the sum of saturated fatty acids (SFAs), monounsaturated fatty acids (MUFAs), and PUFAs in adipose tissue in the present study were compared with published data (24–26) (Table 2Go). The studies in the 1990s showed a decrease in the amount of SFAs and an increase in the amount of PUFAs in adipose tissue compared with data from 1964, eg, 18:2 increased from 7.2% in 1964 to 14.4% in 1991. The amount of 9c,11t-18:2 in adipose tissue in the present study ranged from 0.27% to 0.72% of total fatty acid methyl esters, with a mean of 0.50%. Significant correlations between the amounts of 9c,11t-18:2 and other fatty acids in adipose tissue are shown in Figure 1Go. Strong correlations were observed between 9c,11t-18:2 and myristoleic acid (14:1) and between 9c,11t-18:2 and palmitoleic acid (16:1). On the other hand, weak but significant correlations were found between 9c,11t-18:2 and the odd-chain fatty acid pentadecanoic acid (15:0) and between 9c,11t-18:2 and total t-oleic acid.


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  		TABLE 2. Fatty acid composition of adipose tissue triacylglycerol in men1,
 


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  		FIGURE 1. Relations between one isomer of conjugated linoleic acid—9-cis,11-trans-octadecadienoic acid (9c,11t-18:2)—and 14:1, 16:1, 15:0, and total t-18:1 in adipose tissue in men (n = 103).

 
Relations between milk fat intake and adipose tissue fatty acid composition
Correlations between the amounts of long-chain fatty acids in adipose tissue and dietary milk fat intake were calculated by using data from both the dietary records and the 24-h dietary recall interviews (Table 3Go). Similar correlations were found with both methods. The amount of 9c,11t-18:2 in adipose tissue was significantly, positively correlated with the proportion of milk fat intake to total fat intake (r = 0.42, data from weighed dietary records), whereas a negative correlation was found for 18:2 (r = -0.46). The relation between the amount of 9c,11t-18:2 in adipose tissue and milk fat intake is shown in Figure 2Go. The correlation was similar to that between 9c,11t-18:2 in adipose tissue and the estimated total dietary CLA intake (r = 0.39).


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  		TABLE 3. Spearman correlation coefficients between the composition of 18-carbon fatty acids in adipose tissue and estimated dietary milk fat intake (milk fat intake/total fat intake) in men
 


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  		FIGURE 2. Relations between dietary milk fat intake and one isomer of conjugated linoleic acid—9-cis,11-trans-octadecadienoic acid (9c,11t-18:2)—in adipose tissue in men (n = 103). Intake was measured by using weighed dietary records for 2 wk.

 
CLA in serum
The content of 9c,11t-18:2 in serum samples ranged from 0.12% to 0.50% of total fatty acids. The mean value was 0.25%, which was about half the value found in adipose tissue. The relation between 9c,11t-18:2 in serum and in adipose tissue is shown in Figure 3Go. No significant correlation was found between serum CLA and adipose tissue CLA. The amounts of 9c,11t-18:2 and 14:1 in serum were also positively correlated (Figure 4Go).



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  		FIGURE 3. Relations between one isomer of conjugated linoleic acid—9-cis,11-trans-octadecadienoic acid (9c,11t-18:2)—in adipose tissue and serum in men (n = 103).

 


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  		FIGURE 4. Relations between one isomer of conjugated linoleic acid—9-cis,11-trans-octadecadienoic acid (9c,11t-18:2)—and 14:1 in serum in men (n = 103).

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
The occurrence of CLA in human blood and human milk has been reported in the literature (12, 14, 15, 17) and 9c,11t-18:12 has been identified as the major conjugated diene in human serum (15). The amount of 9c,11t-18:2 in human serum and milk was shown to be 0.30–0.54% and 0.31–1.25% of total fatty acids, respectively (12). The amount of 9c,11t-18:2 was interpreted initially as an indicator of free radical attack on PUFAs (27), but other studies indicated that the concentration of 9c,11t-18:2 in human serum and milk is influenced by the diet, mainly by diets containing dairy and ruminant meat fats (12, 17). Jack et al (28) also found that certain pathogenic bacteria can generate 9c,11t-18:2 in vitro. Consequently, the use of 9c,11t-18:2 as a marker of free radical activity in humans has been questioned.

