Effects of "Bioactive" amino acids leucine, glutamate, arginine and tryptophan on feed intake and mRNA expression of relative neuropeptides in broiler chicks

ABSTRACT: Feed intake control is vital to ensuring optimal nutrition and achieving full potential for growth and development in poultry. The aim of the present study was to investigate the effects of L-leucine, L-glutamate, L-tryptophan and L-arginine on feed intake and the mRNA expression levels of hypothalamic Neuropeptide involved in feed intake regulation in broiler chicks. Leucine, glutamate, tryptophan or arginine was intra-cerebroventricularly (ICV) administrated to 4d-old broiler chicks respectively and the feed intake were recorded at various time points. Quantitative PCR was performed to determine the hypothalamic mRNA expression levels of Neuropeptide Y (NPY), agouti related protein (AgRP), pro-opiomelanocortin (POMC), melanocortin receptor 4 (MC4R) and corticotrophin releasing factor (CRF). Our results showed that ICV administration of L-leucine (0.15 or 1.5 mumol) significantly (P < 0.05) increased feed intake up to 2 h post-administration period and elevated both hypothalamic NPY and AgRP mRNA expression levels. In contrast, ICV administration of L-glutamate (1.6 mumol) significantly (P < 0.05) decreased feed intake 0.25, 0.5 and 2 h post-injection, and increased hypothalamic CRF and MC4R mRNA expression levels. Meanwhile, both L-tryptophan (10 or 100 mug) and L-arginine (20 or 200 mug) had no significant effect on feed intake. These findings suggested that L-leucine and L-glutamate could act within the hypothalamus to influence food intake, and that both orexigenic and anorexigenic Neuropeptide genes might contribute directly to these effects.     

Methylamine induced hypophagia is mediated via dopamine D1 and D2 receptors in neonatal meat chicks

Recently, methylamine has been found as an endogenous amine, which is controling food intake in mammals. However, there is no evidence about the effect of methylamine on feeding behavior in poultry. So, the present study was designed to evaluate the effect of intracerebroventricular (ICV) injection of methylamine and involvement of central methylamine/dopaminergic systems on feeding behavior in neonatal meat type chicks. In experiment 1, chicks were ICV injected with different doses of methylamine (0.48, 0.96, 1.44, 1.92 and 2.40 μmol). In experiment 2, chicks received a dose of either the control solution, 2.40 μmol methylamine, 125 nmol L-DOPA (dopamine precursor) or a combination of methylamine plus L-DOPA. Experiments 3–7 were similar to experiment 2 except that 150 nmol 6-OHDA (dopamine synthase inhibitor), 5 nmol SCH23390 (D1 receptor antagonist), 5 nmol AMI-193 (D2 receptor antagonist), 6.4 nmol NGB2904 (D3 receptor antagonist) and 6 nmol L-741, 742 (D4 receptor antagonist) were used instead of 125 nmol L-DOPA, respectively. Cumulative food intake was determined until 2 h post-injection. According to the results, methylamine significantly decreased food intake in a dose dependent manner (p < 0.05). The inhibitory effect of methylamine on food intake was significantly attenuated by 6-OHDA, SCH23390 and AMI-193 (P < 0.05), but NGB2904 and L-741, 742 had no effect on food intake induced by methylamine. In addition, hypophagic effect of methylamine significantly amplified by L-DOPA (P < 0.05). These results suggest that methylamine decrease food intake and there is an interaction between methylamine and dopaminergic system via D1 and D2 receptors in chickens.     

Effect of oral administration of L-pipecolic acid on food intake in chicks and mice

It has been demonstrated that L-pipecolic acid (L-PA), a major metabolic intermediate of L-lysine (L-Lys) in the brain, is involved in the functioning of the γ-aminobutyric acid-ergic system. Previous study has shown that intracerebroventricular injection of L-PA suppressed feeding and induced sleep-like behavior in neonatal chicks. The present study examines whether the action of L-PA was induced by gavage in both chicks and mice. Oral administration of L-PA significantly inhibited food intake at 2 h after treatment in neonatal chicks, although no significant effect of L-Lys was detected. In mice, oral L-PA suppressed food intake compared to the control after 2 h of treatment. It was concluded that L-PA was effective for suppression of food intake after oral administration in both avian and mammalian species.     

