Jerry L. Sell

Three experiments were conducted to determine the effect of dietary vitamin K₁ (K₁) on selected plasma characteristics and bone ash in poults. In Experiment 1, diets were supplemented with 0, 0.5, 1.0, or 2.0 mg of K₁/kg. All diets contained 1,650 IU of vitamin D₃ (D₃)/kg. Dietary K₁ had no effect on tibia ash at 7 d or incidence of a severe, rickets-like condition. Tibia ash of poults fed 2.0 mg of K₁/kg, however, was greater at 14 d of age than that of poults fed the basal diet. Dietary inclusion of 0.5 mg of K₁/kg was as effective as 1 or 2 mg of K₁/kg in reducing plasma prothrombin time. In Experiment 2, a 2 x 4 factorial arrangement was used consisting of 1,650 or 550 IU of D₃/kg and 0.1, 0.45, 1.0, and 2.0 mg of K₁/kg. Dietary D₃ and K₁ had no effect on bone ash. Dietary inclusion of 0.1 mg of K₁/kg seemed to be enough to minimize plasma prothrombin time. In Experiment 3, dietary treatments consisted of a control (1,650 IU of D₃ and 2.0 mg of K₁/kg) and K₁ concentrations of 0, 0.37, 2.28, or 5.33 mg/kg in diets containing 275 IU of D₃/kg. Poults fed the low-D₃ diet without K₁ consumed less feed, gained less weight, and had increased plasma alkaline phosphatase activity, decreased inorganic phosphorus level, and decreased tibia ash (P < 0.05) compared with those of poults fed the control diet. Feed intake and body weight gain were improved, plasma alkaline phosphatase activity decreased, and plasma inorganic phosphorus increased or tended to increase when poults were fed the low-D₃ diet supplemented with 0.37 or 2.88 mg of K₁/kg compared with poults fed the low-D₃ diet without K₁ supplementation. Tibia ash of poults fed the low-D₃ diet was not affected by K₁ supplementation. The results of this research show that dietary K₁ concentration had little, if any, effect on bone development in 1- to 14-d-old turkeys.

In a preliminary experiment, the inclusion of vitamin K₁ (K₁) at a dietary level of 0.1 mg/kg was as effective as 1 or 2 mg/kg in reducing plasma prothrombin time (PT). To obtain an estimate of the dietary K₁ requirement and to compare the biopotency of different vitamin K sources for poults, three additional experiments were conducted. In Experiment 1, an incomplete factorial arrangement of treatments was used in which five dietary concentrations of K₁ (0, 0.1, 0.25, 0.5, or 2.0 mg/kg) were tested and two concentrations of neomycin (0 or 75 mg/L) in drinking water were used in conjunction with 0, 0.1, and 0.5 mg of K₁/kg of diet. Thus, we used a total of eight treatments. Each treatment was given to two pens of poults, with eight poults per pen. Prothrombin time and prothrombin concentration (PC) in plasma were not influenced by inclusion of neomycin in drinking water. The K₁ requirement was estimated, on the basis of PT and PC, to be 0.099 and 0.13 mg/kg, respectively, in Experiment 1. Dietary K₁ concentrations tested in Experiment 2 were 0, 0.08, 0.31, or 0.44 mg/kg. A similar protocol to that of Experiment 1 was used in this experiment. The results of Experiment 2 indicated that the dietary K₁ requirement was 0.079 mg, based on the influence of dietary K₁ on PT. In Experiment 3, dietary treatments consisted of the equivalent of 0.22, 0.55, or 1.11 microM of menadione equivalent/kg from vitamin K₁, menadione dimethypyrimidinol bisulfite (MPB) or menadione nicotinamide bisulfite (MNB), respectively, and a control without supplementation of any vitamin K source. The results of Experiment 3 showed that the biopotency of K₁ was greater than that of MPB or MNB. The biopotencies of MPB and MNB were similar, although MNB was more potent in reducing plasma PT when supplemented at the level of 0.1 mg of menadione/kg. A nadir of PT and a plateau of PC were evident with a dietary supplementation of MPB or MNB at a level of 0.25 mg of menadione/kg. Results of this research show that the dietary K₁ requirement of young turkeys is in the range of 0.079 to 0.13 mg/kg, and ingestion of neomycin did not affect estimates of the requirement. The biopotency of vitamin K₁ in reducing plasma PT and increasing plasma PC was greater than that of MPB or MNB. The biopotency of MNB was greater than that of MPB when menadione supplementation was equivalent to 0.10 mg of K₁/kg.

