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Department of Animal Science, Cornell University, Ithaca, NY 14853 and * School of Biosciences, University of Nottingham, Loughborough, Leicestershire, LE12 5RD, UK
4To whom correspondence should be addressed. E-mail: Andrew.Salter{at}nottingham.ac.uk or debb{at}cornell.edu.
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ABSTRACT |
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 TOP ABSTRACT MATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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KEY WORDS: • conjugated linoleic acid • vaccenic acid • plasma cholesterol • functional food • human health
Conjugated linoleic acid (CLA)5 isomers have been shown to possess a number of properties that may be beneficial to human health (1,2). Ruminant products are the principal source of CLA in human diets with 
70 and 25% coming from dairy products and red meat, respectively (3); the cis-9, trans-11 isomer (rumenic acid; RA) represents 75–90% of total CLA in dairy foods (4). The predominant source of RA in dairy products is through endogenous synthesis in the mammary gland via 
9-desaturase from vaccenic acid (trans-11 18:1; VA), the major biohydrogenation intermediate produced in the rumen (5). Due to the precursor:product relation between these 2 fatty acids, foods rich in RA are also a rich source of VA. Endogenous synthesis of RA from VA has also been reported in humans (6) and other species (7,8).
Most investigations concerning the health benefits of RA have examined its anticarcinogenic properties which are now well established for several types of cancer (1). We demonstrated that consumption of a VA/RA-enriched butter fat is effective in reducing the risk of mammary cancer in rats treated with a chemical carcinogen (8–10). By comparison, studies investigating the effect of CLA isomers on cholesterol and lipoprotein metabolism and atherosclerosis are limited. Synthetic CLA isomer mixes were shown to inhibit the development of cholesterol-induced atherosclerosis in hamsters and rabbits (11–15) and cause the regression of preestablished atherosclerotic lesions (11). Utilizing pure isomers it was shown that RA and trans-10, cis-12 CLA were equally effective in reducing cholesterol-induced atherogenesis in rabbits (16), and a dietary supplement of RA not only retarded further development of atherosclerotic lesions in the ApoE–/– mouse, but also induced regression of the lesions in the aorta (17). Reports on the effects of RA on cholesterol and lipoprotein metabolism have produced inconclusive results, with RA shown to have no effect in some studies (18,19), but having an effect in others (20).
To date, there have been no investigations into the effects of a naturally enriched RA food product on cholesterol and lipoprotein metabolism in a biomedical animal model of atherogenic risk. In addition to RA, dairy products contain VA, which also contributes to the available pool of RA through endogenous synthesis. The objective of the present study was to determine the effects of feeding a VA/RA-enriched butter on cholesterol and lipoprotein metabolism in male Golden Syrian hamsters. Because of concerns regarding trans fatty acids and their association with elevated plasma concentrations of LDL and lower concentrations of HDL cholesterol (21–23), we also compared the VA/RA-enriched butter to a partially hydrogenated vegetable oil (PHVO).
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MATERIALS AND METHODS |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Diet formulation and feeding.
The purpose of the overall dietary treatment scheme was to evaluate the modulation of cholesterol and lipoprotein metabolism by increasing the dietary supply of VA and RA and comparing this with a control diet and a diet containing trans fatty acids derived from PHVO. All 3 diets were supplemented with 0.2% crystalline cholesterol (Sigma) and contained 20% supplemental fat, which was derived from the 2 butter sources, and PHVO either alone or in combination (Table 2). All diets contained comparable amounts of SFA (12:0, 14:0, and 16:0) and linoleic acid. In addition, the proportion of total trans fat in the EB and VO treatments was approximately equal and represented 5% of the energy (Table 3). Hamsters had free access to food and water, and food was replaced completely every 2 d.
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Fatty acid analysis. The –80°C samples of epididymal and perirenal fat pads and liver were pulverized at liquid nitrogen temperature. Total lipids were extracted from pulverized tissues by the procedure of Hara and Radin (27) using a mixture of hexane and isopropyl alcohol. Fatty acids were methylated according to Christie (28) with modifications as described by Corl et al. (8). FAMEs were analyzed by GC (system 6890+ with flame ionization detector; Agilent) using a CP-Sil 88 capillary column (100 m x 0.25 mm i.d. with 0.2-µm film thickness; Varian) according to the methods described by Lock et al. (10). FAME standards were used to identify sample FAME (Nu-Chek-Prep).
