Identification of pheasant ghrelin and motilin and their actions on contractility of the isolated gastrointestinal tract.

Motilin and ghrelin were identified in the pheasant by molecular cloning, and the actions of both peptides on the contractility of gastrointestinal (GI) strips were examined in vitro. Molecular cloning indicated that the deduced amino acid sequences of the pheasant motilin and ghrelin were a 22-amino acid peptide, FVPFFTQSDIQKMQEKERIKGQ, and a 26-amino acid peptide, GSSFLSPAYKNIQQQKDTRKPTGRLH, respectively. In in vitro studies using pheasant GI strips, chicken motilin caused contraction of the proventriculus and small intestine, whereas the crop and colon were insensitive. Human motilin, but not erythromycin, caused contraction of small intestine. Chicken motilin-induced contractions in the proventriculus and ileum were not inhibited by a mammalian motilin receptor antagonist, GM109. Neither atropine (a cholinergic receptor antagonist) nor tetrodotoxin (a neuron blocker) inhibited the responses of chicken motilin in the ileum but both drugs decreased the responses to motilin in the proventriculus, suggesting that the contractile mechanisms of motilin in the proventriculus was neurogenic, different from that of the small intestine (myogenic). On the other hand, chicken and quail ghrelin did not cause contraction in any regions of pheasant GI tract. Since interaction of ghrelin and motilin has been reported in the house musk shrew, interaction of two peptides was examined. The chicken motilin-induced contractions were not modified by ghrelin, and ghrelin also did not cause any contraction under the presence of motilin, suggesting the absence of interaction in both peptides. In conclusion, both the motilin system and ghrelin system are present in the pheasant. Regulation of GI motility by motilin might be common in avian species. However, absence of ghrelin actions in any GI regions suggests the avian species-related difference in regulation of GI contractility by ghrelin.

Effects of dietary coarsely ground corn and 3 bedding floor types on broiler live performance, litter characteristics, gizzard and proventriculus weight, and nutrient digestibility.

The effects of zero or 50% dietary coarsely ground corn (CC) in pelleted and screened grower and finisher diets on broilers reared on 3 bedding floor types (plastic net [NET], new pine wood shavings litter [NEW], or old pine wood shavings litter [OLD]) on broiler live performance, litter characteristics, gizzard and proventriculus weight, and apparent ileal digestibility (AID) were studied in a 2 × 3 factorial arrangement of treatments. Fine corn was produced with a hammermill (271 µm) and CC with a roller mill (1145 µm). Utilization of CC reduced milling cost by 9.47 cents per MT with similar nutrient content of screened pellets. The 50% CC treatment exhibited improved (P ≤ 0.05) feed intake at 42 d (2.5%) and 49 d (3.0%), and BW (5.4%) and FCR from 28 d (1.4%). Birds on NEW litter exhibited improved (P < 0.05) BW at 28 and 35 d and 42 d FCR as compared to NET and 49 d FCR compared to NET and OLD. The 50% CC treatment exhibited increased (P < 0.05) gizzard weight but decreased proventriculus weight at 49 d. NEW litter birds exhibited increased (P ≤ 0.05) gizzard weight at 28 d and 49 d and decreased proventriculus weight as compared to NET at 49 days. The 50% CC treatment exhibited decreased (P ≤ 0.05) litter moisture at 35 and 42 d, litter N at 35 and 49 d, and litter pH at 49 days. OLD litter birds exhibited greater (P < 0.05) litter N at 14, 35, and 49 d, as well as litter moisture, pH, and ammonia concentration at 49 days. The 50% CC group also exhibited improved AID of nitrogen (P < 0.05). Broilers fed pelleted and screened diets containing 50% CC exhibited improved live performance and reduced litter moisture while use of NEW litter resulted in a somewhat similar effect, which indicated that consumption of NEW litter also facilitated gastric development and function.

Molecular cloning of motilin and mechanism of motilin-induced gastrointestinal motility in Japanese quail.

