Feeding broiler chicks diets containing keto- and hydroxy-acids: performance and carcass weight.

This study evaluated reduced dietary CP and supplementing amino acid analogs to sustain growth and carcass weight in 0- to 21-day-old Cobb × Avian-48 male broiler chicks. A total of 6 diets with 3 levels of CP (22.5, 19.5, and 16.5%) and 2 sources of AA analogs, either synthetic amino acids (SA) or keto-/hydroxy-acids (KA), were assigned randomly to 36 cages (8 chicks/cage) in a 3 × 2 factorial design. For SA diets, DL-Met, DL-Met + L-Ile, and D-Met + L-Ile + L-Val were used to supplement 22.5, 19.5, and 16.5% CP diets, respectively, and for corresponding KA diets, DL-Met was replaced with methionine hydroxy analog (MHA), L-Ile was replaced with keto-Ile, and L-Val was replaced with keto-Val. Water and all isocaloric diets (3,050 kcal ME/kg) were given ad libitum. Lowering dietary CP to 16.5% reduced BW at 7, 14, and 21 D (P ≤ 0.0001) and feed intake at 8 to 14, 15 to 21, and 0 to 21 D (P ≤ 0.001). Body weight gain (BWG) was reduced and feed-to-gain ratio (FGR) was increased (P ≤ 0.003 to 0.0001) at all times for chicks fed 16.5% CP; however, chicks fed 22.5 and 19.5% CP had comparable performance. Differences in 0 to 7 D BWG (SA, 122.9 vs. KA, 113.9 g/bird; P ≤ 0.04), a 0 to 21 D FGR cumulative effect (1.45 vs. 1.51; P ≤ 0.02), and a 15 to 21 D (P ≤ 0.04) and 0 to 21 D (P ≤ 0.05) CP × AA interaction were also observed. Greater liver weight among 16.5 vs. 19.5 or 22.5% CP fed chicks was found at 14 and 21 D (P ≤ 0.0001 and P = 0.06, respectively). Lower dietary CP reduced spleen weight on day 21 birds (P ≤ 0.0005) with lighter spleens among 16.5 and 19.5% vs. the 22.5% CP fed group (0.090, 0.095, 0.119 g/100 g BW, respectively). Breast weight at 21 D was significantly less for 16.5 vs. 22.5% CP fed chicks. Fat pad weight on day 21 was heaviest among 16.5% chicks (P ≤ 0.0004). Overall, lowering dietary CP to 16.5% had a negative effect, but keto-acid supplementation supported 0 to 21 D broiler growth compared to SA; however, transamination efficiency of KA may be lower for 0 to 7D old chicks compared to older birds.

Dietary camelina meal versus flaxseed with and without supplemental copper for broiler chickens: live performance and processing yield.

An experiment was conducted to compare the responses of young broiler chickens to corn-soybean meal diets supplemented with flaxseed or camelina meal versus a corn-soybean meal control and the factorial effect of 150 mg/kg of Cu supplementation on performance and processing yield. A randomized complete block design with a 2 x 3 factorial arrangement was used with 7 replicates from hatch to 21 d of age (n = 294; 7 chicks per replicate). Body weight of birds fed 10% camelina meal or 10% flaxseed was significantly reduced compared with the control birds. Addition of Cu significantly increased BW and feed consumption of the birds fed the control diet throughout the study. Copper supplementation to the 10% camelina meal diet also increased BW (P < 0.001) with no effect on feed consumption or feed conversion at 21 d. In addition, hot carcass weight, yield, and carcass parts were significantly improved among birds fed the Cu-supplemented control diet. A significant Cu x diet interaction was observed for hot carcass weight and yield, indicating Cu supplementation to the control diet was superior for carcass weight to the other treatments. However, yield was greater for the camelina diets and the control + Cu versus the other treatments. Results from the present study demonstrated that either 10% camelina meal or 10% flaxseed diets will reduce broiler BW when fed the first 3 wk of life. However, birds fed the camelina diet responded to Cu sulfate supplementation with improved live performance and carcass characteristics. Birds fed the 10% flaxseed diets showed no beneficial effect resulting from Cu supplements.