Statistical analyses. Data were analyzed by the general linear model procedure of SAS (SAS Institute). ANOVA was used to identify the effect of treatment, and differences between treatment means were identified using the probability of difference option of the LSMeans command. Results are expressed as means ± SE; treatment effects and differences between means were considered significant when P < 0.05.
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RESULTS |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Cholesterol and TAG concentrations in plasma and liver. Dietary treatments had significant effects on total plasma cholesterol and cholesterol levels in individual lipoprotein fractions (Table 4). Total (P < 0.001), chylomicron (P < 0.01), LDL (P < 0.01), and IDL (P < 0.001) cholesterol concentrations were reduced in hamsters fed VA/RA-enriched butter (EB treatment) and PHVO (VO treatment) compared with hamsters fed the control diet (CT treatment). However, VLDL concentrations were significantly reduced only in hamsters administered the EB treatment compared with those administered the CT and VO treatments (P < 0.01). HDL cholesterol concentrations did not differ among treatment groups. Overall, the ratio of potentially atherogenic lipoproteins (VLDL + IDL + LDL) to antiatherogenic HDL was lower in hamsters fed VA/RA-enriched butter (0.60) than in those fed either the control (1.70) or PHVO diet (1.04).
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Hamsters administered the EB treatment had a greater concentration of cholesterol ester in their livers than those administered either the CT or VO treatment (P < 0.001), whereas liver free cholesterol concentration did not differ between treatment groups (Table 5).
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DISCUSSION |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Each dietary treatment produced a unique pattern of fatty acid composition of liver and adipose tissue lipids. Compared with those fed the control diet, hamsters administered the EB treatment had higher tissue lipid concentrations of both RA and VA. This was predominantly at the expense of oleic acid and, to a lesser extent, palmitic acid. Increases in other trans 18:1 isomers were also seen, but these were much less pronounced and in general reflected the composition of the VA/RA-enriched butter. The tissues of hamsters administered the VO treatment also reflected dietary fatty acid composition with a much more uniform distribution of trans 18:1 isomers. It is of note, however, that even though RA was not present in the dietary fat, RA concentrations were higher in hamsters administered the VO treatment compared with those administered the CT treatment. We believe this is evidence of VA, present in the VO diet, being converted to RA through the action of 9-desaturase in these tissues of the hamsters.
In general, hydrogenated fat rich in trans 18:1 isomers has been considered to be associated with increased risk of developing cardiovascular disease (21–23). Human nutrition studies suggest that consuming partially hydrogenated vegetable oils increases plasma LDL cholesterol compared with monounsaturated fatty acids or PUFA, but they are less potent than SFA (32,33). However, compared with diets rich in saturated fat, trans fatty acid consumption may also be associated with reduced HDL cholesterol concentrations (32,33). Human nutrition studies have concentrated on the effect of trans fatty acids present in hydrogenated vegetable oils rather than those naturally occurring in ruminant milk and meat. However, epidemiologic evidence indicates that it is consumption of trans fatty acids derived from PHVO that is associated with increased risk of cardiovascular disease, whereas no clear relation exists for trans fatty acid intake from animal-derived foods (34–38). This suggests that the isomer profile of trans fatty acids may be an important consideration in evaluating the risk for coronary heart disease.
In hamsters, elaidic acid (trans-9 18:1) has been described as being biologically neutral in terms of its effect on plasma LDL concentrations and regulation of LDL receptor activity (39). This contrasted with an increase in LDL when myristic acid was fed and a decrease when oleic acid was fed (39). Nicolosi et al. (40) reported similar LDL cholesterol concentrations in hamsters fed oleic and elaidic acid, which were reduced compared with concentrations in those fed myristic acid. In a comparison of the effects of elaidic and VA, Meijer et al. (41) found no significant difference in VLDL, LDL, or HDL cholesterol concentrations in hamsters fed low-cholesterol (0.01%) diets.