Motilin, a peptide hormone produced in the upper intestinal mucosa, plays an important role in the regulation of gastrointestinal (GI) motility. In the present study, we first determined the cDNA and amino acid sequences of motilin in the Japanese quail and studied the distribution of motilin-producing cells in the gastrointestinal tract. We also examined the motilin-induced contractile properties of quail GI tracts using an in vitro organ bath, and then elucidated the mechanisms of motilin-induced contraction in the proventriculus and duodenum of the quail. Mature quail motilin was composed of 22 amino acid residues, which showed high homology with chicken (95.4%), human (72.7%), and dog (72.7%) motilin. Immunohistochemical analysis showed that motilin-immunopositive cells were present in the mucosal layer of the duodenum (23.4±4.6cells/mm(2)), jejunum (15.2±0.8cells/mm(2)), and ileum (2.5±0.7cells/mm(2)), but were not observed in the crop, proventriculus, and colon. In the organ bath study, chicken motilin induced dose-dependent contraction in the proventriculus and small intestine. On the other hand, chicken ghrelin had no effect on contraction in the GI tract. Motilin-induced contraction in the duodenum was not inhibited by atropine, hexamethonium, ritanserin, ondansetron, or tetrodotoxin. However, motilin-induced contractions in the proventriculus were significantly inhibited by atropine and tetrodotoxin. These results suggest that motilin is the major stimulant of GI contraction in quail, as it is in mammals and the site of action of motilin is different between small intestine and proventriculus.

Peripheral "chicken" obestatin administration does not affect feed intake and gut muscle contractility of meat-type and layer-type chicks (Gallus gallus domesticus).

Obestatin has recently been discovered in the rat stomach. As for ghrelin, the 23-amino acid obestatin is also derived from post-translational processing of the prepro-ghrelin gene but seems to have opposite effects on feed intake. In avian species, ghrelin is mainly present in the proventriculus and decreases feed intake, as opposed to its orexigenic properties in mammals. An obestatin-like sequence was also found in the avian ghrelin precursor protein but the potential involvement of this peptide in appetite regulation of chickens is unclear. We therefore investigated the effects of a single peripheral administration of this predicted "chicken" obestatin peptide on voluntary feed intake of 7- to 9-day-old meat-type and layer-type chicks. "Chicken" obestatin was injected intraperitoneally or intravenously at a dose of 1 nmol or 10 nmol/100 g body weight and feed intake was measured up to 4 h post injection. None of these treatments did reveal any effect of the putative "chicken" obestatin on appetite of either meat-type of layer-type chicks. Furthermore, "chicken" obestatin also failed to affect the in vitro contractility of muscle strips from crop and proventriculus. In conclusion, in the given experimental settings, the putative "chicken" obestatin has indistinctive physiological effects on feed intake and in vitro muscle contractility of gut segments, and hence its functional properties in ingestive behavior of avian species remain obscure.

Effect of anesthesia, positioning, time, and feeding on the proventriculus: keel ratio of clinically healthy parrots.

Healthy, adult Hispaniolan Amazon parrots (Amazona ventralis) were imaged on three occasions to determine the effects of anesthesia, patient rotation, feeding, and short/long-term temporal factors on the proventriculus:keel ratio. Increasing rotation up to 15 degrees from right lateral resulted in increased inability to measure the proventriculus in up to 44% of birds, meaning that the proventriculus:keel ratio could not be calculated from those radiographs. There was a significant difference between the proventriculus:keel ratio for individual parrots when quantified 3 weeks apart. Despite this difference, all ratios remained within normal limits. No significant effect was identified due to anesthesia, feeding, fasting, or repeated imaging through an 8-h period. Interobserver agreement for measurability and correlation for the proventriculus:keel ratio values was high. It is recommended that the proventriculus:keel ratio be calculated from anesthetized parrots to attain images in true lateral recumbency. Ratio fluctuations within the normal range between radiographs obtained on different dates may be observed in normal parrots.

