Food Intake In Chicks Research Articles

Relationships between feeding and locomotion behaviors after central administration of CRF in chicks

The effect of intracerebroventricular injection of corticotropin-releasing factor (CRF) on various behaviors in chicks was determined at 15-min intervals over a 30-min period. Food intake of chicks was significantly decreased, and pecking rhythm was significantly delayed by CRF during the first 15-min post-injection. The similar tendencies were observed in the second 15-min post-injection, but not significantly different. Stepping, as an indicator of locomotion, was not different at 15-min post-injection, but was increased by CRF, thereafter. These results suggest that CRF acts within the central nervous system to decrease food intake and increase locomotion in the chick.

The Role of Central Catecholaminergic Systems in Regulation of Food Intake of Chicks.

To clarify catecholaminergic systems on the regulation of food intake in the neonatal chick, we examined the effects of intracerebroventricular (ICV) injection of prazosin (α1-adrenoceptor antagonist), yohimbine (α2-adrenoceptor antagonist) and benserazide (an inhibitor of L-aromatic amino acid decarboxylase). We found that food intake was significantly suppressed by ICV injection of yohimbine (25 and 50μg) over 60min (P 0.05). ICV administration of benserazide induced a hypophagia after 60min postinjection (P<0.05). It is suggested that catecholaminergic systems play an important role in the neural regulation of food intake in chicks, especially through α2-adrenoceptor.

Involvement of Central Gastrin and Cholecystokinin in the Regulation of Food Intake in the Neonatal Chick

Furuse, M., Bungo, T., Ao, R., Ando, R., Shimojo, M., Masuda, Y. and Denbow, D.M. 2000. Involvement of central gastrin and cholecystokinin in the regulation of food intake in the neonatal chick. J. Appl. Anim. Res., 18: 129–136. The effects of intracerebroventricular (ICV) injection of chicken gastrin and cholecystokinin (CCK) on food intake were compared in the neonatal chick. In Experiment 1, the effect of 131 pmol of chicken gastrin (36 amino acid residues) on food intake was compared with 66 and 131 pmol of CCK-8S over 2h. Chicken gastrin strongly inhibited food intake, but both levels of CCK-8S did not. The similar effect of 131 pmol chicken gastrin was obtained by 262 pmol CCK-8S at Ih after ICV injection in Experiment 2. This suppressive effect of chicken gastrin continued over 2h after ICV injection, though the effect of CCK-8S had disappeared by 2h. In Experiment 3, the effects of 131 pmol of CCK-8S, CCK-33S and chicken gastrin were compared. The effect of CCK-8S was weak, but CCK-33S and chickengastrin similarly and strongly inhibited food intake of chicks. These results suggested that the suppressive effect of food intake of gastrin/CCK family may be dependent upon the length of amino acid sequence.

Leptin-induced decrease in food intake in chickens

The effect of intracerebroventricular (i.c.v.) injection of leptin was investigated using broiler and Single Comb White Leghorn (SCWL)-type chickens. These represent relatively fast- and slow-growing birds, respectively. The i.c.v. injection of leptin decreased food intake in both broilers and Leghorns in a dose-dependent manner. The most efficacious dose appeared to be 10 μg in both types of chickens. Water intake was generally not affected by leptin, indicating that this effect was not due to general malaise. It appears that leptin can act within the central nervous sytstem of birds to decrease food intake.

Protein and body weight accretion of chicks on diets with widely varying contents of soyabean meal supplemented or unsupplemented with its limiting amino acids