Intracerebroventricular administration of chicken glucagon‐like peptide‐2 potently suppresses food intake in chicks

Glucagon‐related peptides, such as glucagon‐like peptide (GLP)‐1, GLP‐2 and oxyntomodulin (OXM), are processed from an identical precursor proglucagon. In mammals, all of these peptides are suggested to be involved in the central regulation of food intake. We previously showed that intracerebroventricular administration of chicken OXM and GLP‐1 significantly suppressed food intake in chicks. Here, we show that central administration of chicken GLP‐2 potently suppresses food intake in chicks. Male 8‐day‐old chicks (Gallus gallus domesticus) were used in all experiments. Intracerebroventricular administration of chicken GLP‐2 significantly suppressed food intake in chicks. Plasma glucose concentration was significantly decreased by chicken GLP‐2, whereas plasma nonesterified fatty acid concentration was significantly increased. Intracerebroventricular administration of chicken GLP‐2 did not affect plasma corticosterone concentration. In addition, the anorexigenic effect of GLP‐2 was not reversed by the corticotropin‐releasing factor (CRF) receptor antagonist α‐helical CRF, suggesting that CRF is not a downstream mediator of the anorexigenic pathway of GLP‐2 in chicks. Intracerebroventricular administration of an equimolar amount of GLP‐1 and GLP‐2, but not OXM, significantly suppressed food intake in both broiler and layer chicks. All our findings suggest that GLP‐2 functions as a potent anorexigenic peptide in the brain, as well as GLP‐1, in chicks.     

Changes in ghrelin levels of plasma and proventriculus and ghrelin mRNA of proventriculus in fasted and refed layer chicks

This is a test-report of ghrelin levels in plasma and proventriculus, the glandular portion of the avian stomach, by using a specific radioimmunoassay for acylated ghrelin, as well as the expression of the ghrelin gene in the proventriculus after a 12-h fasting period followed by a 6-h feeding period with 6-day-old layer chicks. After fasting, the plasma ghrelin levels increased from 21.3 ± 4.5 to 32.9 ± 5.0 fmol/ml, but once refed it returned to the control value. After fasting, the ghrelin mRNA and the peptide levels in the proventriculus increased, and ghrelin mRNA levels remained high but once refed the ghrelin content returned to the control level. Furthermore, in order to examine the effect of increased circulating ghrelin on food intake, a bolus intravenous injection of 500 pmol of chicken ghrelin was given to 8-day-old chicks. The ghrelin injection did not cause any significant changes in food intake. These results indicate that the levels of ghrelin and its mRNA with layer chicks are altered according to the feeding state and this in a similar manner as has been observed in mammals. Unlike in mammals, an increase in circulating ghrelin does not cause the promotion of food intake in chicks.     

Influence of ketone body and the inhibition of fatty acid oxidation on the food intake of the chick

1. Fatty acid oxidation is known to be involved in the control of food intake in mammals. The effect of fatty acid oxidation on food intake in chickens was studied using a ketone body (beta-hydroxybutyrate (beta-HB)) and mercaptoacetate (MA) (an inhibitor of fatty acid oxidation). 2. Central and peripheral injection of beta-HB decreased food intake in a dose-dependent manner, while low doses of MA had no effect. Higher doses of MA inhibited feeding but also caused mortality. 3. These results indicate that ketone bodies act as an inhibitory signal for food intake in both the central and peripheral nervous systems but that inhibition of fatty acid oxidation may not be associated with feeding behaviour in chicks.     

