Fishy-egg tainting is recessively inherited when brown-shelled layers are fed canola meal

Abstract

Feeding canola meal to brown-shelled laying hens can result in the production of eggs with a fishy odor. This fishy taint is caused by the accumulation of trimethylamine (TMA) in the yolk. Trimethylamine is produced by the bacterial fermentation of choline in the lower gut. Fishy-egg tainting is caused by a SNP in flavin-containing monooxygenase 3 (FMO3 c.984A > T), rendering the hen unable to metabolize TMA into the nonodorous TMA N-oxide. The purpose of this study was to characterize the inheritance pattern of fishy-egg tainting when hens are fed canola meal at levels reflecting maximum use based on conventional formulation of laying hen diets. Additionally, we wished to examine the effect of choline source (choline chloride vs. canola meal) on egg tainting. In the first of 2 experiments, 6 hens per genotype (AA, AT, and TT) were allocated to each of 5 dietary treatments (0, 6, 12, 18, or 24% canola meal) for 4 wk. Three yolks per hen collected in the last week of the trial were analyzed for TMA concentration. There was a significant linear regression (P < 0.05) between yolk TMA concentration and dietary canola meal level for hens of the TT but not the AA or AT genotypes. In the second experiment, 6 hens of the TT (homozygous tainting) genotype were each assigned to 1 of 9 dietary treatments: the 5 diets used in the first experiment plus 4 diets that used choline chloride to match the total choline concentration of the 6, 12, 18, and 24% canola meal diets, respectively. Three yolks per hen were analyzed for TMA concentration. A significant response in yolk TMA concentration was seen with the canola meal diets but not the choline chloride diets. We conclude that fishy-egg tainting is recessively expressed when hens are fed canola meal at levels from 12 up to 24% inclusion. We also conclude that choline chloride, at levels typical of commercial egg production, will not lead to egg tainting.