1. Two studies were conducted to evaluate the effects of relative deficiencies of methionine and threonine on the growth performance of 8- to 21-d-old chicks fed on isoenergetic diets containing a wide range of crude protein (CP) concentrations from dehulled soyabean meal (SBM). 2. Chicks fed on graded levels of SBM containing supplemental methionine and threonine (BAL) accreted whole-body protein more efficiently (P < 0.05) than those receiving graded levels of unsupplemented SBM (DEF), and superior (P < 0.05) growth performance was also obtained at lower CP levels when chicks were fed on the BAL diets. 3. Voluntary food intake increased between 30 and 220 g CP/kg in chicks fed on DEF diets, whereas food intake of chicks fed on BAL diets increased only between 30 and 100 g CP/kg, after which it decreased between 100 and 220 g CP/kg. 4. Protein efficiency ratio (g gain per g protein intake) decreased with each incremental increase in CP between 30 and 260 g CP/kg, regardless of whether diets were BAL or DEF. 5. These data indicate that maintaining a balanced ratio of amino acids is a preferable approach when poultry producers are interested in employing low CP diets for economic, physiological or environmental reasons.

Intracerebroventricular injection of orexins does not stimulate food intake in neonatal chicks

1. Recently, 2 novel neuropeptides were discovered, both derived from the same precursor by proteolytic processing, which bind and activate 2 closely related orphan G protein-coupled receptors, Named orexin-A and-B (Sakurai et al., 1998). Both stimulate food intake when administered centrally to rats. 2. Our aim was to elucidate whether central injection of mammalian orexin-A or-B stimulates food intake in the chick. 3. Under conditions of free access to food, orexin-A did not alter the food intake of chicks, but cumulative food intake was significantly suppressed by orexin-B. 4. The orexin-B was then administered to chicks deprived of food for 3 h to confirm its suppressive effect. No significant effect of orexin-B on food intake was detected. 5. Central injection of orexin-B did not modify food intake when appetite was stimulated by fasting. 6. Neither of these orexins appears to stimulate feeding in chicks.

Intracerebroventricular administration of mouse leptin does not reduce food intake in the chicken

Recently, it has been suggested that leptin plays an important role in regulation of food intake and metabolism in rats and mice, however, the effect of central administration of leptin on food intake in chicks has not been reported. We have investigated the anorexigenic effect of leptin administered by intracerebroventricular (i.c.v.) injection in chicks using mouse leptin, which shows 97% homology to chicken leptin. Three experiments were conducted. After being deprived of food for 3 h, male broiler chicks were administered leptin by i.c.v. injection at dose levels of 0, 0.2, 1.0 and 5.0 μg (Experiment 1) or 0, 2.5 and 5.0 μg (Experiment 2). The birds were allowed free access to the diet for 2 h (Experiment 1) and 24 h (Experiment 2) after treatment. Male Single Comb White Leghorn chicks were used in Experiment 3 and were treated in the same manner as in Experiment 1. In all experiments, central administration of mouse leptin did not influence food intake in the time periods examined. It appears that either mouse leptin does not bind to the chicken leptin receptor or in the chicken brain the leptin receptor may be absent.

Effect of acute histamine and pentagastrin on voluntary food intake in growing chickens

To study the action of histamine (a potent secretagogue in mammals and chickens) on food intake, 5-week-old male chickens ( n = 7) were injected intraperitoneally with 0, 500 or 1000 μg/kg body weight of histamine. Food intake was measured at 6, 15, 30, 45, 60, 90 and 120 min after injection of histamine. Water intake was measured at 15, 30, 45, 60, 90 and 120 min after injection of histamine. A second experiment was carried out to see if another potent secretagogue, pentagastrin, exhibits a similar effect on food intake in chickens. In the first trial a group of chickens ( n = 8) received 0, 25 or 50 μg/kg body weight of pentagastrin intraperitoneally. Food and water intake were measured at 15, 30, 45, 60, 90 and 120 min after injection of pentagastrin. In the second trial, another group ( n = 8) received higher doses of pentagastrin (0, 100 or 200 μg/kg body weight) under similar conditions as above but only food intake was measured. In all cases the animals were starved for 16 h before injection of drugs. The results obtained were different for the two secretagogues utilized. Whereas histamine decreased consumption ( P < 0.05), pentagastrin did not show a similar response either in low or high doses. No differences were observed for water intake in any cases. These results suggest that histamine, but not pentagastrin, plays an inhibitory effect on the regulation of food intake in chickens. From these findings, it could be assumed that histamine's secretory property is not the primary mechanism by which histamine inhibits eating. Since peripherally administered histamine decreases food intake in chickens, the H1, H2 or H3 receptors could very possibly be involved in such response and this requires further research.

