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Feeding laying hens a bioavailable soy sterol mixture fails to enrich their eggs with phytosterols or elicit egg yolk compositional changes

Department of Poultry Science, The Pennsylvania State University, University Park 16802

¹ Corresponding author: relkin{at}psu.edu

	ABSTRACT

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Coronary heart disease (CHD) is the leading cause of death in the United States. Elevated levels of plasma total cholesterol (TC), and particularly plasma low density lipoprotein-cholesterol (LDLC), are primary contributing factors to CHD. Dietary plant sterols (phytosterols) have been shown to significantly reduce plasma TC and LDLC in humans, primarily through inhibition of intestinal cholesterol absorption, and are potentially effective agents for reduction of CHD risk. Although a variety of phytosterol-containing foods are currently available, phytosterol-enriched eggs, which represent a potential value-added product, are conspicuously absent from the marketplace. Therefore, the objectives of this study were 1) to enrich shell eggs with phytosterols; and 2) to determine if feeding phytosterols to hens elicits egg compositional changes, particularly that of yolk cholesterol content. Sixteen 32-wk-old White Leghorn hens were fed a corn-soy-based layer diet without (n = 8) or with (n = 8) 1 g of supplemental soy sterols/100 g of diet for 28 d.. Hen performance was determined on an individual basis, and 1 egg/hen per week was collected, processed, and analyzed for yolk cholesterol, CP, crude fat (CF), and phytosterol content. There was no effect (P > 0.05) of supplemental dietary phytosterols on 28-d weight gain, feed consumption, feed efficiency, plasma TC, hen-day egg production, egg weights, egg component weights, and yolk cholesterol, CP, and CF contents. Small amounts of campesterol were present in most of the eggs (average of 0.29 and 1.02 mg/yolk for control vs. soy sterol-fed hens, respectively; P 0.05), whereas only 3 of the 80 analyzed eggs contained trace amounts of β-sitosterol and none contained any detectable stig-masterol. It was concluded that phytosterols are either poorly absorbed from the chicken intestine or, if they are absorbed, they are efficiently secreted back into the intestinal lumen, most likely via as yet uncharacterized adenosine triphosphate-binding cassette transporters.

Key Words: campesterol • cholesterol • egg yolk • laying hen • phytosterol

	INTRODUCTION

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Phytosterols are plant-derived sterols that are structurally similar and functionally analogous to cholesterol in vertebrate animals (Ostlund, 2002). Campesterol, sitosterol, and stigmasterol, which are the most commonly encountered phytosterols in higher plants (Moreau et al., 2002), share an identical ring structure to cholesterol but are distinguished by the presence of methyl (campesterol) and ethyl (sitosterol and stigmasterol) groups at the C24 position of the side chain. Stigmasterol also contains an unsaturated double bond between carbons 22 and 23 of the side chain.

Phytosterols have been used as blood cholesterol-lowering agents for more than 50 yr (Kritchevsky and Chen, 2005). They are thought to act primarily in the intestinal lumen, where they compete with cholesterol for incorporation into absorptive micelles and thereby decrease the solubility of cholesterol and inhibit the intestinal uptake of both dietary and endogenously produced (biliary) cholesterol (Ostlund, 2007). Because coronary heart disease (CHD) is the leading cause of death in the United States, and elevated levels of plasma total cholesterol (TC) and plasma low density lipoprotein-cholesterol (LDLC) are primary contributing factors to CHD, phytosterols are recognized today as an important component of diets designed to reduce the risk of CHD (Ostlund, 2007).

Peterson (1951) was the first to show that dietary soybean sterols could inhibit the elevations of plasma and liver cholesterol in cholesterol-fed animals (Single Comb White Leghorn chicks), and the initial report of their effectiveness in humans appeared shortly thereafter (Pollak, 1953). Originally presented as a pharmaceutical formulation, phytosterols have since been incorporated into a variety of human foodstuffs, where they have been shown to be effective and safe (Kritchevsky and Chen, 2005). However, phytosterol-enriched eggs, which represent a potential value-added product, are conspicuously absent from the marketplace because the avian egg (chicken and quail) appears to be refractory to phytosterol enrichment through alteration of the hens’ diet (Boorman and Fisher, 1966; Weiss et al., 1967; Godfrey et al., 1976; Kudchodkar et al., 1976; Dam et al., 1979).