Possible role of central interleukins on the anorexigenic effect of lipopolysaccharide in chicks

1. The purpose of the present study was to determine if central interleukin-1β (IL1β), interleukin-6 (IL6) and interleukin-8 (IL8) affect feeding behaviour in chicks (Gallus gallus) and examine if central interleukins are related to the lipopolysaccharide (LPS)-induced anorexia.

2. Intra-abdominal (IA) injection of LPS significantly suppressed feeding behaviour and significantly increased mRNA expression of IL1β and IL8 in the diencephalon when compared to the control group, while IL6 tended to be increased.

3. Intracerebroventricular (ICV) injection of 200 ng IL1β significantly decreased food intake at 60 min after the injection while IL6 and IL8 had no effect.

4. IA injection of these ILs (200 ng) had no effect on food intake in chicks.

5. ICV injection of 200 ng IL1β did not affect water intake and plasma corticosterone concentration, suggesting that central IL1β might not be related to the regulation of drinking behaviour and the hypothalamus–pituitary–adrenal axis.

6. The present study demonstrated that central IL1β but not IL6 and IL8 might be related to the inhibition of feeding in chicks.     

Effect of intracerebroventricular orexin-B on food intake in sheep.

Orexin is a hypothalamic neuropeptide that regulates feeding behavior in rats. Orexin-B has recently been cloned in pigs and was shown to stimulate food intake after intramuscular injection. This study was designed to determine whether intracerebroventricular (ICV) and intravenous injections of orexin could regulate appetite in sheep. Suffolk wethers were moved to indoor facilities, adapted to diets for 6 wk, and trained to stand in stanchions for 3 to 6 h each day for 2 wk before indwelling ICV cannulas were installed. These sheep were provided water and they consumed feed ad libitum. On the day before an experiment, each sheep was cannulated in a jugular vein. On the day of an experiment, sheep were placed in stanchions and allowed to stand for 1 h before use. Sheep were then monitored over a 2-h control period before i.v. injection with saline or porcine orexin-B (3 micrograms/kg BW) or ICV injection with artificial cerebrospinal fluid (CSF), orexin (0.03, 0.3, or 3 micrograms/kg BW) or in a second experiment with either orexin B (0.03, 0.3, 3 micrograms/kg BW), neuropeptide-Y (NPY; 0.3 microgram/kg BW), or orexin plus NPY. Food intake was monitored for consecutive 2-h periods. The i.v. injections of orexin did not affect food intake or metabolite or hormone concentrations. In ICV sheep, orexin increased food intake at 2 (P < 0.04) and at 4 h (P < 0.02). Food intake was greatest with the 0.3 microgram/kg BW dosage of orexin (P < 0.05). In the first 2 h after injection, orexin had an effect similar to that of NPY (0.23 kg for orexin and 0.2 kg for NPY). The combination of NPY and orexin had a greater effect on food intake (to 0.34 kg) than did either orexin (P < 0.05) or NPY (P < 0.008) alone. Differences were not apparent in the subsequent 2-h interval. No differences were noted in free fatty acid, glucose, growth hormone, luteinizing hormone, or insulin concentrations following orexin injection. There was an effect of ICV orexin treatment on plasma cortisol concentrations (P < 0.002). Cortisol was increased by orexin at the 0- to 2-h (P < 0.008) and in the 2- to 4-h (P < 0.009) intervals after orexin injection. These data indicate that central administration of orexin stimulates feed intake in sheep.     