CCK is involved in both peripheral and central mechanisms controlling food intake in chickens.

The aim of this work was to study the involvement of cholecystokinin (CCK) in the control of food intake in chickens. The following aspects were studied: 1) the effects of intravenous and intracerebroventricular sulfated octapeptide of CCK (CCK-8s) on voluntary food intake; 2) the effects of two CCK-receptor antagonists. L-365,260 and L-364,718, on food intake; and 3) the ability of such drugs to block the effects of CCK-8s on food intake in the chicken. Intravenous and intracerebroventricular CCK-8s caused a decrease in food intake. Intraperitoneal L-365,260, a CCK-receptor antagonist with low affinity for the two CCK receptors described in the chicken, increases food intake. Intracerebroventricular L-364,718, a drug that has high affinity for the chicken central CCK-receptor type, increased food intake. The effect of intravenous CCK-8s on food intake was not blocked by L-364,718 or L-365,260, whereas that of intracerebroventricular CCK-8s was blocked by intracerebroventricular L-364,718. It is concluded that central endogenous CCK plays a role in the control of food intake, which is dependent on central CCK-receptor type; nevertheless, peripheral CCK also decreases food intake acting on the peripheral CCK-receptor type. The fact that intracerebroventricular L-364,718 is able to increase food intake is related to its high affinity for the central CCK-receptor type of this species. Finally, three different speculations that might explain the fact that intraperitoneal L-365,260 increases food intake are discussed.

L-364,718 AND L-365,260, two CCK antagonists, have no affinity for central benzodiazepine binding sites in chickens

It has recently been demonstrated that L-365,260, a CCK-B antagonist in mammals, causes an increase in food intake in chickens. In contrast, L-364,718, a CCK-A antagonist in mammals, shows this effect only at very high dose levels. It has been shown that L-365,260 has very low affinity for chicken CCK receptors. Thus, the mechanism of action of L-365,260 remains unknown. As L-365,260 is a benzodiazepine derivative, one may hypothesize that it would be acting on benzodiazepine binding sites. The aims of this work were to establish the existence of benzodiazepine binding sites in the chicken brain, and to check the possibility that L-365, 260 was acting on these receptors, determining the affinity of L-364,718 and L-365, 260 for them. We have found specific binding for tritiated flunitrazepam (a benzodiazepine agonist) ([ 3H]-flunitrazepam) in chicken brain membranes. A single binding site was detected with a K d of 3.58 ± 0.97 nM and a B max of 451.6 ± 23.3 mol/mg protein. L-365,260 and L-364,718 exhibited very low affinity for these binding sites (K i = 1.17 × 10 −6 ± 0.16 × 10 −6 M and K i > 10 −5 M, respectively). Thus, these results demonstrate that the increase in food intake caused by L-365,260 in the chicken is not due to a direct action on benzodiazepine receptors. Other possible explanations for its effect are discussed.

S-57-5 - Synthetic CCK modulators: Update on current pharmacology

It has recently been demonstrated that L-365,260, a CCK-B antagonist in mammals, causes an increase in food intake in chickens. In contrast, L-364,718, a CCK-A antagonist in mammals, shows this effect only at very high dose levels. It has been shown that L-365,260 has very low affinity for chicken CCK receptors. Thus, the mechanism of action of L-365,260 remains unknown. As L-365,260 is a benzodiazepine derivative, one may hypothesize that it would be acting on benzodiazepine binding sites. The aims of this work were to establish the existence of benzodiazepine binding sites in the chicken brain, and to check the possibility that L-365, 260 was acting on these receptors, determining the affinity of L-364,718 and L-365, 260 for them. We have found specific binding for tritiated flunitrazepam (a benzodiazepine agonist) ([3H]-flunitrazepam) in chicken brain membranes. A single binding site was detected with a Kd of 3.58 ± 0.97 nM and a Bmax of 451.6 ± 23.3 mol/mg protein. L-365,260 and L-364,718 exhibited very low affinity for these binding sites (Ki = 1.17 × 10−6 ± 0.16 × 10−6 M and Ki > 10−5 M, respectively). Thus, these results demonstrate that the increase in food intake caused by L-365,260 in the chicken is not due to a direct action on benzodiazepine receptors. Other possible explanations for its effect are discussed.