Effects of dietary zinc supplementation on hen performance, ammonia volatilization, and nitrogen retention in manure.

This investigation was undertaken to evaluate the effects of dietary ZnSO4 supplementation on ammonia volatilization and nitrogen retention in hen manure. One hundred twenty, 45-wk-old commercial Leghorn laying hens were sequentially fed diets with 1000, 2000, and 3000 ppm Zn as ZnSO4 (Zn-1000, Zn-2000, and Zn-3000), then followed by two control dietary periods with 114 ppm Zn (Control-1 and Control-2) for a total of five consecutive eight-day experiment periods, respectively. When hens were fed the 1000 and 2000 ppm Zn treatment diets, room ammonia levels were significantly reduced compared to the control diets. Dietary Zn treatments reduced the decomposition of uric acid, resulting in an increase in manure total-N retention compared to the control fed birds. The 1000 ppm Zn supplement had no adverse effects on hen body weight, feed consumption, egg production, egg weight, albumen height, or shell thickness. However, hens fed the diet containing 3000 ppm Zn had significantly depressed body weight, feed consumption, egg production, egg weight, and shell thickness. Zinc levels of egg contents increased linearly as dietary Zn levels increased. These levels in eggs would not be a problem for human consumption because these are much less than the daily Zn recommended dietary allowance. Although land application of such manure will not cause environmental problems or crop toxicity, proper monitoring of soil and crop Zn levels and effective nutrient management planning would be well advised.

Effects of dietary zinc supplementation on broiler performance and nitrogen loss from manure.

An experiment was conducted to evaluate the effects of ZnSO4 or ZnO supplementation of broiler diets on growth performance and loss of uric acid N and total N from manure. A total of 240, 1-d-old broiler males were used for this experiment. Each dietary treatment was replicated 3 times with 10 birds per replicate. Chicks were fed a control diet for the first 6 d and then treatment diets for the next 12 d. There were 8 dietary treatments: the control, CuSO4-20, ZnSO4-500, ZnSO4-1,000, ZnSO4-1,500, ZnO-500, ZnO-1,000, and ZnO-1,500 containing 0, 0, 500, 1,000, 1,500 ppm supplemental Zn as ZnSO4 and 500, 1,000, and 1,500 ppm supplemental Zn as ZnO, respectively. A 300-g sample of the broiler manure from each treatment was incubated in a pan for 3 wk at room temperature. After incubation, samples were collected for the measurement of total N and uric acid N. Weight gain, feed consumption, and feed efficiency of chicks fed the diets supplemented with 1,500 ppm Zn as ZnSO4 were significantly lower than those of the other treatments, whereas the ZnO treatments had no negative effects on growth performance. After the 21-d incubation, the uric acid-N levels of manure from chicks fed the ZnO-1,000 treatment were significantly higher than those of manure from chicks fed the ZnSO4-500. The manure from chicks fed the Zn-supplemented diets had significantly less total N loss compared with that from chicks fed the control. The manure from chicks fed ZnO-1,500 had significantly less total N loss than that from chicks fed the other treatment diets. This study indicated that the Zn treatments significantly reduced nitrogen loss in poultry manure, and ZnO could be a better Zn source to prevent nitrogen loss to the atmosphere without any detrimental effect on growth performance.

In situ evaluation of hen mortality meal as a protein supplement for dairy cows.

A study was conducted to evaluate the nutritional composition and in situ degradation of hen mortality meals. There were four treatments: control autoclaved hen meal (C-HM), enzyme-treated, fermented, autoclaved hen meal (E-HM), NaOH-treated, fermented, autoclaved hen meal (NaOH-HM), and soybean meal (SBM). For the E-HM or NaOH-HM, hen mortality was treated with a feather digesting enzyme or NaOH to improve digestibility of feathers on the carcass. After the enzyme or NaOH treatment, treated hen mortality was preserved by a fermentation procedure. The crude protein levels of the C-HM and SBM were higher than the E-HM and NaOH-HM, and the concentration of fat in the C-HM was higher than the other treatments. Levels of Lys, Thr, Arg, Ile, Leu, Val, and Phe for the C-HM and SBM were higher than in the E-HM and NaOH-HM. The Met, Cys, and Gly levels in the C-HM were higher than the soybean meal. In situ ruminal degradation data showed that the C-HM had lower dry matter and crude protein degradation than the other treatments, whereas the E-HM or NaOH-HM was more susceptible to ruminal degradation. These results indicate that the C-HM has higher levels of crude protein, amino acids, and resistance to ruminal degradation, whereas the E-HM or NaOH-HM was more digestible to ruminal microorganisms.