The effect of Nesfatin-1 on food intake in neonatal chicks: role of CRF<Subscript>1</Subscript> /CRF2 and H1/ H3 receptors

The present study was designed to determine the effect of central injection of Nesfatin-1 and corticotropin and histaminergic systems on food intake in neonatal meat-type chicks. In this study, 7 experiments were designed, each with 4 treatment groups. In experiment 1, four groups of chicks received the ICV injection of (A) phosphate-buffered saline (PBS), (B) Nesfatin-1 (10 ng), (C) Nesfatin-1 (20 ng) and (D) Nesfatin-1 (40 ng). In experiment 2, (A) PBS, (B) Astressin-B (CRF₁/CRF₂ receptors antagonist; 30 µg), (C) Nesfatin-1 (40 ng) and (D) Nesfatin-1?+?Astressin-B were injected. In experiments 3–6, chicken received ICV injection of the Astressin2-B (CRF₂ receptor antagonist; 30 µg), α-FMH (alpha fluoromethyl histidine; as inhibitor of histidine decarboxylase, 250 nmol), Chlorpheniramine (histamine H₁ receptors antagonist, 300 nmol), Famotidine (histamine H₂ receptors antagonist, 82 nmol) and Thioperamide (histamine H₃ receptors antagonist, 300 nmol) instead of the Astressin-B. Then the cumulative food intake measured until 120 min post-injection. According to the results, ICV injection of Nesfatin-1 dose dependently decreased food intake in neonatal chicks (P?<?0.05). Co-injection of the Nesfatin-1 and Astressin-B (CRF₁/CRF₂) inhibited Nesfatin-1 induced hypophagia (P?<?0.05). ICV inejction of the Nesfatin-1?+?Astressin-B significantly inhibited the effect of Nesfatin-1 on food intake (P?<?0.05). In addition, α-FMH and chlorpheniramine attenuated Nesfatin-1-induced hypophagia in chicks (P?<?0.05); while thioperamide significantly amplified the effect of Nesfatin-1 on food intake in chicks (P?<?0.05). These results suggested Nesfatin-1 has an anorectic effect in 3-hour food deprived neonatal meat-type chicks and this effect was mediated by corticotropin CRF₁/CRF₂ as well as histamine H₁ and H₃ receptors.     

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.     

Modulatory function of NMDA glutamate receptor on MC<Subscript>3</Subscript>/MC<Subscript>4</Subscript> receptors agonist-induced hypophagia in neonatal meat-type chicken

Melanocortin 3 and 4 receptors (MC₃R and MC₄R) are known as the main receptors for melanocortin-induced hypophagia in mammalian and poultry. Also, central glutamatergic system has mediatory role on function of the melanocortin system in some brain areas. So, the aim of the current study was to determine the role of MC₃/MC₄ receptors agonist on food intake and its interaction with glutamatergic in 3-h food-deprived (FD₃) neonatal broilers. In experiment 1, chickens were intracerebroventricular (ICV) injected with control solution, MTII (MC₃/MC₄ receptors agonist; 2.45, 4.8 and 9.8 pmol). In experiment 2, control solution, SHU9119 (MC₃/MC₄ receptors antagonist; 0.5, 1 and 2 nmol) were ICV injected. In experiment 3, birds ICV injected with control solution, SHU9119 (0.5 nmol), MTII (9.8 pmol) and co-injection of the SHU9119 + MTII. Experiments 4–8 were similar to experiment 3, except birds injected with MK-801 (NMDA glutamate receptors antagonist, 15 nmol), CNQX (AMPA glutamate receptors antagonist; 390 nmol), AIDA (mGLUR₁ glutamate receptors antagonist; 2 nmol), LY341495 (mGLUR₂ glutamate receptors antagonist; 150 nmol) and UBP1112 (mGLUR₃ glutamate receptors antagonist; 2 nmol) instead of SHU9119. Then, cumulative food intake was recorded until 120 min after injection. According to the results, dose dependent hypophagia observed after ICV injection of the MTII (p < 0.05). ICV injection of SHU9119 significantly increased food intake in birds (p < 0.05). Co-injection of SHU9119 + MTII significantly inhibited MTII- induced hypophagia in neonatal chicks (p < 0.05). In addition, hypophagia- induced by MTII was significantly attenuated with co-injection of MTII + MK-801(p < 0.05). These results suggested MC₃ and MC₄ receptors have inhibitory role on food intake and this effect is probably mediated by NMDA glutamate receptors in neonatal chickens.     