406 Measurement of nitrite and nitrate in the cerebellum of awake rats by using in vivo brain microdialysis

We investigated the effect of peripheral or central administration of NG-nitro-L-arginine methyl ester (L-NAME), a nitric oxide (NO) synthase inhibitor, on food intake in layer and broiler chicks (Gallus gallus). The intraperitoneal administration of L-NAME significantly decreased food intake in both broiler and layer chicks while the administration of D-NAME, an inactive form of L-NAME, had no effect. The intracerebroventricular (ICV) injection of L-NAME did not affect food intake in broiler chicks. However, ICV injection of L-NAME increased food intake in layer chicks while the injection of D-NAME had no effect. In addition to this, L-NAME-induced feeding was negated with the co-injection of L-arginine, suggesting that NO acts as a feeding-inhibitor signal in the brain of layer chicks. The present study revealed that administration of NO synthase inhibitor affected food intake in chicks, but the effect might be changed by chick strain and position of the injection.

The interaction of clonidine and nitric oxide on feeding behavior in the chicken

Central administration of α 2-receptor agonists stimulate food intake in mammalian and avian species. Recently we reported that inhibition of nitric oxide (NO) synthase (NOS) decreased food intake in chickens. In the present study, we investigated whether the increased eating induced by clonidine (Clon), and α 2-receptor agonist, is attenuated by NOS inhibition. In the first experiment, four levels (0, 9.4, 18.8 or 37.5 nmol/10 μl) of Clon were administered into the right lateral ventricle of chickens, and food intake was monitored. Clon increased 30 min-food intake in a dose-dependent manner. In a co-administration study of l- N G-nitro-arginine methyl ester HCl (LNNA), a NOS inhibitor, and Clon, LNNA (0, 1.5, 3.0 or 5.9 μmol) attenuated food intake induced by Clon (37.5 nmol) in a dose-dependent manner. Our results suggest the possibility that NO interacts with adrenergic neurons in the central nervous system to modulate feeding behavior in the chicken.

Gastrin, somatostatin and histamine release by bombesin from the dog stomach

It has recently been demonstrated that L-365,260, a CCK-B antagonist in mammals, causes an increase in food intake in chickens. In contrast, L-364,718, a CCK-A antagonist in mammals, shows this effect only at very high dose levels. It has been shown that L-365,260 has very low affinity for chicken CCK receptors. Thus, the mechanism of action of L-365,260 remains unknown. As L-365,260 is a benzodiazepine derivative, one may hypothesize that it would be acting on benzodiazepine binding sites. The aims of this work were to establish the existence of benzodiazepine binding sites in the chicken brain, and to check the possibility that L-365, 260 was acting on these receptors, determining the affinity of L-364,718 and L-365, 260 for them. We have found specific binding for tritiated flunitrazepam (a benzodiazepine agonist) ([3H]-flunitrazepam) in chicken brain membranes. A single binding site was detected with a Kd of 3.58 ± 0.97 nM and a Bmax of 451.6 ± 23.3 mol/mg protein. L-365,260 and L-364,718 exhibited very low affinity for these binding sites (Ki = 1.17 × 10−6 ± 0.16 × 10−6 M and Ki > 10−5 M, respectively). Thus, these results demonstrate that the increase in food intake caused by L-365,260 in the chicken is not due to a direct action on benzodiazepine receptors. Other possible explanations for its effect are discussed.

Adverse effects of low concentrations of dietary RNA addition on the growth, food intake and kidney weight of young chickens.