One exception to the current dogma is the work of Clarenburg et al. (1971), who reported that feeding either 2 or 4% β-sitosterol to laying hens resulted in a marked incorporation of β-sitosterol (~42 mg maximal) into egg yolks. However, this observation, as well as a concomitant β-sitosterol-mediated 35% reduction in egg yolk cholesterol content, has never been confirmed by others. One possible explanation for these discrepant findings is that Clarenburg et al. (1971) did not measure yolk phytosterol contents directly by conventional gas chromatographic methods; instead, they determined total yolk sterol contents using a nonspecific FeCl₃ color reaction and calculated sitosterol contents based on the total radioactivity of the egg yolk samples and the specific activity of tritiated dietary β-sitosterol, which was fed to the hens along with the unlabeled β-sitosterol. Thus, actual mass determination of β-sitosterol was not made and, as pointed out by Kudchodkar et al. (1976), the high values for β-sitosterol absorption reported by Clarenburg et al. (1971) might have been due to bacterial degradation of the sterol ring structure during intestinal transport.

The phytosterol formulation can also contribute to the variability of response, as demonstrated in human clinical studies (Moreau et al., 2002; Ostlund, 2002). Purified phytosterols form highly stable crystals that are not readily soluble in bile salt solutions. Thus, consistent plasma LDLC lowering in humans has been most effectively attained with phytosterol preparations dissolved in oil or egg fat, emulsified in aqueous medium with monooleate or lecithin, or finely micronized and mixed with fatty foods (Ostlund, 2002). A newer approach to enhancing the bioavailability of unesterified sterols and stanols involves rendering them water-dispersible through the formation of lecithin micelles (Ostlund et al., 1999).

Because some uncertainty remains as to whether phytosterol enrichment of eggs can be attained at the expense of yolk cholesterol by feeding laying hens plant sterols, the objectives of this study were 2-fold: 1) to determine if phytosterols can be incorporated into egg yolk by feeding hens a highly bioavailable (lecithin micelle) formulation; and 2) to determine the influence of dietary phytosterols on egg yolk composition, particularly that of cholesterol content.

	MATERIALS AND METHODS

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Birds, Housing, and Management

Sixteen 32-wk-old White Leghorn hens were selected from The Pennsylvania State University flock. The birds were housed in individual 40 x 45 x 50 cm cages in an environmentally controlled room (24°C and 16 h of light daily) in the Layer Research Unit of the Poultry Education and Research Center. Hens were assigned to 1 of 2 dietary treatments [control layer diet or the control diet plus 1% soy sterols (n = 8); see below] based on egg production and egg weights during the 14 d immediately preceding the initiation of the study. During this preexperimental period, both groups averaged 97.32% hen-day egg production [(100 x number of eggs laid)/(number of hens x d); data not shown]. Egg weights (mean ± SD) averaged 55.09 ± 3.49 g and 54.73 ± 3.04 g for the birds subsequently fed the control and soy sterol-supplemented diets, respectively (data not shown).

Diets and Ingredients

The soy sterol product [450 g of ChoLESStolife active substance + 450 g of soy lecithin + 100 g of maltrin (a maltodextrin used as a spray-drying aid)] and placebo (450 g of cellulose + 450 g of soy lecithin + 100 g of maltrin) were prepared according to Ostlund et al. (1999) and provided by Lifeline Technologies Inc. (Chesterfield, MO) in the form of a lyophilized powder. The phytosterol product contained 33.20% β-sitosterol, 14.90% campesterol, and 6.17% stigmasterol by analysis, whereas the placebo contained 0.07% β-sitosterol, 0.01% campesterol, and 0.01% stigmasterol by analysis (Table 1). Two pounds (907.2 g) each of the soy sterol product or the placebo were mixed with 98 pounds (44.453 kg) of a corn-soybean meal-based commercial layer diet (MW-122; Wenger Feeds, Rheems, PA) that was calculated to contain 17.4% CP, 2,900 kcal of ME/ kg, 3.86% calcium, and 0.42% available phosphorus. Analyses of the 2 diets (Table 1) confirmed that the ChoLESStolife active substance had been appropriately diluted and provided a total of approximately 1% of the diet as soy sterols (0.603% β-sitosterol + 0.272% campesterol + 0.118% stigmasterol) whereas the control diet contained a small amount of β-sitosterol and campesterol, which most likely were of plant origin (i.e., from corn and soybean meal). Because the proprietary layer diet contained poultry by-product meal (Joseph M. Garber, Wenger Feeds; personal communication), a small amount of cholesterol (0.011% by analysis) was detected in both the control and the soy sterol-supplemented diets, which also contained similar amounts of calcium and CP (Table 1).

Eight hens each were fed the control diet or the soy sterol-containing diet for 28 d. Feed and water were provided for ad libitum consumption throughout the study. Body weights were determined on d 0 and 28, and feed consumption and egg weights were determined daily. Egg component (yolk, albumen, and shell) weights were obtained on an individual basis from 1 egg per hen per week on d 0, 7, 14, 21, and 28. On d 28, blood samples were obtained via brachial vein puncture from each hen using heparinized 21-gauge x 3.81 cm needles and 4.5-mL syringes (Sarstedt Inc., Newton, NC). The blood samples were kept on ice and subsequently centrifuged at 1,000 x g for 10 min at 4°C. Plasma was stored at –80°C until analysis for TC content. All animal handling protocols were approved by The Pennsylvania State University Institutional Animal Care and Use Committee.