Pharmacological characterization of 5-hydroxytryptamine-induced contraction in the chicken gastrointestinal tract.

5-Hydroxytryptamine (5-HT) receptor subtypes involved in 5-HT-induced contraction of the chicken gastrointestinal tract were characterized pharmacologically using subtype-selective agonists and antagonists. The proventriculus (area of stomach adjacent to the oesophagus) and ileum are examined. 5-HT applied cumulatively caused sustained contraction of the proventriculus that was not decreased by tetrodotoxin, atropine or l-nitro-arginine methylester (l-NAME). alpha-Methyl-5-HT showed the same potency as that of 5-HT, indicating the involvement of the 5-HT(2) receptor. (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-amino-propane (DOI), 5-methoxytryptamine and 1-(3-chlorophenyl)piperazine hydrochloride (mCPP) were potent, and 2-methyl-5-HT, 5-carboxamidotryptamine, BW723C86 and 6-chloro-2-(1-piperazinyl)pyrazine hydrochloride (MK212) were moderate, but (+/-)-8-hydroxy-2-dipropylaminotetralin hydrobromide (8-OH-DPAT), [endo-N-8-methyl-8-azabicyclo-(3,2,1)oct-3-yl]-2,3-dihydro-(1-methyl)ethyl-2-oxo-1H-benzimidazol-1-carboxamide (BIMU-8) and cisapride were weak agonists. Correlation of pEC(50) values of these agonists with documented pEC(50) values for 5-HT(2C) receptor was higher than 5-HT(2A) and 5-HT(2B). Cinanserin, ketanserin, methiothepin, methysergide, mianserin, (8-[5-(2,4-dimethoxy-5-(4-trifluoromethylphenylsulphonamido)phenyl-5-oxopentyl)-1,3,8-triazaspiro[4,5]decane-2,4-dione hydrochloride (RS102221), N-(1-methyl-1H-indolyl-5-yl)-N'-(3-methyl-5-isothiazolyl)urea (SB204741), spiperone and N-desmethylclozapine concentration-dependently inhibited the contractile responses to 5-HT. Correlation of pK(b)/pA(2) of antagonists with documented pK(i) for 5-HT(2C) receptor was highest among 5-HT(2) receptor subtypes. In the methysergide- and ketanserin-treated proventriculus, 5-HT, 2-methyl-5-HT and cisapride did not enhance the electrical field stimulation (5 Hz)-induced cholinergic contractions. 5-HT applied non-cumulatively caused transient contraction of ileum, and the responses were partly decreased by atropine or tetrodotoxin. 5-Methoxytryptamine, alpha-methyl-5-HT, 5-carboxamidotryptamine, L692,247 and DOI were potent agonists. However, 2-methyl-5-HT, cisapride, BW723C86, 8-OH-DPAT and 5-nonyloxytryptamine, mCPP and MK212 were less effective. Ketanserin and methysergide decreased the 5-HT-induced ileal contraction, but neither GR113808 nor SB269970 inhibited the responses. In conclusion, 5-HT causes contraction of the proventriculus via 5-HT(2C)-like receptors present on smooth muscle. 5-HT also causes contraction of the ileum, but the underlying mechanisms are complex, involving neural and smooth muscle components, and both 5-HT(1)- and 5-HT(2)-like receptors. Neural 5-HT receptors similar to 5-HT(3)/5-HT(4) receptors were not found in the chicken proventriculus and ileum.

Exogenous administration of octanoic acid accelerates octanoylated ghrelin production in the proventriculus of neonatal chicks.

