Effects on Nutrient Digestibility and Growth

Two experiments were conducted to delineate the effect of dietary sinapic acid on broiler chickens, in terms of performance, toxicity and nutrient digestibility (Qiao et al., 2008). In the first experiment on 80 male broiler chicks with feeding of sinapic acid, performance from 0 to 18 days of age and the relative size of aU the internal organs and intestines were not affected by dietary treatment. The result also implied that there was no damage to skeletal muscle, heart muscle, liver, kidneys, or brain as assumed from the no change of on the serum activity of creatine kinase and lactate dehydrogenase. 

Qiao et al. (2008) in their second experiment investigated the effect of sinapic acid on nutrient retention and the retention of sinapic add in the digestive tract of 

Qiao and Classen (2003) also reported minor effects cansed by dietary treatment of sinapine on tissue measurements. The authors proposed that the hind gut might be an important metabolic site for sinapine because aU the diets containing sinapine reduced the empty weight of caeca. The ileal digestibility of SNP was 35-42%, 27-38% and 30-46% for sinapine bisulphate, sinapine ethanol extract and rapeseed meal sinapine, respectively, while faecal digestibility values were 68-72%, 65-75% and 54-63% for the same treatment groups. A major metabolic pathway of sinapine via hydrolysis into sinapic acid and choline in the digestive tract was identified. 

In an earlier stndy, Josefesson and Uppstrom (1976) evaluated the influence of sinapine on the nutritional value of rapeseed meal and white mustard meal. However, the effect of sinapine was not highly significant. In another in vivo study, Pearson et al. (1980) found that sinapine did not reduce the ability of chicks or laying hens to oxidize trimethylamine. Since the amount included in the diet was similar to that which would be provided by a diet containing 10% rapeseed meal, it was concluded that sinapine is not involved in the depression of TM A oxidation that occurs when the meal is fed and acts solely as a source of TMA in the consequent production of egg taint. 

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