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Cardiovascular Nutrition Laboratory, Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA and * National Public Health Institute, Department of Molecular Medicine, Biomedicum, Helsinki, Finland
3To whom correspondence should be addressed. E-mail: Alice.Lichtenstein{at}tufts.edu.
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ABSTRACT |
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KEY WORDS: • reverse cholesterol transport • lecithin-cholesterol acyltransferase • lipid transfer • scavenger receptor B class 1 • apolipoprotein A-I
The majority of cholesterol in blood circulates in LDL and HDL particles. Epidemiologic observations and clinical trials have consistently documented a positive relation between LDL cholesterol concentrations and cardiovascular disease (CVD)4 risk and a negative relation between HDL cholesterol concentrations and CVD risk (1). With respect to HDL, in vitro work demonstrated that this relation is mediated by the ability of HDL particles to facilitate the egress of cholesterol from peripheral tissues and its transport to the liver in a process of reverse cholesterol transport (2).
There are a number of factors that determine circulating HDL cholesterol concentrations. Apolipoprotein (apo) A-I is the main structural protein of HDL, and its concentration in plasma is positively correlated with HDL cholesterol concentrations (2,3). Lecithin-cholesterol acyltransferase (LCAT), an enzyme associated with HDL, esterifies free cholesterol in the particle, resulting in a shift from the particle surface to the core. The creation of a free cholesterol–poor HDL surface is a critical component in sustaining reverse cholesterol transport. Alterations in LCAT activity have been associated with changes in HDL cholesterol concentrations (4–7).
Another critical component of reverse cholesterol transport is the uptake of HDL-associated cholesteryl ester by scavenger receptor B class 1 (SR-B1) located on the surface of hepatocytes and steroidogenic tissues. SR-B1 is a high affinity cell surface HDL receptor that mediates the selective uptake of HDL cholesteryl ester, thus modulating HDL cholesterol concentrations as well as delivering cholesteryl esters to the liver, adrenals, ovaries, and/or testes (8). Upregulation of SR-B1 expression has been associated with decreased HDL cholesterol concentrations and atherosclerotic lesion development in experimental animal models (9).
Two transfer proteins, cholesterol ester transfer protein (CETP) and phospholipid transfer protein (PLTP), also play crucial roles in reverse cholesterol transport. CETP transfers the LCAT-generated cholesteryl ester from HDL to VLDL and LDL in exchange for triglyceride (10,11). PLTP facilitates the transfer of surface phospholipids from postlipolytic chylomicron and VLDL particles to HDL particles (12). An increase in CETP activity and a decrease in PLTP activity are both associated with an increase in aortic lesion formation (13). Although recent observations have broadened the scope of PLTP functions, a clear understanding of its role either as a pro- or antiatherogenic factor is still rather limited (12).
The fatty acid profile of the diet alters the HDL cholesterol concentrations in humans and animals. Dietary monounsaturated fatty acids (MUFA) and PUFA lower HDL cholesterol concentrations, as well as total and LDL cholesterol concentrations, relative to SFA (14,15). Dietary trans fatty acids lower HDL cholesterol concentrations relative to SFA and raise total cholesterol and LDL cholesterol concentrations relative to their cis isomers (16). This effect is thought to be mediated in part by changes in LCAT and apo A-I mRNA levels, and the activities of CETP and PLTP (3,13,17,18).
In the present study, we investigated the effect of common sources of dietary fat on components of reverse cholesterol transport with the aim of further describing the mechanism(s) by which circulating HDL cholesterol concentrations are altered. First we assessed the effect of the 3 types of dietary fat, i.e., butter, canola oil, and soybean oil, commonly found in Western type diets, that contribute relatively high levels of SFA, MUFA, and PUFA, respectively. Second, we assessed the differential effect of 2 types of saturated fat, coconut oil and butter, and hydrogenated fat (trans fatty acids), as provided by traditional stick soybean oil based margarine, relative to soybean oil in the natural state (cis fatty acids). The Charles River (CR) Golden-Syrian hamster was chosen as the experimental animal model because it is one of the few rodents that has endogenous CETP activity and was shown previously to be responsive to dietary fat type (19).
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MATERIALS AND METHODS |
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Western blot analyses of plasma apo A-I. Plasma apo A-I was determined by immunoblotting using a polyclonal rabbit antibody specific to human apo A-I (Calbiochem) that crossreacts with hamster apo A-I due to considerable consensus between primary amino acid sequences. Briefly, apo B–containing lipoproteins were precipitated using dextran-sulfate MgCl2 reagent. The proteins remaining in the supernatant were separated by homogeneous 10% SDS-PAGE after which the Western blot analysis was performed (21). Membranes were blocked with 5% nonfat milk-TBS-Tween-20, and incubated for 2 h with a 1:1000 dilution of rabbit anti- apo A-I and then for 1 h with a 1:5000 dilution of the secondary antibody, goat anti-rabbit with horseradish peroxidase (Bio-Rad). Apo A-I was normalized to glyceraldehyde-3-phosphate dehydrogenase.