Ghrelin is modified by fatty acid at the third serine residue. In this study, derivation of fatty acid for acylation of ghrelin was investigated using a hatchling chicken model. We first studied ghrelin gene expression and production in the neonatal chick proventriculus and then investigated the effect of exogenous octanoic acid (OA) administration on acylated ghrelin production. In a free-feeding condition on day 2.5 after hatching, the density of ghrelin mRNA-expressing (ghrelin-ex) cells was greater than that of ghrelin-immunopositive (ghrelin-ip) cells, but no difference was found between those densities in adult chickens. Intraperitoneal or oral administration of OA for a few days significantly increased the density of ghrelin-ip cells without any changes in ghrelin-ex cells and elevated only octanoylated ghrelin levels in the proventriculus. The results indicate that fatty acid absorbed from food is directly utilized in acylated ghrelin production in the chicken.

Involvement of the signal transduction pathway mediated by epidermal growth factor receptor in the differentiation of chicken glandular stomach.

During the development of the chicken proventriculus (glandular stomach), the initially undifferentiated epithelium differentiates into two distinct cell populations: the glandular epithelium, cells of which secrete embryonic chicken pepsinogen (ECPg), and luminal epithelial cells, which express the chicken spasmolytic polypeptide gene (cSP). Based on knowledge of the adult mouse stomach, the ligands of epidermal growth factor (EGF) receptor (EGFR) were expected to affect differentiation of the proventricular epithelium. When EGF was added to the medium in which proventriculi were cultured in vitro, gland formation was suppressed in a dose-dependent manner and the amount of ECPg mRNA decreased, whereas morphological differentiation of luminal epithelium was stimulated. Simultaneous treatment of the proventriculus with EGF and tyrphostin 47 resulted in the attenuation of the effect of EGF, suggesting that EGF, or other ligands of EGFR, may actually be involved in the normal course of development of the proventricular epithelium.

Potentiation of motilin-induced contraction by nitric oxide synthase inhibition in the isolated chicken gastrointestinal tract.

The present experiments were designed to determine whether or not endogenous nitric oxide (NO) modifies the contractile response to chicken motilin (ch-MT) in the gastrointestinal (GI) tract (proventriculus and small intestine) of the chicken. ch-MT (1 nmol L(-1)-1 micromol L(-1)) caused contractions of longitudinal muscle strips of the proventriculus through both myogenic and neurogenic (mostly cholinergic) mechanisms. On the other hand, ch-MT (0.1 nmol L(-1)-100 nmol L(-1)) contracted the small intestine (duodenum, jejunum and ileum) only through a myogenic mechanism. L-Nitroarginine methylester (L-NAME) potentiated, and L-arginine inhibited, the ch-MT- induced contraction without affecting the responsiveness of acetylcholine (ACh) or 5-hydroxytryptamine in the proventriculus. Electrical field stimulation (EFS)- and 1,1-dimethyl-4-phenylpiperazinium (DMPP)- induced contractions were also potentiated by L-NAME. The potentiation by L-NAME was prevented by L-arginine but not by D-arginine. However, in the presence of atropine or tetrodotoxin, neither L-NAME nor L-arginine modified the responses to ch-MT and DMPP. In contrast to the proventriculus, L-NAME and L-arginine were both ineffective in modifying the ch-MT-induced contraction in the small intestine. These results indicate that NO synthase inhibition potentiates the contractile response of ch-MT, EFS and DMPP in the chicken proventriculus through reduction of endogenous NO-mediated presynaptic inhibition on neural ACh release. However, NOS inhibition did not modify the myogenic (direct) action of ch-MT in gastric and intestinal smooth muscles of the chicken.

Effects of biogenic amines in broiler chickens.

Biogenic amines in spoiled animal by-product feeds have been implicated in causing poor performance and intestinal lesions in broilers. This study was designed to determine if biogenic amines, at the concentrations found in animal by-product meals, would reduce performance in broilers or cause lesions. Twelve treatments were used in a 2 x 6 factorial arrangement with the main effects being either a corn-soybean meal diet or a corn-soybean meal diet with 10% animal by-products added and either no amines added or added levels of phenylethylamine (4.8 mg/kg), putrescine (49 mg/kg), cadaverine (107 mg/kg), histamine (131 mg/kg), or a combination of all these amines. Levels of biogenic amines used in this study simulated those found in areas with reported problems attributed to biogenic amines. Broilers were monitored for performance, gross lesions, and histologic evidence of lesions at 2, 4, and 6 wk. No consistent effects were observed on performance, and by the conclusion of the trial, no statistical differences were noted in the performance of any of the treatments. No gross lesions were observed on a consistent basis in any of the treatments. Histopathology was likewise unremarkable. On the basis of this study, it would appear that these four biogenic amines, at levels detected in the United States, do not pose a serious health concern for the broiler industry.