1. Appetite suppressant activity of supplemental dietary amino acids and subsequent compensatory growth of broilers.

This study was conducted to take advantage of the appetite-suppressant effect of excessive dietary amino acids in reducing feed intake and, in turn, restricting the early rapid growth of broilers to minimize metabolic disorders. Dietary amino acids were supplemented to a basal diet to yield a total of 1.57, 2.57, and 3.57% His; 2.7, 4.3, and 5.9% Lys; 1.36, 2.16, and 2.96% Met; 2.8, 3.8, and 4.8% Thr; and 1.27, 2.27, and 3.27% Trp and were fed to 408 chicks from 4 to 11 d of age. Fifteen dietary treatments of His, Lys, Met, Thr, and Trp were compared to the basal diet. Feed consumption was measured daily. Body weight measurements were taken at 0, 4, 7, 11, 14, and 21 d. At 21 d, pectoralis major and minor muscles, liver, and abdominal fat pad were weighed. High levels of Met and His caused the greatest depression in appetite from 4 to 11 d, and Thr, Trp, and Lys were found to be less potent. The exponential growth rate (EGR) of birds from 4 to 11 d of age was significantly reduced by the intermediate and high levels of the amino acid supplementation. From 11 to 14 d, EGR was greatest with high levels of Met or Trp, indicating more potential compensatory growth realized with these treatments. The high level of His decreased the percentage of pectoralis minor muscle yield, whereas the high level of Lys and Met increased the percentage of liver compared to those fed the basal diet. These results indicate that it is possible to use excessive individual amino acids in diets to suppress the appetite and early rapid growth to alleviate or minimize metabolic disorders.

Nutritional value of enzyme- or sodium hydroxide-treated feathers from dead hens.

Two feather digestion processes to remove the feathers from the carcasses of dead hens were evaluated for their impact on the nutritional quality of the resulting feather meal. There were three treatments: control (untreated feathers), a feather-digesting enzyme, and NaOH treatment. Both enzyme- and NaOH-treated feathers were easily separated from the hen carcasses. The CP level of enzyme-treated feathers after autoclaving (49.90%) was significantly less than the control and NaOH-treated feathers (94.48 and 87.31%, respectively) because of elevated ether extract levels resulting from skin and abdominal fat release during the 12-h enzyme incubation. Before autoclaving, pepsin digestibilities of enzyme- and NaOH-treated feathers were significantly higher than the control. However, after autoclaving, no significant difference was found in pepsin digestibility between the control and enzyme treatments or control and NaOH treatments. The typical limiting amino acids, methionine, lysine, and histidine, in feathers were present at greater levels in the resulting enzyme-feather meal (E-FM) compared with the NaOH-feather meal (N-FM) or control-feather meal (C-FM) on a percentage of CP basis. Cystine levels, however, were significantly lower in the E-FM and N-FM compared with that of the C-FM. In chick bioassays, no significant differences were found in protein efficiency ratio (PER) and net protein ratio (NPR) among C-FM, E-FM, and N-FM. The AMEn of E-FM (4.52 kcal/g) was significantly higher than the C-FM (3.58) or N-FM (2.79). These findings indicated that although enzyme treatment could improve the nutritional quality of feathers from dead hens, NaOH treatment was a more rapid means of separating feathers from the carcass.

Activins as candidate cholinergic differentiation factors in vivo.

