2-keto-4-(methylthio)butyric acid (keto analog of methionine) is a safe and efficacious precursor of L-methionine in chicks.

Relative bioefficacy and toxicity of Met precursor compounds were investigated in young chicks. The effectiveness of DL-Met and 2-keto-4-(methylthio)butyric acid (Keto-Met) to serve as L-Met precursors was quantified using Met-deficient diets of differing composition. Efficacy was based on slope-ratio and standard-curve methodology. Using L-Met as a standard Met source added to a purified diet, DL-Met and Keto-Met were assigned relative bioefficacy values of 98.5 and 92.5%, respectively, based on weight gain. Relative bioefficacy values of 98.5 and 89.3% were assigned to DL-Met and Keto-Met, respectively, when chicks were fed a Met-deficient, corn-soybean meal-peanut meal diet. Thus, both DL-Met and Keto-Met are effective Met precursor compounds in chicks. Additionally, growth-depressing effects of L-Met, DL-Met, and Keto-Met were compared using a nutritionally adequate corn-soybean meal diet supplemented with 15 or 30 g/kg of each compound. Similar reductions in weight gain, food intake, and gain:food ratio were observed for each compound. Subjective spleen color scores, indicative of splenic hemosiderosis, increased linearly (P < 0.01) with increasing intakes of each compound, suggesting a similarity in overall toxicity among these compounds. Because conversion of Keto-Met to L-Met in vivo merely requires transamination, Keto-Met may prove to be a useful supplement not only in food animal production, but also as a component of enteral and parenteral formulas for humans suffering from renal insufficiency.

Dietary encapsulated glycine influences Clostridium perfringens and Lactobacilli growth in the gastrointestinal tract of broiler chickens.

Three experiments were conducted to determine whether there is a causative relation between dietary glycine concentration and intestinal Clostridium perfringens growth in broiler chickens. Expt. 1 showed that glycine concentrations were higher (P < 0.05) in jejunum and ileum of birds fed fat-encapsulated glycine compared with crystalline glycine. In Expt. 2, 2 cages of 6 birds were assigned to 1 of 6 experimental diets formulated to contain 7.6 and 10.6, 17.8 and 40.6, 27.8 and 30.6, 37.8 and 20.6, 47.7 and 10.6, and 7.8 and 50.6 g/kg total glycine and proline, respectively, provided primarily by supplementation with encapsulated glycine or proline as required. In Expt. 3, 12 groups of 6 birds were fed 4 different diets supplemented with encapsulated glycine to achieve 7.6, 21.0, 34.3, or 47.7 g/kg total glycine. The birds were orally challenged with C. perfringens type A on d 1 and d 14-21 and killed on d 28. In Expt. 2, C. perfringens populations were higher (P < 0.05) in ileum and cecum of birds, which received either 37.8 or 47.7 g/kg total glycine compared with those fed 7.6 g/kg glycine. In Expt. 3, C. perfringens numbers were higher (P < 0.05) in ileum of birds fed either 34.3 or 47.7 g/kg dietary glycine than those given either 7.6 or 21.0 g/kg glycine. Conversely, lactobacilli counts in ileum and cecum were significantly lower in birds fed the higher levels of glycine in both experiments. High C. perfringens colonization and high intestinal lesion scores were associated with reduced performance (P < 0.05). We conclude that glycine is an important determinant of C. perfringens growth in the intestinal tract of broiler chickens.