Neurotensin decreases pepsin output and gastrointestinal motility in chickens.

Two experiments were conducted to determine the effect of neurotensin on gastric secretion and gastrointestinal motility in conscious chickens. Chickens were surgically fitted with a cannula to collect secretions from the proventriculus and strain gauge transducers sutured to the gizzard, duodenum, and ileum in order to detect contractions. Peripheral intravenous infusion of physiological levels of neurotensin inhibited pepsin output from the proventriculus, but had no effect on the volume or pH of gastric secretions. Neurotensin also inhibited both the frequency and strength of gastrointestinal contractions when compared to motility patterns following infusion of isotonic 0.9% (wt/vol) saline. The frequency of occurrence of small intestinal refluxes was not affected by neurotensin. These results coupled with our earlier work, which demonstrated that neurotensin is released by the presence of oleic acid in the duodenum, indicate that neurotensin may function as an enterogastrone released by lipids in the gastrointestinal tract of the chicken. This overall inhibitory effect of neurotensin on the avian gut indicates that it is involved in the postprandial regulation of digestion, especially lipid digestion.

Functional characterization of neural and smooth muscle motilin receptors in the chicken proventriculus and ileum.

To characterize the motilin receptors present in the chicken, the effects of chicken motilin (Phe-Val-Pro-Phe-Phe-Thr-Gln-Ser-Asp-Ile-Gln-Lys-Met-Gln-Glu-Lys-Glu-Arg -Asn-Lys-Gly-Gln), Leu13 porcine motilin, canine motilin and three erythromycin derivatives (EMA, EM523, GM611) on the contractility of the chicken gastrointestinal (GI) smooth muscles were investigated in vitro and compared with those in the rabbit duodenum. In the proventriculus longitudinal and circular muscle layers, chicken motilin (3 nM-1 microM) caused an atropine- and a tetrodotoxin-sensitive contraction (EC50 = 39-49 nM), and potentiated the EFS-induced contraction without affecting the responsiveness of acetylcholine. EM523 and GM611 (3-100 microM) contracted the proventriculus longitudinal muscle, and the maximum amplitudes of contraction were about 60% of that induced by chicken motilin. Chicken motilin (0.1 nM-100 nM) also caused contraction of the ileum (EC50 = 7 nM) through direct action on the smooth muscle cells. On the other hand, erythromycin derivatives showed only a weak contractile efficacy (about 20% of the maximum response of chicken motilin) even at high concentrations (10-100 microM). The rank order of potency in the ileum was chicken motilin > canine motilin > or = Leu13 porcine motilin > > GM611 > or = EM523 > or = EMA. GM109 slightly inhibited the ideal contractions induced by Leu13 porcine motilin at 100 microM (pA2 = 3.86). In the rabbit duodenum, chicken motilin was a full agonist with the same intrinsic activity as Leu13 porcine motilin, canine motilin and the erythromycin derivatives. However, the rank order of potency (Leu13 porcine motilin > or = canine motilin > chicken motilin > GM611 > or = EM523 > EMA) was different from that in the chicken ileum. In conclusion, chicken motilin causes an excitatory response in the chicken GI tract through activation of neural (proventriculus) and smooth muscle motilin receptors (ileum). The motilin receptor present in the ileum is different from that demonstrated in the rabbit intestine, because of a different rank order of motilin peptides in producing the contraction, low contracting activity of erythromycin derivatives and low antagonistic efficacy of GM109. Different pharmacological characteristics of the mechanical response induced by motilin peptides and erythromycin derivatives between the proventriculus and the ileum are discussed.