Central regulation of food intake in the neonatal chick

Regulating food intake is complicated in animals including domestic birds. Just after hatching, neonatal chicks find their food by themselves and they can control food intake, since domestic chicken belongs to the precocial type of avian species. Thus, domestic chickens have relatively well-developed mechanisms of food-intake control at hatching. While many aspects of food-intake regulation in chickens appear similar to that in mammals, there are some responses that are unique to chickens. For instance, some neurotransmitters such as neuropeptide Y (NPY), orexin-A, orexin-B, motilin, melanin-concentrating hormone (MCH), galanin, growth hormone releasing factor (GRF) and ghrelin stimulate feeding in mammals. Only NPY strongly stimulates food intake in birds similar to that observed in mammals; however, both orexins, motilin, MCH and galanin failed to alter food intake of the chick. Moreover, GRF and ghrelin suppressed feeding of chicks. On the other hand, cholecystokinin (CCK), gastrin, glucagon-like peptide-1 (GLP-1), corticotropin-releasing factor (CRF), histamine, α-melanocyte stimulating hormone (α-MSH), leptin and bombesin are known to suppress feeding in mammals. These responses are similar to those of mammals except for leptin. Therefore, the inhibitory mechanisms for feeding are well conserved in chicks.     

Intracerebroventricular injection of mammalian motilin, melanin-concentrating hormone or galanin does not stimulate food intake in neonatal chicks

1. Several neural peptides are known to stimulate feeding behaviour in mammalian species. The aim of this study was to elucidate whether central injection of mammalian motilin, melanin-concentrating hormone (MCH) or galanin stimulates feeding in the neonatal chick. 2. None of the peptides applied here enhanced the food intake of the chick. 3. It is suggested that motilin, MCH and galanin, at least those of mammalian origin, may not regulate feeding in neonatal chicks, when administered to the central nervous system.     

Physiological responses to central and peripheral injection of polyinosinic-polycytidylic acid in chicks

1. The purpose of the present study was to determine if intracerebroventricular (ICV) and intraperitoneal (IP) injection of polyinosinic-polycytidylic acid (poly I:C), a viral mimetic that binds to toll-like receptor-3 (TLR3), affects food intake, voluntary activity, cloacal temperature, plasma corticosterone (CORT) and glucose concentrations, and crop emptying rate in chicks (Gallus gallus).

2. Both ICV and IP injection of poly I:C significantly decreased food intake.

3. IP but not ICV injection of poly I:C significantly suppressed voluntary activity, whereas ICV injection decreased time spent sitting. Both ICV and IP injection of poly I:C significantly increased plasma CORT and glucose concentration. Neither ICV nor IP injection of poly I:C significantly affected cloacal temperature.

4. In addition, ICV injection of poly I:C significantly reduced crop emptying rate, whereas IP injection had no effect.

5. These results suggested that central TLR3 is related to anorexia, stress response and retardation of crop emptying while peripheral TLR3 is related to anorexia, change in behaviour and stress responses during viral infection in chicks.     

Ingestive responses to mu and delta opioid receptor agonists in the domestic fowl

1. Four experiments were conducted using the highly specific mu and delta opioid receptor agonists morphiceptin (B-casomorphin 1-4, amide) or [Met5]-enkephalin, respectively, to evaluate the effect of mu and delta opioid receptor agonists on ingestive behaviour in the domestic fowl. 2. Intracerebroventricular (ICV) administration of 0.625, 1.25, 2.5 and 5.0 micrograms of morphiceptin significantly stimulated drinking, while having no effect on feeding. Intramuscular injection of 0.5, 1.5 and 3.0 mg morphiceptin/kg body weight induced a significant increase in feeding, whereas drinking was not altered. 3. ICV administration of 0.625, 1.25, 2.5 and 5.0 micrograms [Met5]-enkephalin, as well as intramuscular injection of 0.5, 1.5 and 3.0 mg [Met5]-enkephalin significantly stimulated feeding while having no effect on drinking. 4. These results suggest that, in the central nervous system, mu opioid receptor agonists stimulate drinking and delta receptor agonists stimulate feeding. At sites outside the blood-brain barrier, both mu and delta opioid receptor agonists stimulate feeding.     