The present experiment suggests that compared with CT, both EB and VO treatments reduce LDL cholesterol. This may be related to the slightly higher SFA concentration of the CT diet. In comparison with both CT and VO treatments, feeding EB specifically reduced VLDL cholesterol concentration. We demonstrated previously that development of atherosclerosis in hamsters was directly correlated with the concentration of VLDL, IDL, and LDL; hence each of these fractions can be considered to be "proatherogenic" (30). When considering the sum of these lipoproteins, or when expressing them as a ratio to the "antiatherogenic" HDL fraction, hamsters fed EB display the least atherogenic lipoprotein profile of the 3 treatments. Thus, some component(s) of EB appear to induce favorable changes in lipoprotein cholesterol concentrations.
The question remains concerning what fatty acid components of the EB diet are having these effects. Previous studies in hamsters suggested that purified mixtures of CLA isomers may have beneficial effects on plasma lipoprotein profiles (15,18,19). However, studies specifically investigating the effects of pure isomers yielded conflicting results, with one (20) showing that RA was effective in lowering plasma cholesterol levels, but others (18,19) indicating that this isomer had no effect. Differences in results may relate to the background diet of the animals, particularly cholesterol concentration, or the amount of CLA fed. Furthermore, most of these studies, with the exception of that of de Deckere et al. (18), have fed CLA isomers as FFA. Recent work from our laboratory (Salter et al., unpublished) suggests that RA is more readily absorbed when incorporated into dietary TAG. If RA is responsible for the beneficial effects of EB, then the conversion of dietary VA to RA through the action of 9-desaturase may further contribute to the effect. This may also explain some of the differential effects of the EB and VO diets, with the former containing considerably more VA.
Mechanisms for the effects of EB on cholesterol and lipoprotein metabolism remain to be established, but are presumably related to effects on hepatic cholesterol metabolism. Previous work showed that hamsters respond to diets supplemented with cholesterol by increasing hepatic stores of cholesterol ester in a dose-dependent manner (29). However, the storage of such cholesterol is modulated by the type of fatty acid in the diet (29,39,42). The current study suggests that consumption of the EB diet leads to a greater accumulation of cholesterol ester compared with either CT or VO. Whether this effect is related to the relative affinity of fatty acids as substrates (perhaps either RA or VA) for esterification or to some less direct effect remains to be established. Such sequestration of dietary cholesterol may explain, at least in part, why EB reduced plasma concentrations of VLDL, IDL, and LDL cholesterol. In addition, we showed previously that different dietary fatty acids modulated the fecal excretion of cholesterol (29,31). Other mechanisms, such as increased conversion to and/or excretion of bile acids or decreased cholesterol synthesis may also play a role.
To date, there have been 2 studies that examined the effects of RA on blood lipids in healthy humans. Differences in response were observed when the proportions of RA and trans-10, cis-12 CLA were altered in a CLA supplement; a 50:50 mixture of RA and trans-10, cis-12 CLA significantly improved plasma TAG and VLDL metabolism, whereas an 80:20 blend of the same 2 CLA isomers significantly reduced VLDL cholesterol concentrations (43). Utilizing relatively pure CLA isomers, it was recently reported that RA and trans-10, cis-12 CLA had opposing effects on blood lipids in healthy humans; plasma TAG, total plasma cholesterol, LDL cholesterol, and the LDL:HDL cholesterol ratio were all lower during supplementation with RA compared with trans-10, cis-12 CLA (44). Although data are limited at present, these 2 studies provide support that some of the cardioprotective effects of RA observed in the current study and previously may extend to humans. Additional studies are required to extend these results and examine the dissimilar effects of RA and trans-10, cis-12 CLA, and their possible interaction, on cholesterol and lipoprotein metabolism.
In conclusion, we produced butter with a modified fatty acid composition that yielded a more favorable lipoprotein cholesterol profile when fed to hamsters than standard butter or a diet containing partially hydrogenated vegetable oil. This is despite the fact that this butter was enriched in trans fatty acids. Current public health policy strongly recommends a reduction in the intake of trans fatty acids principally due to their putative association with elevated plasma concentrations of cholesterol and LDL along with lower concentrations of HDL (21–23). Although CLA are exempt from the imminent nutrition labeling of the trans fatty acid content of all food products in the United States, there will be no distinction between individual trans 18:1 fatty acids. Data presented here, and previously published studies on effects on cancer (8,10) suggest that perhaps VA should also be considered for an exemption. The VA/RA-enriched butter used in these studies is thus worthy of further consideration as a "Functional Food" that may offer benefits for human health.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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2 Supported in part by a grant from the National Dairy Council, Rosemont, IL; support was also received from Northeast Dairy Foods Research Center and Cornell University Agricultural Experimental Station.
