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

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 < or = 0.05), whereas only 3 of the 80 analyzed eggs contained trace amounts of beta-sitosterol and none contained any detectable stigmasterol. 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.