Involvement of histaminergic and noradrenergic receptors in the oxytocin-induced food intake in neonatal meat-type chicks

Oxytocin neurons have a physiological role in food intake and energy balance. Several studies have shown that central histaminergic and adrenergic systems synapse on oxytocin neurons but there is no information for their interaction on food intake regulation in birds. The purpose of this study was to examine the effects of intracerebroventricular (ICV) injection of α-fluoromethylhistidine (α-FMH, histidine decarboxylase inhibitor), chlorpheniramine (histamine H1 receptors antagonist), famotidine (histamine H2 receptors antagonist), thioperamide (histamine H3 receptors antagonist), prazosin (α1 receptor antagonist), yohimbine (α2 receptor antagonist), metoprolol (β1 adrenergic receptor antagonist), ICI 118,551 (β2 adrenergic receptor antagonist) and SR59230R (β3 adrenergic receptor antagonist) on oxytocin-induced hypophagia in 3-h food-deprived (FD₃) neonatal broiler chicken. In Experiment 1, 3 h-fasted chicks were given an ICV injection of saline, α-FMH (250 nmol), oxytocin (10 μg) and co-injection of α-FMH + oxytocin. Experiments 2–9 were similar to experiment 1 except birds were injected with chlorpheniramine (300 nmol), famotidine (82 nmol), thioperamide (300 nmol), prazosin (10 nmol), yohimbine (13 nmol), metoprolol (24 nmol), ICI 118,551(5 nmol) and SR59230R (20 nmol) instead of α-FMH, respectively. After injection cumulative food intake was measured until 120 min post injection. According to the results, ICV injection of oxytocin significantly decreased food intake in broiler chickens (P < 0.001). ICV injection of α-FMH significantly attenuated hypophagic effect of oxytocin (P < 0.001). Also, co-injection of chlorpheniramine plus oxytocin significantly decreased the effect of oxytocin on food intake (P < 0.001). Co-administration of thioperamide and oxytocin significantly amplified hypophagic effect of oxytocin in chickens (P < 0.001). In addition, ICI 118,551 attenuated hypophagic effect of oxytocin (P < 0.001); while famotidine, prazosin, yohimbine, metoprolol and SR59230R had no effect on oxytocin- induced food intake in FD3 broiler chickens. These results suggest that the effect of oxytocin on food intake is probably mediated by histaminergic (via H1 and H3 receptors) and noradrenergic (via β2 receptors) systems in broiler chickens.     

The role of glutamatergic and GABAergic systems on serotonin- induced feeding behavior in chicken

It has been reported that serotonin can modulate glutamate and GABA release in central nervous system (CNS). The present study was designed to examine the role of glutamatergic and GABAergic systems on serotonin- induced feeding behavior in chickens. In Experiment 1 intracerebroventricular (ICV) injection of MK- 801(NMDA receptor antagonist, 15 nmol) performed followed by serotonin (10 μg). In experiments 2, 3, 4, 5, 6 and 7 prior to serotonin injection, chickens received CNQX (AMPA/kainate receptor antagonist, 390 nmol), AIDA (mGluR1 antagonist, 2 nmol), LY341495 (mGluR2 antagonist, 150 nmol), UBP1112 (mGluR3 antagonist, 2 nmol), picrotoxin (GABA A receptor antagonist, 0.5 μg), CGP54626 (GABAB receptor antagonist, 20 ng) respectively. Cumulative food intake was determined at 3 h post injection. The results of this study showed that the hypophagic effect of serotonin was significantly attenuated by pretreatment with MK- 801 and CNQX (p?<?0.05) but AIDA, LY341495 and UBP1112 had no effect (p?>?0.05). Also, the inhibitory effect of serotonin on food intake was amplified by picrotoxin (p?<?0.05) while CGP54626 had no effect (p?>?0.05). These results suggest that serotonin as a modulator probably interacts with glutamatergic (via NMDA and AMPA/Kainate receptors) and GABAergic (via GABAA receptor) systems on feeding behavior in chicken.     