Analytical Methodologies

Supplements and Diets. The placebo, soy sterol supplement, and both the control and phytosterol-supplemented diets were analyzed for CP (method 990.03; AOAC International, 2000) and sterol contents (method 994.10; AOAC International, 2000), whereas only the 2 diets were analyzed for calcium content (method 968.08; AOAC International, 2000). All analyses were conducted by a commercial laboratory (Ralston Analytical Laboratories, St. Louis, MO). In all instances, the analytical laboratory personnel were unaware of the sample treatments.

Egg Yolks and Blood Plasma Samples. Eggs were collected as described above, weighed, and the yolks were separated as described previously (Elkin et al., 1999). Each yolk was then transferred to an individual 150-mL polypropylene sample cup, stirred to homogeneity with a spatula, and lyophilized. Yolk CP (method 990.03; AOAC International, 2000), crude fat (CF; method 920.39; AOAC International, 2000), and cholesterol (method 941.09; AOAC International, 2000) contents were determined by a commercial laboratory (Experiment Station Chemical Laboratories at the University of Missouri, Columbia). Blood plasma TC and egg yolk phytosterol contents were determined by Ralston Analytical Laboratories based on AOAC International (2000) method 994.10. Yolk and plasma sample identification numbers were coded before submission to the commercial laboratories such that the analysts were unaware of the dietary treatments.

Statistical Analyses

Analysis of variance (Steel and Torrie, 1980) was performed on all data using the GLM procedure (SAS Institute, 1989). Arc sin transformations (Steel and Torrie, 1980) were performed on all percentage data. Because the statistical patterns were similar for both transformed and untransformed results, only the latter are presented. In situations where egg components or nutrient contents were assessed over time, a 2-way ANOVA was conducted to account for the effects of diet, day, and the interaction of diet x day. Individual treatment differences were tested by Duncan’s multiple range test (Steel and Torrie, 1980). Treatment differences at P 0.05 were considered significant.

	RESULTS

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Hen BW and Overall Performance

There was no significant effect of dietary soy sterols on BW gain, daily feed consumption, feed efficiency, hen-day egg production, or weights of all eggs laid during the 28-d study (Table 2). In addition, no birds died during the experiment (data not shown).

Diet had no significant influence on egg, yolk, albumen, or shell weights; only yolk weights were significantly affected by day (age of the hen; Table 3). However, because the birds were 32 wk old at the onset of the trial, it was not unexpected that egg or egg component weights might increase as the study progressed. No 2-way (diet x day) interactions were observed for egg or egg component weights (Table 3). Although hens were allocated to diets based on 14-d preexperimental egg production and egg weights to equalize these variables, eggs from phytosterol-fed hens had an overall greater relative percentage of albumen than eggs from control hens, and the difference was evident beginning on d 0 (Table 4). In contrast, there was no influence of diet on the relative percentages of yolk or shell (Table 4). Egg component percentages were also unaffected by day, and there were no significant 2-way (diet x day) interactions (Table 4).

Diet did not significantly affect either yolk cholesterol contents (expressed as mg/g of yolk or as mg/ yolk; Table 5) or mean 28-d plasma TC concentrations (control hens, 158.3 mg/100 mL; soy sterol-fed hens, 157.1 mg/100 mL; data not shown). In contrast, relative yolk cholesterol contents (mg/g of yolk) decreased (P 0.05) as the study progressed (Table 5). Because yolk weights increased weekly (Table 3), total yolk cholesterol contents (mg/yolk) were not significantly affected by day (Table 5). Significant (P 0.05) 2-way interactions for cholesterol content (expressed as mg/g of yolk or as mg/yolk) were observed because, compared with control eggs, the cholesterol contents of eggs from soy sterol-fed birds increased between d 7 and 14, whereas the opposite occurred between d 14 and 21 (Table 5). A biological explanation for this observation is not readily apparent.

View larger version (22K): [in this window] [in a new window]   Figure 1. Relative (mg/g of yolk) and total (mg/yolk) campesterol contents of eggs of hens fed a corn-soybean meal-based layer diet without (control) or with 1% soy sterols for 28 d. Regardless of how campesterol content was expressed (i.e., as mg/g of yolk in the upper panel or as mg/yolk in the lower panel), significant main effects (diet, day) as well as the 2-way interaction (diet x day) were observed. a–cBars with no common letters are significantly different (P 0.05).