A number of cytokine families have been implicated in shaping neuronal survival, growth and gene expression. The neuropoietic and transforming growth factor-beta (TGF-beta) cytokines, in particular, have emerged as candidates for regulating the phenotype of sympathetic neurons. Culture studies have shown that neuropoietic cytokines (such as leukemia inhibitory factor, ciliary neurotrophic factor, oncostatin M, growth promoting activity) can induce the cholinergic enzyme, choline acetyltransferase (ChAT) and several neuropeptides, whereas certain members of the TGF-beta family (activin A, bone morphogenetic proteins-2 and -6) induce partially overlapping but distinct sets of transmitter and neuropeptide genes in sympathetic neurons. Since activins can induce ChAT in cultured neurons, we have investigated whether these cytokines are expressed by the appropriate cells and tissues to make them candidates for the cholinergic differentiation factor that is known to alter the phenotype of sympathetic neurons that innervate the sweat gland in the footpad in vivo. In-situ hybridization with the anti-sense probe for activin beta B specifically labels the sweat glands but not other tissues in the footpads of developing rats. Ribonuclease protection assays indicate that beta B as well as the other activin and inhibin subunit mRNAs are expressed by a number of tissues, including footpad, hairy skin and submaxillary gland. Homogenates of developing rat footpads, however, failed to induce the set of neuropeptide genes in cultured sympathetic neurons that is characteristic for activins, although neuropoietic cytokine activity was readily detectable in this assay. Thus, while activin beta B mRNA is expressed in the sweat gland, this tissue does not contain detectable activin protein as assayed by its ability to regulate neuronal gene expression. Moreover, activin subunit mRNAs are expressed by targets of noradrenergic sympathetic neurons in vivo, indicating that activin expression is not limited to targets of cholinergic neurons.

Potassium-stimulated purine release by cultured sympathetic neurons.

Environmental factors can influence cultured sympathetic neurons to acquire several different neurotransmitter phenotypes. Cholinergic and noradrenergic transmitter status can be influenced by heart cell conditioned medium, chronic depolarization (Patterson, P. H. (1978) Annu. Rev. Neurosci. 1:1-17), and rat serum (Wolinsky, E. J., and P. H. Patterson, (1985) J. Neurosci. 5:1509-1512); formation of electrical synapses can be induced by insulin (Wolinsky, E. J., H. Patterson, and A. L. Willard (1985) J. Neurosci., 5:1675-1679). Purine release has also been proposed as a possible transmission mode for sympathetic neurons (Potter, D. D., E. J. Furshpan, and S. C. Landis (1983) Fred. Proc. 42:1626-1632), and as such, it is another candidate for environmental modulation. In this report, we assess the ability of sympathetic neuron cultures grown with and without serum to release metabolically labeled tritriated purine compounds in response to depolarization. Exposure to 54 mM potassium stimulated release of adenosine, inosine, and hypoxanthine from both serum-supplemented and defined-medium cultures. However, depolarization-stimulated release of adenine nucleotides was observed only from serum-supplemented cultures and not from serum-free cultures. The release of adenine nucleotides from serum-containing cultures is affected by divalent cations in the manner expected for a neurosecretory process. The failure of serum-free cultures to release detectable adenine nucleotides raises the possibility that they do not share with, or that they differ from, serum-supplemented cultures in the purinergic aspect of the multiple transmission modes available to sympathetic neurons, and that this difference may be due to effects of the culture medium.

Rat serum contains a developmentally regulated cholinergic inducing activity.

Sympathetic neurons cultured in defined medium do not develop the ability to produce acetylcholine, as do neurons grown with serum supplementation (lacovitti, L., M. I. Johnson, T. H. Joh, and R. P. Bunge (1982) Neuroscience 7:2225-2239; Wolinsky, E. J., S. C. Landis, and P. H. Patterson (1985) J. Neurosci. 5: 1497-1508). The implication that rat serum contains cholinergic inducing activity is further explored here. Dependence of cholinergic induction on serum concentration is demonstrated, and the activity is shown to reside in a macromolecular fraction. Very little cholinergic inducing activity is present in serum obtained from animals younger than 9 postnatal days. This age dependence correlates with the time of transition from noradrenergic to cholinergic transmitter status by the sympathetic innervation of the rat sweat gland in vivo (Landis, S. C., and D. Keefe (1983) Dev. Biol. 98: 349-372).