Opioid modulation of feeding and drinking in fowls

1. D-ala2-methionine enkephalinamide (DME), the stable analogue of met-enkephalin (an opioid agonist), stimulated food intake of immature hens in the first 30 min after intracerebroventricular injection (2 and 8 micrograms/kg), but had no effect on either food or water intake when injected intravenously (15 and 60 micrograms/kg). 2. Naloxone (an opioid antagonist) had no effect on food intake after either intracerebroventricular (50 and 200 micrograms/kg) or intravenous (1 and 4 mg/kg) injection, but inhibited water intake in the second 30 min after intravenous injection. 3. Water intake was not measured after the intracerebroventricular injections of DME and naloxone. 4. Both feeding and drinking were inhibited in a dose-related way in the 7 h after intramuscular injection of nalmefene (0.2, 0.4, 0.8 and 1.6 mg/kg), a more potent and longer-lasting antagonist than naloxone. 5. These data are compared with published results from similar work with birds and mammals. It is concluded that central release of endogenous opioids may reinforce both feeding and drinking in fowls, but whereas opioid blockage affects feeding more than drinking in pigeons and quail, the opposite appears to be the case in fowls.     

Intracerebroventricular melanin-concentrating hormone stimulates food intake in sheep

Melanin-concentrating hormone (MCH) stimulates feeding when injected intracerebroventricularly (ICV) in rats. At present it is not clear whether the function of MCH is similar in ruminants, which are species with a continuous delivery of nutrients. Therefore the current investigation sought to determine the role of MCH in sheep. In the first experiment, six, castrate male sheep were satiated and received one of four treatments [saline, 0.1, or 1.0 nmol/kg MCH, and NPY (0.1 nmol/kg)] injected ICV over 30s, then infused ICV for 6 h ( approximately 500 microl/h). Food intake was measured for 2 h before and at 2, 4, 6, 8, 12 and 24 h. In this experiment, feed intake was increased (P相似文献   

Peripheral leptin effect on food intake in young chickens is influenced by age and strain

The acute effect of leptin on the regulation of food intake was investigated in layer and broiler chickens. In an initial study, we observed that a single intraperitoneal injection of recombinant chicken leptin (1 mg/kg BW) dramatically reduced (38%) food intake in 56-day-old layer chickens, more moderately reduced (15%) food intake in 9-day-old layer chicks, and had no significant effect in 9-day-old broiler chicks. In a subsequent study, body weight and plasma concentrations of leptin were measured weekly in layer and broiler chicks from day 1 to 35 of age and brain leptin receptor and neuropeptide Y (NPY) mRNA expression were analyzed at 1, 9, and 35 days of age. At day 1 of age, peripheral concentrations of leptin were significantly greater in layer than broiler chicks. Subsequently, despite increases in body weight and differences in growth rates between layer and broiler chicks from day 8 to day 35 of age, peripheral concentrations of leptin were constant and similar in both genotypes. Leptin receptor and NPY mRNA were expressed in brain from day 1 in chicks of both genotypes and increased significantly to day 35 of age. These observations provide evidence that the inhibitory effect of leptin on the regulation of food intake in growing chicks is an age dependent process. Furthermore, acquisition of the anorectic effect of leptin is likely to be associated with greater expression of the leptin receptor and NPY mRNAs than to changes in blood levels of leptin. Finally, this study provides evidence that chickens selected for high growth rates may be less sensitive or responsive to peripheral concentrations of leptin than chickens with low growth rates (layers), suggesting that the faster growth of broiler chicks may be related to a lessened responsiveness to anorexigenic factors.