Effects of feeding Fusarium moniliforme culture material, containing known levels of fumonisin B1, in the young turkey poult.

The effects of feeding Fusarium moniliforme culture material, containing known concentrations of fumonisin B1 (FB1), were studied in turkey poults. Day-old poults were allotted randomly to dietary treatments containing 0, 0.41, 0.82, 1.23, 1.64. 2.87, 4.10, 5.33, 6.56, and 7.79% fumonisin culture material (FCM). These levels of FCM supplied 0, 25, 50, 75, 100, 175, 250, 325, 400, and 475 mg FB1/kg of feed. Each dietary treatment was fed to six pen replicates of six poults each for 21 d. Poults fed FCM that supplied 325 to 475 mg FB1/kg diet had lower (P < 0.05) feed intakes and BW gains. Increased (P < 0.05) liver and pancreas weights were observed in poults fed FCM that supplied > or = to 175 mg FB1/kg. Poults fed FCM that supplied 400 and 475 mg FB1/kg diet had increased (P < 0.05) red blood cell counts and increased (P < 0.05) serum concentrations of gamma glutamyl transferase and aspartate aminotransferase. Compared with controls, poults fed FCM that supplied 25, and 75 to 475 mg FB1/kg had increased (P < 0.05) liver sphinganine:sphingosine ratios. Hepatocellular hyperplasia was mild at 75 and 100 mg FB1/kg diet, moderate to severe at 250 mg/kg FB1, and severe at 325 to 475 mg FB1/kg. Multifocal to generalized loss of cross striations and thinning of cardiomyocytes was observed in poults fed FCM that supplied 475 mg FB1/kg diet. Results indicated that diets containing < or = to 1.23% FCM that supplied > or = to 75 mg FB1 /kg are toxic to young turkeys.

The effect of dietary copper sulfate on infectious proventriculitis.

Oral inoculation of day-old broiler chicks with a crude homogenate of affected proventricular tissue, or the same homogenate filtered through a .2 micron filter caused proventricular lesions similar to those responsible for carcass contamination of broilers at processing. Dietary copper sulfate (CUS) has also been shown to produce similar lesions. In this study, we investigated the interaction between crude proventriculus homogenate or filtered proventriculus homogenate and 1 g/kg CUS added to a standard chicken diet. Cobb x Cobb female broiler chicks were distributed into six groups with four replicate battery pens per group. Birds were fed either a standard broiler starter diet or the same diet with 1 g/kg CUS. Each dietary treatment was inoculated per os with 1 mL of either sterile saline, unfiltered homogenate, or filtered homogenate. Both crude and filtered homogenates had a much stronger affect on proventriculus score than did Cu by itself, resulting in no interaction between either homogenate or filtrate and CUS. There was a significant and possibly antagonistic interaction on proventriculus relative weights in the CUS by filtrate group during Week 1 and a synergistic interaction in the CUS by homogenate group during Week 4. Body weights were decreased in birds fed homogenate or CUS, but not in birds fed filtrate. There was a protective effect shown by filtrate on body weight of birds fed both filtrate and CUS only during Week 1. There was a synergistic decrease in body weight of birds fed homogenate and CUS during Week 2. Overall feed conversion efficiency was significantly decreased in the homogenate treatment (P = .04) and decreased in the birds fed CUS (P = .1). There was a (4.2 vs 2.3) (P = .1) decrease in feed conversion efficiency in birds fed both homogenate and CUS. Natural exposure to low levels of the infectious agent present in the homogenates may interact with excess dietary CUS, resulting in increased proventriculus size and decrease in body weight and feed conversion efficiency.

Effects of Fusarium moniliforme culture material containing known levels of fumonisin B1 in ducklings.