Although there were significant effects of day on yolk CP content (mg/g of yolk), no consistent pattern was noted (Table 6). However, when expressed on a per-yolk basis, CP contents increased each week. A similar trend was noted for CF (per-yolk basis; exception of d 21 value). This most likely was a reflection of relatively constant protein and fat contents (on a per gram of yolk basis) combined with increasing weekly yolk weights (Table 3).

	DISCUSSION

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Because eggs are among the most cholesterol-rich foodstuffs consumed by humans, their enrichment with phytosterols might initially seem paradoxical in terms of developing a human food product designed to decrease plasma TC concentrations. However, the present work was conducted with the anticipation that supplemental dietary phytosterols would also competitively replace a significant amount of cholesterol and cholesterol esters in hepatically synthesized very low density lipoprotein (VLDL) particles, which are the major yolk precursor macromolecules. In sexually mature hens, VLDL is secreted by the liver into the bloodstream, taken up by growing oocytes via receptor-mediated endocytosis, and is intracellularly transformed into yolk, where it constitutes approximately 60% of its dry matter (Burley et al., 1993) and 95% of its cholesterol (Griffin, 1992).

Unfortunately, in the present study, less than 1% of yolk cholesterol was replaced by campesterol (~1.5 mg/187 mg), and virtually no β-sitosterol or stigmasterol was incorporated into the yolks of eggs of soy sterol-fed hens. However, because the rank order of intestinal sterol absorption rates in mammals is cholesterol > cholestanol > campesterol > sitosterol (von Bergmann et al., 2005; Yu, 2008), it was not surprising that campesterol was the main phytosterol incorporated into the eggs of soy sterol-fed hens. This finding agreed with the report of Boorman and Fisher (1966), who fed laying hens a semipurified, isolated soy protein-based diet supplemented with 3% corn sterols (89.0% β-sitosterol, 9.6% campesterol, and 1.3% stigmasterol) and observed that all 5 of the analyzed eggs contained campesterol and cholesterol (approximately 0.5 and 99.5% of total detectable sterols, respectively). β-Sitosterol was found to be present in only 1 of the 5 eggs (0.2% of total detectable sterols), whereas no detectable phytosterols were found in the eggs of hens fed the semipurified diet containing no supplemental corn sterols.

Phytosterols are inherently hydrophobic and tend to form stable crystals, which are not very bioavailable (Ostlund, 2007). In contrast, the bioavailability of purified phytosterols can be greatly enhanced by formulation with lecithin (Ostlund et al., 1999). Thus, although the dietary soy sterols were present in a highly bioavailable form (phytosterol/lecithin complexes) and may have been readily absorbed by the laying hens in this study, it is likely that the phytosterols were re-secreted into the intestine via as yet uncharacterized (in the chicken) adenosine triphosphate-binding cassette transporter G5 (ABCG5) and G8 (ABCG8), which function together as a heterodimer and are located in both enterocytes and hepatocytes (Wang et al., 2006). It has been hypothesized that the ABCG5 and ABCG8 co-transporters are able to discriminate between cholesterol and other sterols and pump noncholesterol sterols out of the enterocyte back into the intestinal lumen and also into bile (Igel et al., 2003). Another recently identified major player in intestinal sterol transport is Niemann-Pick C1 Like 1 protein (NPC1L1), which has been shown to be essential for intestinal cholesterol absorption (Altmann et al., 2004). Niemann-Pick C1 Like 1 protein also mediates the intestinal absorption of phytosterols albeit with unequal affinities (Yu, 2008).

The results of the present study suggest that the chicken egg is refractory to phytosterol enrichment through alterations of the laying hens’ diet. Moreover, it is likely that, as in mammals, as yet uncharacterized avian homologs of ABCG5, ABCG8, and NPC1L1 function cooperatively to limit the net intestinal absorption of phytosterols in the chicken. In theory, it might be possible to overcome this putative gatekeeping system by feeding laying hens greater amounts or different combinations of phytosterols or phytostanols (which are saturated plant sterols) than were employed in the present study. However, the successful enrichment of hepatic VLDL particles and, consequently, egg yolks with phytosterols will most likely be achieved via a combination of dietary (phytosterol feeding) and biotechnological approaches (i.e., the knock down of ABCG5, ABCG8, and NPC1L1 genes). However, analogous to the envisioned production of low-cholesterol eggs via transgenic technology (Elkin, 2007), the commercial availability of phytosterol-enriched eggs will ultimately be influenced by regulatory issues, public acceptance, and economics.

	ACKNOWLEDGMENTS

 
This work was supported in part by a grant from Lifeline Technologies Inc. (Chesterfield, MO). The helpful comments of Curtis A. Spilburg (Lifeline Technologies Inc.) are greatly appreciated.

Received for publication July 3, 2008. Accepted for publication September 29, 2008.

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Elkin, R. G. Articles by Lorenz, E. S. Search for Related Content PubMed Articles by Elkin, R. G. Articles by Lorenz, E. S.