Real-time PCR analysis of LCAT, apo A-I, and SR-B1.
Total RNA was extracted from liver using Qiagen Rneasy kits (Qiagen). Reverse transcription of RNA into cDNA was performed using the Pharmacia first strand synthesis kit (Amersham Pharmacia Biotech). mRNA levels were quantified using an ABI Prism 7700 Sequence Detection System (Applied Biosystems). Primers used for genes are as follows: LCAT forward primer 5'-CCA-TTG-TTA-ACC-AGA-TTC-TGT-ACC-3' reverse primer 5'-TGT-CCA-ATG-CTC-CTG-GTG-TA-3' (22), apo A-I forward primer 5'-ACC-GTT-CAG-GAT-GAA-AAC-TGT-AG-3', reverse primer 5'-GTG-ACT-CAG-GAG-TTC-TGG-GAT-AAC-3' (23) and SR-B1 forward primer 5'-AAG-CCT-GCA-GGT-CTA-TGA-AGC-3' and reverse primer 5'-AGA-AAC-CTT-CAT-TGG-GTG-GGT-A-3' (24). ABI fluorescence probes specific to each gene were used. For each sample, both the threshold cycle (Ct) for the LCAT, apo A-I, and SR-B1, and for the endogenous control, ribosomal subunit 18s, were determined to calculate 
Ct,sample (Ct,target gene – Ct, 18s) to normalize the data and correct for the differences in amount and/or quality among the RNA samples. mRNA expression levels are reported as fold differences compared with hamsters fed the control diet.
LCAT activities. LCAT activity with endogenous substrate (endogenous LCAT activity) in plasma provides a measure of enzyme activity within the context of available substrate and cofactors and was measured as previously described (25). LCAT activity with exogenous substrate (exogenous LCAT activity) provides an approximation of LCAT mass and was measured as previously described (26,27). Both endogenous and exogenous activities are expressed as µmol/(L · h).
Transfer protein activities. CETP activity was analyzed as described by Groener et al. (28). PLTP activity was measured by monitoring the transfer of radiolabeled [14C]-dipalmitoyl phosphatidylcholine from phosphatidylcholine-vesicles to HDL3 (29). The results for both CETP and PLTP activity are expressed as µmol/(L · h) (29,30).
Aortic lesion area. The aortic arch was separated from the heart immediately superior to the aortic valve and cleaned of adventitia. The section of the aorta between the aortic valve and the first bifurcation was rinsed in 60% isopropanol, bisected longitudinally, and the inner surface stained with oil red O (31). Tissues were mounted on a glass slide and a mean of 28 consecutive microscope fields per aorta were analyzed. Movement of the slide was standardized to avoid duplication of any region. Images were captured directly and digitized using the C.IMAGING system (Compix). Measurements are expressed as the percentage of the area affected.
Statistical analysis. All data are reported as the means ± SD and were analyzed among treatment groups with ANOVA (SAS). The data were analyzed to determine the effect of butter relative to canola and soybean oils and the effect of margarine relative to saturated fat and unsaturated fatty acids in the cis configuration. Transformations were used to normalize the data when appropriate and are so indicated. The Student-Newman-Keuls test was used for post hoc analysis after ANOVA. Pearson correlation coefficients were used to determine the association between selected variables. Differences were considered significant at P < 0.05.
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RESULTS |
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2 times greater than that observed in either of the groups fed the canola or soybean oil diets (Table 3). When the data were pooled, there was a positive relation between serum HDL cholesterol and plasma apo A-I concentrations (r = 0.452, P < 0.0001). The extent of aortic lesion development was small in all of these hamsters (<0.5% of surface area) and the lesion areas did not differ among the experimental diet groups (Table 3).
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Triglyceride concentrations in hamsters fed the coconut oil were significantly higher than those fed the soybean oil diet (Table 3). The butter- and margarine-fed hamsters did not differ. Both of the SFA, coconut oil and butter, significantly increased plasma apo A-I levels compared with margarine or soybean oil, in the absence of differences in HDL cholesterol levels. These data suggest that saturated fat induces a shift to more dense HDL particles enriched with apo A-I. The effect of diet on aortic lesion surface area was minimal and no differences were observed among the groups (Table 3).
Hepatic LCAT and apo A-I mRNA concentrations were 4 and 1.5 times greater, respectively, in hamsters fed the diet enriched in soybean oil relative to the other diets (Fig. 2). This effect was not reflected in rates of enzyme activity or HDL apo A-I levels, again suggesting as for the first comparison an alternative regulating factor, not accounted for in this study (Fig. 1). Differences in hepatic SR-B1 mRNA abundance were small and unlikely to have a biological effect.