3 Supplemental tables with complete tissue fatty acid data and diet composition are available as Online Supporting Material with the online posting of this paper at www.nutrition.org.
5 Abbreviations used: CLA, conjugated linoleic acid; CT, control diet containing standard butter; EB, diet containing vaccenic acid/rumenic acid-enriched butter; IDL, intermediate density lipoprotein; PHVO, partially hydrogenated vegetable oil; RA, rumenic acid (cis-9, trans-11 conjugated linoleic acid); TAG, triacylglycerol; VA, vaccenic acid; VO, diet containing partially hydrogenated vegetable oil.
Manuscript received 14 March 2005. Initial review completed 15 April 2005. Revision accepted 26 April 2005.
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LITERATURE CITED |
|---|
|
TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
|---|
1. Belury, M. A. (2002) Dietary conjugated linoleic acid in health: physiological effects and mechanisms of action. Annu. Rev. Nutr. 22:505-531.[Medline]
2. Parodi, P. W. (2004) Milk fat in human nutrition. Aust. J. Dairy Technol. 59:3-59.
3. Ritzenthaler, K. L., McGuire, M. K., Falen, R., Shultz, T. D., Dasgupta, N. & McGuire, M. A. (2001) Estimation of conjugated linoleic acid intake by written dietary assessment methodologies underestimates actual intake evaluated by food duplicate methodology. J. Nutr. 131:1548-1554.
4. Lock, A. L. & Bauman, D. E. (2004) Modifying milk fat composition of dairy cows to enhance fatty acids beneficial to human health. Lipids 39:1197-1206.[Medline]
5. Bauman, D. E., Corl, B. A. & Peterson, D. G. (2003) The biology of conjugated linoleic acids in ruminants. Sébédio, J.-L. Christie, W. W. Adlof, R. O. eds. Advances in Conjugated Linoleic Acid Research 2:146-173 AOCS Press Champaign, IL.
6. Turpeinen, A. M., Mutanen, M., Aro, A., Salminen, I., Basu, S., Palmquist, D. L. & Griinari, J. M. (2002) Bioconversion of vaccenic acid to conjugated linoleic acid in humans. Am. J. Clin. Nutr. 76:504-510.
7. Santora, J. E., Palmquist, D. L. & Roehrig, K. L. (2000) Trans-vaccenic acid is desaturated to conjugated linoleic acid in mice. J. Nutr. 130:208-215.
8. Corl, B. A., Barbano, D. M., Bauman, D. E. & Ip, C. (2003) cis-9, trans-11 CLA derived endogenously from trans-11 18:1 reduces cancer risk in rats. J. Nutr. 133:2893-2900.
9. Ip, C., Banni, S., Angioni, E., Carta, G., McGinley, J., Thompson, H. J., Barbano, D. & Bauman, D. E. (1999) Conjugated linoleic acid–enriched butter fat alters mammary gland morphogenesis and reduces cancer risk in rats. J. Nutr. 129:2135-2142.
10. Lock, A. L., Corl, B. A., Barbano, D. M., Bauman, D. E. & Ip, C. (2004) The anticarcinogenic effect of trans-11 18:1 is dependent on its conversion to cis-9, trans-11 CLA by 9-desaturase in rats. J. Nutr. 134:2698-2704.
11. Kritchevsky, D., Tepper, S. A., Wright, S., Tso, P. & Czarnecki, S. K. (2000) Influence of conjugated linoleic acid (CLA) on establishment and progression of atherosclerosis in rabbits. J. Am. Coll. Nutr. 19:472S-477S.
12. Kritchevsky, D., Tepper, S. A., Wright, S. & Czarnecki, S. K. (2002) Influence of graded levels of conjugated linoleic acid (CLA) on experimental atherosclerosis in rabbits. Nutr. Res. 22:1275-1279.
13. Lee, K. N., Kritchevsky, D. & Pariza, M. W. (1994) Conjugated linoleic acid and atherosclerosis in rabbits. Atherosclerosis 108:19-25.[Medline]
14. Wilson, T. A., Nicolosi, R. J., Chrysam, M. & Kritchevsky, D. (2000) Conjugated linoleic acid reduces early aortic atherosclerosis greater than linoleic acid in hypercholesterolemic hamsters. Nutr. Res. 20:1795-1805.