Fusarium moniliforme culture material containing fumonisin B1 (FB1) was fed to white Pekin ducklings from 1 to 21 days of age. Four dietary treatments were prepared with 0, 100, 200, and 400 mg FB1/kg ration. Ducklings fed rations containing FB1 had a dose-dependent decrease in feed intake and weight gain. Increasing levels of FB1 in the ration were associated with increasing absolute organ weights of liver, heart, kidney, pancreas, and proventriculus. Liver sphinganine to sphingosine ratios increased significantly in ducklings fed FB1. Two of eight ducklings fed a ration containing 400 mg FB1/kg died prior to the termination of the experiment. Mild to moderate hepatocellular hyperplasia was evident in all ducklings fed FB1. Mild to moderate biliary hyperplasia was also noted in the liver sections of ducklings fed 400 mg FB1/kg in the ration. Ducklings, like other poultry, are relatively resistant to the toxic effects of FB1.

Excitatory action of [Leu13]motilin on the gastrointestinal smooth muscle isolated from the chicken.

The effects of a porcine motilin analogue, [Leu13]motilin (LMT) on the smooth muscle preparations isolated from the chicken gastrointestinal (GI) tract were investigated in vitro. In the proventriculus, LMT (100 nM to 30 microM) caused an atropine-sensitive contraction and enhanced the electrical field stimulation (EFS)- or 1,1-dimethyl-4-phenyl-piperazinium (DMPP)-induced contraction without affecting the response to acetylcholine (ACh). LMT also caused a concentration-dependent contraction of the intestinal tract (duodenum, jejunum, ileum, and colon). The responsiveness to LMT was strongest in the jejunum and weakest in the colon. The responses to LMT in the intestinal segments were not affected by tetrodotoxin, atropine, hexamethonium, pyrilamine, spantide, and 5-hydroxyltryptamine-induced desensitzation, but significantly decreased by verapamil or removal of external Ca2+. LMT did not enhance the EFS- or DMPP-induced contraction in the ileum. Canine motilin also contracted the intestinal segments in a similar concentration range to LMT with an equal potency, but erythromycin A (EMA) and N-ethyl-N-demethyl-8,9-anhydroerythromycin A, 6-9-hemiketal (EM523) showed only a weak contractile activity even at high concentration (up to 100 microM), indicating that motilin receptors in the chicken intestine were somewhat different from those of mammals. In conclusion, LMT produces an excitatory response in the chicken GI tract with a different sensitivity from region to region. The mechanisms of the action were different between the proventriculus and small intestine; that is, LMT contracts the small intestine through the direct action on the smooth muscle cells, but this peptide acts on the enteric cholinergic neurones and stimulates ACh release, and thus regulates autonomic neuroeffector transmission in the proventriculus.

The inhibitory action of lead on mechanical responses of the proventricular smooth muscle in the chick.

The purpose of the present experiments was to examine the mechanism of the proventricular dilatation caused by lead in the isolated vagus nerve-proventricular smooth muscle preparation of the chick. Lead caused dose- and time-dependent inhibition of contractions induced by vagal stimulation, transmural stimulation and externally applied acetylcholine (ACh). Vagally evoked contraction was much more sensitive to the inhibitory action of lead than the contractile response to ACh. The lower the frequency of transmural stimulation, or the lower the concentration of ACh was applied, the greater the inhibitory action of lead on the evoked smooth muscle contraction. The results suggest that proventricular impaction occurring in lead poisoning results from the pre- and post-synaptic inhibition of the vagus nerve-smooth muscle transmission.

Growth of the parathyroid glands in omeprazole-treated chickens.