Plasma CETP activity did not differ among the diet groups, whereas PLTP activity was significantly higher in hamsters fed coconut oil relative to the other diet groups (Fig. 1B, C). This difference in PLTP activity was not mirrored in HDL cholesterol concentrations (Fig. 1C). Although saturated fat and hydrogenated fat had small effects on the variables assessed, it appears that the response of Golden-Syrian hamsters to trans fatty acids is not similar to that of humans.
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DISCUSSION |
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Elevated concentrations of plasma HDL cholesterol protect the arterial wall from the development of atherosclerotic plaque facilitated by reverse cholesterol transport (2). In plasma, HDL cholesterol concentrations are modulated in a number of ways, including the uptake of the entire HDL particle (33,34), the selective uptake of cholesteryl ester by the liver and steroidogenic organs via SR-B1 (33,35), and the transfer of individual components of HDL by CETP and PLTP (13).
Apo A-I and LCAT, 2 essential components of reverse cholesterol transport, were also shown to modulate HDL cholesterol concentrations. HDL cholesterol concentration is highly correlated with the amount of apo A-I; thus, apo A-I gene expression may be an important determinant of HDL cholesterol levels (17,36). In humans, SFA were shown to increase apo A-I protein concentration, paralleling the increase in HDL cholesterol concentration, whereas PUFA and trans fatty acids decrease HDL cholesterol concentrations (4,16,37,38). Consistent with the literature, these findings show that plasma apo A-I protein and HDL cholesterol concentrations were higher in butter-fed than canola- and soybean oil–fed hamsters. The response to saturated fatty acids, trans fatty acids, and cis fatty acids with respect to HDL cholesterol levels did not differ. Apo A-I concentrations were lowest in the margarine and soybean oil groups; however, apo A-I mRNA levels were significantly higher in response to soybean oil relative to saturated and trans fatty acids. Margarine feeding decreased plasma apo A-I and hepatic apo A-I mRNA concentrations, suggesting either a potential decrease in the biosynthesis or an increase in the catabolism of HDL particles. Within the realm of the dietary fatty acid profiles used in this study, differences in hepatic apo A-I mRNA expression were not reflected in plasma apo A-I concentrations. Azrolan et al. (17) hypothesized that the lack of change in apo A-I mRNA concentration in response to dietary perturbations that alter HDL cholesterol concentrations suggests regulation at the level of translation. Importantly, inducing changes in the composition of the HDL particle can determine the lipoprotein particle’s subsequent metabolic fate.
LCAT activity depends in part on the mass of the enzyme in plasma, and in part on the substrate and cofactors available to the enzyme (5,6). In humans, LCAT deficiency is associated with lower levels of both HDL cholesterol and apo A-I. In rodents, LCAT deficiency in a gene knockout mouse model decreases both HDL cholesterol and apo A-l concentrations relative to wild-type mice. In contrast, the overexpression of LCAT has the opposite effect, i.e., higher HDL cholesterol and apo A-l concentrations relative to wild-type mice (7,39). In response to dietary perturbation in the whole animal, LCAT activity was greater in the presence of exogenous substrate after the hamsters were fed canola oil relative to butter or soybean oil diets, which was not reflected in higher LCAT activity in the presence of endogenous substrate. The lower LCAT activity with exogenous substrate observed in the butter and soybean oil groups is consistent with reports suggesting that SFA and PUFA, relative to MUFA, are a poor substrate for LCAT activity [i.e., when incorporated into the sn2-position of phosphatidylcholine (4,6)].
LCAT endogenous and exogenous activities did not differ in response to saturated and hydrogenated fat relative to polyunsaturated fat, despite a higher LCAT mRNA abundance in the soybean oil–fed group of hamsters. This may be due to lower levels of apo A-I and/or other factors such as a post-translational modification of the LCAT protein, or different levels of other factors that may alter enzyme activity such as apo A-II, an inhibitor of LCAT activity. SFA heterogeneity had little effect on components of HDL cholesterol metabolism; however, LCAT mRNA levels were higher in hamsters fed butter relative to soybean or canola oils, without an apparent change in LCAT mass as approximated by exogenous LCAT activity. This observation is in contrast to earlier work suggesting little or no change in mRNA levels of LCAT in response to saturated relative to other classes of fatty acids (40).