15. Nicolosi, R. J., Rogers, E. J., Kritchevsky, D., Scimeca, J. A. & Huth, P. J. (1997) Dietary conjugated linoleic acid reduces plasma lipoproteins and early aortic atherosclerosis in hypercholesterolemic hamsters. Artery 22:266-277.[Medline]
16. Kritchevsky, D., Tepper, S. A., Wright, S., Czarnecki, S. K., Wilson, T. A. & Nicolosi, R. J. (2004) Conjugated linoleic acid isomer effects in atherosclerosis: growth and regression of lesions. Lipids 39:611-616.[Medline]
17. Toomey, S., Roche, H., Fitzgerald, D. & Belton, O. (2003) Regression of pre-established atherosclerosis in the apoE(–/–) mouse by conjugated linoleic acid. Biochem. Soc. Trans. 31:1075-1079.[Medline]
18. de Deckere, E.A.M., van Amelsvoort, J.M.M., McNeill, G. P. & Jones, P. (1999) Effects of conjugated linoleic acid (CLA) isomers on lipid levels and peroxisome proliferation in the hamster. Br. J. Nutr. 82:309-317.[Medline]
19. Gavino, V. C., Gavino, G., Leblanc, M. J. & Tuchweber, B. (2000) An isomeric mixture of conjugated linoleic acids but not pure cis-9, trans-11-octadecadienoic acid affects body weight gain and plasma lipids in hamsters. J. Nutr. 130:27-29.
20. Valeille, K., Gripois, D., Bloquit, M. F., Souidi, M., Riottot, M., Bouthegourd, J. C., Serougne, C. & Martin, J. C. (2004) Lipid atherogenic risk markers can be more favourably influenced by the cis-9, trans-11-octadecadienoate isomer than a conjugated linoleic acid mixture or fish oil in hamsters. Br. J. Nutr. 91:191-199.[Medline]
21. Katan, M. B. (2000) Trans fatty acids and plasma lipoproteins. Nutr. Rev. 58:188-191.[Medline]
22. Mensink, R. P., Zock, P. L., Kester, A.D.M. & Katan, M. B. (2003) Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Am. J. Clin. Nutr. 77:1146-1155.
23. Institute of Medicine, Food, and Nutrition Board (2002) Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Letter Report on Dietary Reference Intakes for Trans Fatty Acids National Academy of Science Washington, DC.
24. Bauman, D. E., Barbano, D. M., Dwyer, D. A. & Griinari, J. M. (2000) Technical note: production of butter with enhanced conjugated linoleic acid for use in biomedical studies with animal models. J. Dairy Sci. 83:2422-2425.[Abstract]
25. McAteer, M. A., Grimditch, D. C., Vidgeon-Hart, M., Benson, G. M. & Salter, A. M. (2003) Dietary cholesterol reduces lipoprotein lipase activity in the atherosclerosis-susceptible Bio F(1)B hamster. Br. J. Nutr. 89:341-350.[Medline]
26. Bennett, A. J., Billett, M. A., Salter, A. M., Mangiapane, E. H., Bruce, J. S., Anderton, K. L., Marenah, C. B., Lawson, N. & White, D. A. (1995) Modulation of hepatic apolipoprotein B, 3-hydroxy-3-methylglutaryl-CoA reductase and low-density-lipoprotein receptor mRNA and plasma-lipoprotein concentrations by defined dietary fats. Comparison of trimyristin, tripalmitin, tristearin and triolein. Biochem. J. 311:167-173.