1. The effects of 0, 10 and 50 g/kg of RNA in diets on the growth and food intake of chicks from 6 to 21 d of age were examined. Their effects on renal tissue were examined by light microscopy at the end of experiment. 2. Total food intake and growth decreased with the increase in dietary RNA content and kidney weight was significantly increased by 50 g/kg RNA addition. A significant increase in liver weight was also observed in chickens fed on the diet-supplemented with 10 g RNA/kg. 3. The enlarged kidney caused by dietary RNA contained many crystals which were composed mainly of calcium salts but did not contain purines. 4. It is concluded that relatively low dietary RNA concentrations decrease food intake and growth and cause enlarged kidneys which contains many crystals composed mainly of calcium salts.

Genetic Control of Food Intake in Chickens

Genetic selection for body weight in broiler-type chickens has created a highly efficient omnivore capable of attaining a 2.0 kg body weight in 40-42 d of age with an overall feed conversion (feed consumed per unit of body weight) of less than two. The primary correlated response to the huge increases in the growth of chickens over the last 50 years has been increased feed intake. Although there is much independent data regarding the physiological systems controlling feed intake, there is a dearth of information regarding the inheritance of central and peripheral feed intake control mechanisms. Using four lines of chickens from a double selection experiment for exponential growth rate at different ages, we are investigating changes in both peripheral and central feed intake control mechanisms in response to selection. We have observed a genetic basis for neurotransmitter levels in the hatching chick, which seems to be related to selection for body weight. Diallel crossing experiments have demonstrated that catecholamine levels are inherited in a nonadditive manner, as is feed consumption immediately post-hatch, suggesting that sympathetic nervous activity (as defined by catecholamine and metabolite levels) may be involved in the inheritance of early feed intake in chickens. Further, the use of pharmacological substances (such as monosodium glutamate) known to alter food intake in mammals exhibit signs of genotype by treatment interactions for growth and hypothalamic neurotransmitter levels. These data suggest a research strategy to separate genetic changes in food intake from those related to responses in metabolism.

Effect of cholecystokinin receptor antagonists on voluntary food intake in chickens

The effect of two cholecystokinin (CCK) receptor antagonists (L-364718 and L-365260) and of diazepam on voluntary food intake in chicken was studied. L-365260 significantly increased cumulative food intake at 30 and 60 min, whereas L-364718 had no effect. Diazepam also increased food intake at 30 minutes. It was therefore concluded that anxiolytic effects could account for an increase in food intake in the conditions under which the study was carried out. Consequently, the effect of L-365260 could either be due to its anxiolytic properties or to its direct effects on food intake control.

Evaluation of the effect of extrusion cooking of jackbean ( Canavalia ensiformis L.) seed on short-term feed intake in chicks

Experiments were conducted to investigate the relationship between various extrusion cooking conditions, the chemical composition of jackbean samples and the short-term control of food intake in chicks. All data were analysed using a principal component analysis computerized program. Ground jackbean was extruded on a pilot-scale twin-screw extruder. Water addition at the feed inlet, filling rate of the screws, barrel temperature in the last section of the extruder and reverse-screw element position were tested as operating variables. Three sets of experiments (A, B and C) and a total of 20 trials were performed. Process variables were specific mechanical energy, product temperature measured at the die and resulting pressure exerted on the shafts. Also, colour values were determined on all jackbean samples. Experimental diets containing 300 g kg −1 extruded jackbean were fed to 7-day-old chicks to measure the short-term variations in food intake. Inactivation of the lectin (concanavalin A) was monitored using a haemagglutination assay. In addition, starch solubility, and reactive lysine and canavanine contents were determined on samples from Experiment A. Pilot-scale extrusion cooking of Canavalia appears to be feasible: water addition decreased energy consumption ( r = −0.76), filling rate and position of the reverse-screw element are correlated to product temperature ( r = +0.61 and −0.66, respectively). Food intake inhibition index, used as an expression of toxicity for chicks, was reduced in proportion to a decrease in the amount of water added and to the filling rate ( r = +0.8 and +0.6, respectively). The minimum food intake inhibition index was 70% in Experiment A, 61% in Experiment B and 35% in Experiment C according to our experimental conditions. The lower the food intake inhibition index, the more delayed the inhibition effect on food intake. Lightness and specific mechanical energy appeared to be accurate indicators of the detoxification level ( r = +0.85 and +0.72). No significant relationship was apparent between toxicity and haemagglutination activity of the meal. Additional research is needed to understand the high correlation found among canavanine, reactive lysine content and the reduced feed intake shown by the chicks.