The effect of the consumption of dairy products on plasma CLA concentrations in humans was studied by supplementing the diet of men with cheddar cheese, which resulted in a 19–27% increase in the plasma CLA concentration (16). This finding indicated that dietary modification can increase the CLA concentration in human plasma. It is known that dietary intake is also an important factor that can influence the fatty acid composition of human adipose tissue (29, 30). In the present study, the correlation between the fatty acid profile of adipose tissue and dietary milk fat intake determined by 2 different dietary assessment methods showed similar results, ie, the amount of 9c,11t-18:2 in adipose tissue was significantly correlated with milk fat intake.

In addition to the dietary factor, the endogenous formation of 9c,11t-18:2 was shown in rats by means of desaturation of 11-octadecanoic acid by liver microsomes (31) and by conversion of free 18:2 to CLA by the intestinal flora (32). Similar processes may occur in humans; eg, it was shown that dietary trans fatty acids increase CLA concentrations in human serum, which suggests that CLA in human tissues is partly derived from the diet, but that part of it may be formed via the conversion of dietary trans fatty acids (33). An elevated concentration of CLA in the cervix was observed as a result of bacterial colonization and activity (34). However, a recent study of the possible isomerization of 18:2 to CLA by human intestinal microflora reported that the supplementation of safflower oil with triacylglycerol-esterified 18:2 did not increase plasma concentrations of esterified CLA in total lipids (35).

The incorporation of dietary CLA into various tissues was studied and was found to be tissue dependent, eg, adipose tissue and lung tissue contain the most and brain tissue the least (36). In the present study, it was found that the average amount of CLA in human adipose tissue was twice as high as in serum, and there was no significant correlation between the amount of CLA in adipose tissue and in serum. These results warrant further studies of the incorporation of dietary CLA into human adipose tissue and the turnover rate, endogenous formation, and metabolism of CLA in humans.

Regarding the relations between different fatty acids in adipose tissue, no positive correlation was found between 9c,11t-18:2 and 18:2, which agrees with the results reported for human plasma (16). Jiang et al (37) showed previously a strong correlation between 9c,11t-18:2 and trans-vaccenic acid (11t-18:1) in bovine milk (r = 0.78). However, a weaker correlation (r = 0.20) was observed between 9c,11t-18:2 and total t-18:1 in human adipose tissue in this study. The result that 9c,11t-18:2 was significantly correlated with 15:0 might substantiate the observed correlation between 9c,11t-18:2 and milk fat intake because 15:0 has been shown to be a good biological marker of milk fat intake in human adipose tissue (38). Of interest are the strong correlations between 9c,11t-18:2 and 14:1 and of 9c,11t-18:2 and 16:1 in adipose tissue. The reason for these relations is not understood and thus requires further investigation. The data published in 1964 (24) showed that the amounts of 14:1 and 16:1 in adipose tissue in men were twice as high in the 1960s as in the more recent investigations. This may indicate a higher concentration of CLA in human adipose tissue in the 1960s, as judged from the strong correlations between CLA and 14:1 and 16:1 found in the present study. This observation is consistent with the reduced consumption of total animal fat (eg, butter, full-fat milk, and fat from ruminant meats) in recent decades, although the reason for these differences may be due in part to divergent fat intakes in different countries.

In conclusion, milk fat has been shown to be associated with negative health effects because of its high SFA content. The increased knowledge about the positive health effects associated with CLA, the occurrence of CLA in milk, and the transfer of CLA from milk fat in the diet to human adipose tissue, as shown in this investigation, may warrant reevaluation of the health aspects of milk fat. However, before such a reevaluation can be made, additional scientific data on the nutritional effects of CLA are required.


   ACKNOWLEDGMENTS
 
We thank Lennart Björck for his fruitful suggestions and for reading the manuscript, Zhou Wei and Siv Tengblad for analyzing the adipose tissue samples, and Håkan Ljung for analyzing the data.


   FOOTNOTES
 
2 Supported by the Swedish Cancer Society and Arla, Stockholm. The conjugated linoleic acid standard was a gift from Sou Fei Chin (Food Research Institute, University of Wisconsin, Madison).

3 Address reprint requests to J Jiang, Department of Food Science, Swedish University of Agricultural Sciences, PO Box 7051, S-750 07 Uppsala, Sweden. E-mail: Jin.Jiang{at}lmv.slu.se.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

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Received for publication February 6, 1998. Accepted for publication January 14, 1999.




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