Although overexpression of SR-B1 is associated with lower concentrations of HDL cholesterol relative to wild-type expression, it is also associated with a decreased risk of CVD (8,41). This is thought to be due to increased rates of HDL-mediated transport of cholesteryl ester from peripheral tissues to the liver, thus reducing the CETP-facilitated transfer of cholesteryl ester to apoB-containing lipoproteins. Hepatic SR-B1 mRNA levels were higher in hamsters fed dietary unsaturated fatty acid (canola and soybean oil) relative to SFA (butter and coconut oil) and trans fatty acids (traditional stick margarine). These data suggest that the effect of dietary fatty acids on SR-B1 may be an important factor that regulates the circulatory pool of cholesterol.
Losion et al. (42) reported a correlation between decreased HDL cholesterol concentrations and increased SR-B1 protein concentrations in response to an increase in myristic acid in the diet. The absence of myristic acid in the unsaturated fatty acid groups could in part account for the decrease in HDL cholesterol concentrations and increase in SR-B1 mRNA abundance in the current study. It would be premature at this point to assume on the basis of these data that the absence of myristic acid is solely responsible for decreasing HDL cholesterol levels in these hamsters because of the importance of other factors involved in the modulation of HDL cholesterol concentrations and reverse cholesterol transport.
Due to sample limitations, HDL particle composition was not characterized. However, the data suggest that the modifications made to HDL particles as described by changes in CETP and PLTP activity may not be the major components involved in modulating HDL cholesterol concentration in response to these dietary fatty acid perturbations. CETP and PLTP activities were shown to increase in response to a high-fat and -cholesterol diet (43,44). Although dietary cholesterol is a major factor in this increase, Kurushima et al. (45) determined that the addition of saturated fat to the diet caused a more pronounced increase in activity. In our study, compared with the nonpurified diet, all of the experimental fats had significantly higher activities of both enzymes, suggesting an additive effect of dietary fat and cholesterol (data not shown). However, the butter, canola oil, and soybean oil diets did not differ in either CETP or PLTP activities. Although the groups fed the 2 types of saturated fat, coconut oil and butter, or hydrogenated fat did not differ in CETP activity, PLTP activity was significantly higher in the coconut oil group, potentially contributing to the differences observed in total and nHDL cholesterol concentrations observed among these diet groups.
Higher CETP activity is associated with lower HDL cholesterol concentrations, and an increase in aortic lesion formation and CVD risk (46,47). Higher PLTP activity was shown to be atherogenic due to a decrease in the recycling of apo A-I proteins and a change in the phospholipid composition on the surface of the HDL particle (12,48). Additional work suggested that high PLTP activities are associated with increased synthesis and secretion of hepatic VLDL particles (49). Phospholipids on the surface of HDL particles serve as substrates for LCAT, and surface phospholipid composition can regulate the uptake of cholesterol from peripheral cells (12,29,48). The hamsters in the present study had minimal aortic lesion surface area and the extent of lesion did not differ among any of the diet groups. Taken together, minimal lesion formation combined with changes in hepatic gene expression and no differences in CETP and PLTP activity levels, further suggest that under these conditions, HDL cholesterol concentrations were modulated predominantly by selective cholesterol uptake.
A limitation of this work is that the CR Golden-Syrian hamsters were fed the experimental diets for only 6 wk; it is possible that if they were fed the diets for a longer period of time, larger differences in the variables assessed might have been observed. However, Nicolosi et al. (50) reported no significant difference among plasma total cholesterol, LDL cholesterol, HDL cholesterol in hamsters fed diets enriched in oleic acid (cis 18:1) and elaidic acid (trans 18:1) after 8 wk of consuming the diet. These observations, in conjunction with the present data, suggest that the CR Golden-Syrian hamsters may not be an appropriate model with which to study the relation between trans fatty acids and CVD.
In summary, substituting unsaturated fats, canola or soybean oil, for saturated fatty acids, butter and coconut oil, lowered HDL cholesterol concentrations without altering atherosclerotic lesion formation, and increased the expression of genes involved in reverse cholesterol transport. Trans fatty acids, although having adverse effects on lipoprotein profiles in humans, appeared to be intermediate in effect between the unsaturated fatty acids and SFA in hamsters. Selective cholesteryl ester uptake by SR-B1 may be the main mechanism by which MUFA and PUFA lower HDL cholesterol concentrations.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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2 Any opinions, findings, conclusions, or recommendations expressed in this publication are those of the author(s) and do not necessarily reflect the view of the U.S. Department of Agriculture.
4 Abbreviations used: apo, apolipoprotein; CETP, cholesterol ester transfer protein; CR, Charles River; Ct, threshold cycle; CVD, cardiovascular disease; LCAT, lecithin-cholesterol acyltransferase; MUFA, monounsaturated fatty acid; nHDL, non-HDL; PLTP, phospholipid transfer protein; SR-B1, scavenger receptor B class 1.
Manuscript received 21 October 2004. Initial review completed 24 November 2004. Revision accepted 20 December 2004.
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