Two experiments with broiler chicks and one experiment with laying hens were conducted to determine the MEn value of conjugated linoleic acid (CLA). In Experiment 1, for 8 d, 16-d-old chicks were fed diets in which 4, 8, or 12% of CLA Source A or 4, 8, or 12% of soybean oil (SO) was substituted for glucose. Dietary MEn increased linearly (P < or = 0.001) with increments of CLA Source A or SO. Regression analysis relating increases in dietary MEn and increments of the dietary fat sources showed that the MEn values of CLA Source A and SO, when evaluated separately, were 7,419 and 8,429 kcal/kg, respectively. In Experiment 2, feed was withheld from laying hens for 38 h and then the hens were force-fed diets containing 15% glucose, 15% CLA Source A, or 15% SO (two feedings of 30 g each). Excreta samples were collected for 36 h after the last feeding. The MEn values obtained for CLA Source A and SO were 8,517 and 8,437 kcal/kg, respectively. The MEn of CLA Source B (higher in unsaturated fatty acids than CLA Source A) was determined in Experiment 3 by feeding diets containing 4, 8, or 12% CLA Source B to 14-d-old chicks. Increases in dietary MEn with increments of CLA Source B were curvilinear, with resulting MEn of 9,375 to 9,588 kcal/kg of fat when CLA Source B was fed at 4 or 8% of the diet and 7,917 kcal/kg when fed at 12% of the diet. Results of this research show that CLA sources can contribute substantial energy to diets, but the MEn value of CLA sources for young chicks varies with fatty acid composition and dietary concentration.

There is interest in increasing the conjugated linoleic acid (CLA) content of foods because of purported benefits of CLA for human health. Two experiments were conducted to determine the influence of dietary CLA concentration on CLA content of eggs. In Experiment 1, diets containing 0, 0.5, 2.5, or 5.0% CLA were fed to 26-wk-old White Leghorn hens (Hy-Line W-77) for 29 d. No CLA was detected in the yolk lipids of hens fed the control diet. Concentration of CLA in the yolk lipids linearly increased as dietary CLA increased. The maximum concentrations of CLA in the yolk lipids of hens fed 0.5, 2.5, or 5.0% CLA occurred 11 d after the start of the experiment and were 0.82, 5.82, and 11.20% of the total fatty acids, respectively. Concurrent decreases were observed in concentrations of C18:1, C18:2, C18:3, C20:4, and C22:6. Rate of egg production, body weight gain, and feed intake were not affected by dietary CLA. Average weights of eggs and yolks were decreased for hens fed 5.0% CLA compared with other dietary treatments. In Experiment 2, 62-wk-old hens were fed diets containing 0 or 5.0% CLA. Maximum CLA concentration in the yolk lipids of hens fed 5.0% CLA was less (7.43%) than that observed in Experiment 1. Feeding 5.0% CLA decreased feed intake but did not affect rate of egg production, weight of eggs, albumens, or yolks, or body weight gain through 36 d. Results of these experiments show that eggs produced by hens fed 5.0% CLA will contain 310 to 365 mg of CLA per egg. Such eggs could provide a substantial amount of CLA source in human foods.

Three experiments were conducted with turkeys to determine the influence of delayed access to feed and water on the development of the digestive system. In all experiments, poults were randomly assigned to three placement times, 6, 30, and 54 h posthatch. Experiments 1, 2, and 3 were terminated when poults were 10, 28, and 14 d old, respectively. In Experiment 1, six poults per treatment were sampled on Days 1, 2, 3, 4, 5, 6, 8, and 10. In Experiment 2, 12 poults per treatment were sampled on Days 1, 2, 3, 4, 5, 10, 15, and 28. The objective of Experiment 3 was to determine the effect of delayed placement on dietary MEn. Delaying access to feed and water for 54 h adversely affected BW through 10, 28, and 14 d of age in Experiments 1, 2, and 3, respectively (P < or = 0.01). Delayed access to feed and water for 54 h decreased the absolute weights of the small intestine and pancreas and reduced lengths of the small intestine through 5 d posthatch (P < or = 0.05). The relative weights of the small intestine and proventriculus were reduced by delayed access to nourishment through 4 d posthatch. Poults placed on feed at 54 h posthatch had decreased pancreatic amylase activity (P < or = 0.05) at 3 and 4 d, and trypsin activities were depressed at 3 d posthatch (P < or = 0.05). In Experiment 3, dietary MEn value determined at 4 d of age with poults placed 54 h posthatch was less (P < or = 0.07) than the MEn value obtained with poults placed at 6 h posthatch. A 54-h delay in access to feed and water generally delayed development of the digestive system, impaired nutrient utilization, and reduced BW.