BACKGROUND: Omeprazole, a long-acting inhibitor of gastric acid secretion, is able to increase the circulating concentrations of gastrin. Daily treatment with high doses of omeprazole cause sustained hypergastrinemia. Long-standing hypergastrinemia can be expected to exert numerous effects in the body. For instance, gastrin has been proposed to promote growth in the digestive tract and pancreas. The present study is concerned with the effect of omeprazole on parathyroid glands in the chicken. METHODS: Chickens were treated with omeprazole (400 mumol/kg/day) in methylcellulose (2.5 ml/kg) for 5 or 10 weeks. Controls received vehicle. Blood calcium and serum gastrin concentrations were studied. The weight gain of the animals and of various organs (proventriculus, antrum, thyroids, parathyroids, ultimobranchial glands, and femur) were determined. The DNA content and the size of the parathyroid chief cells were also determined. RESULTS: Omeprazole reduced the body weight gain while greatly increasing the weight of the proventriculus and the parathyroid glands. The weight and density of the femur were reduced. The circulating concentrations of calcium were unaffected. The DNA content of the parathyroid glands was increased, and morphometric analysis of the parathyroid chief cells showed an increased cell size. Thus, the increased parathyroid gland weight seems to reflect both hypertrophy and hyperplasia. There was a slight increase in the weight of the ultimobranchial glands (expressed per kilogram body weight). The weight of the thyroids was unaffected (expressed in relation to body weight). CONCLUSIONS: The results indicate that omeprazole treatment in chickens leads not only to trophic effects in the acid-producing gastric mucosa (probably because of the ensuing hypergastrinemia), as reported earlier, but also to growth of the parathyroid glands (both hypertrophy and hyperplasia) and to bone loss without affecting blood calcium values. The mechanism behind these effects remains unknown.

Fumonisin toxicity in broiler chicks.

The effects of dietary fumonisin B1 were evaluated in young broiler chicks. The experimental design consisted of 5 treatments each with 9 randomly allotted male broiler chicks. Day-old chicks were fed diets containing 0 (feed control), 100, 200, 300, or 400 mg fumonisin B1/kg feed for 21 days. Response variables measured were chick performance, organ weights, serum biochemistry, and histologic parameters. Body weights and average daily gain dramatically decreased with increasing dietary fumonisin B1, and liver, proventriculus, and gizzard weights increased. Diarrhea, thymic cortical atrophy, multifocal hepatic necrosis, biliary hyperplasia, and rickets were present in chicks fed diets containing fumonisin B1. Serum calcium, cholesterol, and aspartate aminotransferase levels all increased at higher fumonisin dietary levels. Results indicate that fumonisin, from Fusarium moniliforme culture material, is toxic in young chicks.

Toxicological evaluation of aflatoxin and cyclopiazonic acid in broiler chickens.

The individual and combined effects of aflatoxin (AF) and cyclopiazonic acid (CPA) were evaluated in day-old Petersen x Hubbard broiler chickens to 3 wk of age. Treatments were arranged in a 2 x 2 factorial with levels of 0 and 3.5 mg AF/kg of feed, and 0 and 50 mg CPA/kg of feed. Production performance, serum biochemistry, and gross pathological observations were evaluated. Body weight gain was significantly (P less than .05) reduced by AF, CPA, and the AF-CPA combination at the end of 3 wk. Aflatoxin significantly increased the relative weight of the kidney and serum concentration of blood urea nitrogen and decreased serum concentrations of protein, albumin, cholesterol, phosphorus, and the activity of lactate dehydrogenase. The toxicity of CPA was expressed through increased relative weights of the liver, kidney, and proventriculus, increased levels of uric acid and cholesterol, and decreased serum phosphorus. The activity of AF-CPA combination was characterized by increased relative weight of the liver, kidney, pancreas, and proventriculus, decreased concentrations of serum albumin and phosphorus, increased concentrations of serum glutamic oxalacetic transaminase and blood urea nitrogen, and decreases in the relative weight of the bursa of Fabricius. Post-mortem examination revealed that the chickens fed CPA and the AF-CPA combination had thickened mucosa and dilated proventricular lumens, hard fibrotic spleen, and atrophy of the gizzard. The data from the present study demonstrate that both AF and CPA alone and the AF-CPA combination can limit broiler performance and adversely affect broiler health. In most cases the effects of AF and CPA were additive.