Effects of different rates of drying cassava root on its toxicity to broiler chicks.

1. The effects of drying cassava root at different rates on its composition and toxicity to broiler chicks were examined. Unpeeled roots from a high-cyanide cultivar of cassava were chipped and dried at 25 degrees C to a moisture content of below 100 g/kg over 24 h for fast-dried meal (FD) or 72 h for slow-dried meal (SD). The meals were incorporated at 250 and 500 g/kg into semi-synthetic diets which were fed to day-old broiler chicks as mash or pellets in separate experiments. 2. The two drying rates produced meals with similar concentrations of polyphenols, but different concentrations of cyanogens, the latter being 38 and 482 mg total cyanide/kg for SD and FD, respectively. The linamarin, acetonecyanohydrin or total cyanide content measurements of pelleted diets were highly correlated. 3. Growth rates of chicks fed on SD-based diets were significantly higher than those of chicks fed on FD-based diets. Compared with a control diet, weight gain of chicks fed on the 500 g FD/kg diet (containing 258 mg total cyanide/kg) was 77% lower, although performance also appeared to be reduced at 142 mg total cyanide/kg. 4. The ratio of water:food intake of chicks was higher in FD than in SD groups, and this was reflected in the high water content of excreta. There was increased bile excretion, the chloretic effect increasing with the cyanogen content of diet. Pancreas weights were lower in FD than in SD groups in experiment 1 (mash diets), but not in experiment 2 (pelleted diets), while there was a significant interaction between drying method and cassava inclusion rate on liver weight in experiment 2, but not in experiment 1. There were no effects on the mortality rate. 5. Pelleting of diets generated high temperatures, but did not significantly alter the cyanogen concentration or the growth of the chicks. 6. Thus, slower rates of drying cassava roots produce meals with lower cyanogen concentration that are, consequently, less toxic to broiler chicks. Cassava root meal of less than 40 mg total cyanide/kg can be fed to broiler chicks at 500 g/kg without any adverse effects.

Effect of concanavalin A from jackbean seeds on short-term food intake regulation in chicks and laying hens

A balanced diet containing 30% jackbean seed meal induces a 50% reduction in food intake in young chicks (7 or 14 days old) after a delay of 30–45 min from the onset of normal consumption. This reduction in food intake, which is the major cause of growth depression in chicks fed on jackbean (JB), is consistent (14 experiments) and can be used as a routine procedure for testing various fractions of JB seeds. Concanavalin A (Con A) was isolated and identified as the major cause of this early reduction in food intake. Dose-response curves show a linear decrease of food intake up to 0.85% of Con A in the diet. From 0.85 to 2.55% of Con A in the diet, the response is less marked. This response is much faster (a few minutes) in adult hens which have been previously exposed to JB than in naive birds (1 h). After repeated distribution, the diet containing JB is probably recognised by cephalic organs (smell or taste), although the initial effect of Con A on food intake is probably independent of taste or smell control. A single oral administration of purified Con A significantly affects the intake of a regular diet for > 6 h. Addition of D (+) mannose partly counteracts the effect of Con A on food intake, both in young chicks and adult hens. The effect of Con A on the initial stage of food intake in chicks is probably not initially associated with taste or smell detection; it is associated with the haemagglutinating capacity of the diet and is dependent on the carbohydrate-binding capacity of this lectin, perhaps involving the glycosylated proteins and lipids of the gut cells.