27. Hara, A. & Radin, N. S. (1978) Lipid extraction of tissues with a low-toxicity solvent. Anal. Biochem. 90:420-426.[Medline]
28. Christie, W. W. (1982) A simple procedure for the rapid transmethylation of glycerolipids and cholesteryl esters. J. Lipid Res. 23:1072-1075.[Abstract]
29. Billett, M. A., Bruce, J. S., White, D. A., Bennett, A. J. & Salter, A. M. (2000) Interactive effects of dietary cholesterol and different saturated fatty acids on lipoprotein metabolism in the hamster. Br. J. Nutr. 84:439-447.[Medline]
30. Mangiapane, E. H., McAteer, M. A., Benson, G. M., White, D. A. & Salter, A. M. (1999) Modulation of the regression of atherosclerosis in the hamster by dietary lipids: comparison of coconut oil and olive oil. Br. J. Nutr. 82:401-409.[Medline]
31. Salter, A. M., Mangiapane, E. H., Bennett, A. J., Bruce, J. S., Billett, M. A., Anderton, K. L., Marenah, C. B., Lawson, N. & White, D. A. (1998) The effect of different dietary fatty acids on lipoprotein metabolism: concentration-dependent effects of diets enriched in oleic, myristic, palmitic and stearic acids. Br. J. Nutr. 79:195-202.[Medline]
32. Lichtenstein, A. H., Erkkila, A. T., Lamarche, B., Schwab, U. S., Jalbert, S. M. & Ausman, L. M. (2003) Influence of hydrogenated fat and butter on CVD risk factors: remnant-like particles, glucose and insulin, blood pressure and C-reactive protein. Atherosclerosis 171:97-107.[Medline]
33. Matthan, N. R., Ausman, L. M., Lichtenstein, A. H. & Jones, P.J.H. (2000) Hydrogenated fat consumption affects cholesterol synthesis in moderately hypercholesterolemic women. J. Lipid Res. 41:834-839.
34. Gillman, M. W., Cupples, L. A., Gagnon, D., Millen, B. E., Ellison, R. C. & Castelli, W. P. (1997) Margarine intake and subsequent coronary heart disease in men. Epidemiology 8:144-149.[Medline]
35. Pietinen, P., Ascherio, A., Korhonen, P., Hartman, A. M., Willett, W. C., Albanes, D. & Virtamo, J. (1997) Intake of fatty acids and risk of coronary heart disease in a cohort of Finnish men. The alpha-tocopherol, beta-carotene cancer prevention study. Am. J. Epidemiol. 145:876-887.
36. Willett, W. C., Stampfer, M. J., Manson, J. E., Colditz, G. A., Speizer, F. E., Rosner, B. A., Sampson, L. A. & Hennekens, C. H. (1993) Intake of trans fatty acids and risk of coronary heart disease among women. Lancet 341:581-585.[Medline]
37. Ascherio, A., Hennekens, C., Buring, J., Master, C., Stampfer, M. & Willet, W. C. (1993) A case-control study of trans fatty acid intake and risk of myocardial-infarction. Circulation 87:702.
38. Bolton Smith, C., Woodward, M., Fenton, S. & Brown, C. A. (1996) Does dietary trans fatty acid intake relate to the prevalence of coronary heart disease in Scotland?. Eur. Heart J. 17:837-845.
39. Woollett, L. A., Daumerie, C. M. & Dietschy, J. M. (1994) Trans-9-octadecenoic acid is biologically neutral and does not regulate the low-density-lipoprotein receptor as the cis isomer does in the hamster. J. Lipid Res. 35:1661-1673.[Abstract]
40. Nicolosi, R. J., Wilson, T. A., Rogers, E. J. & Kritchevsky, D. (1998) Effects of specific fatty acids (8:0, 14:0, cis-18:1, trans-18:1) on plasma lipoproteins, early atherogenic potential, and LDL oxidative properties in the hamster. J. Lipid Res. 39:1972-1980.
41. Meijer, G. W., van Tol, A., van Berkel, T.J.C. & Weststrate, J. A. (2001) Effect of dietary elaidic versus vaccenic acid on blood and liver lipids in the hamster. Atherosclerosis 157:31-40.[Medline]
42. Sessions, V. A. & Salter, A. M. (1994) The effects of different dietary fats and cholesterol on serum-lipoprotein concentrations in hamsters. Biochim. Biophys. Acta 1211:207-214.[Medline]
43. Noone, E. J., Roche, H. M., Nugent, A. P. & Gibney, M. J. (2002) The effect of dietary supplementation using isomeric blends of conjugated linoleic acid on lipid metabolism in healthy human subjects. Br. J. Nutr. 88:243-251.[Medline]
44. Tricon, S., Burdge, G. C., Kew, S., Banerjee, T., Russell, J. J., Jones, E. L., Grimble, R. F., Williams, C. M., Yaqoob, P. & Calder, P. C. (2004) Opposing effects of cis-9, trans-11 and trans-10, cis-12 conjugated linoleic acid on blood lipids in healthy humans. Am. J. Clin. Nutr. 80:614-620.
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