J-STAGE Advance Publication Date: December 25, 2010 The Journal of Poultry Science doi: 10.2141/jpsa.010117
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Hypothalamic Melanocortin System on Feeding Regulation in Birds: A Review
Takashi Bungo*, Jun-ichi Shiraishi and Shin-ichi Kawakami
Department of Bioresource Science, Graduate School of Biosphere Science, Hiroshima
University, Higashi-Hiroshima 739-8528, Japan;
Running head: MELANOCORTIN SYSTEM AND FEEDING REGULATIONProofs
*Correspondence:
Dr. T. Bungo Laboratory of Animal Behavior and PhysiolViewogy, Graduate School of Biosphere Science, Hiroshima University, Higashi-Hiroshima 739-8528, Japan
E-mail: [email protected]
Advance
J-STAGE Advance Publication Date: December 25, 2010 The Journal of Poultry Science doi: 10.2141/jpsa.010117
Abstract
Regulation of feed intake in chickens represents a complex homeostatic
mechanism involving multiple levels of control. Understanding the regulation of
feeding behavior can be a very important theme in animal production. Recently, a
close evolutionary relationship between the peripheral and hypothalamic neuropeptides
has become apparent. In the infundibular nucleus (the avian equivalent of the
mammalian arcuate nucleus), the melanocortin system, which contains neuroendocrine
neurons that regulate endocrine secretions by releasing substances, is an essential site in
the brain for signals about the status of peripheral energy balance. The structure and
function of many hypothalamic neuropeptides, melanocortins, neuropeptide-Y (NPY)
and agouti-related protein (AGRP) have been characterized. ThisProofs review provides as
overview of the various effects and interrelationship of these central and peripheral
neuropeptides, and summarizes the role of the melanocortin system on feeding
regulation in chicks. View Key words: melanocortin system; pro-opiomelanocortin (POMC); neuropeptide-Y
(NPY); agouti-related protein (AGRP); feed intake; chick;
Advance
J-STAGE Advance Publication Date: December 25, 2010 The Journal of Poultry Science doi: 10.2141/jpsa.010117
Introduction
Feeding behavior in domestic chickens is the one of the greatest concerns of
animal scientists and producers because it not only establishes a healthy life but also
holds the key to improvements in productive efficacy for meat and eggs. Thus,
understanding the regulation of feeding behavior can be a very important theme in
poultry production. There are various factors which affect feeding behavior and the
information-processing network of those factors should operate accurately. In
particular, there is a vast amount of research on brain function because the central
nervous system (CNS) is thought to be a critical center of behavioral motivations.
From the initial findings, it is well known that the lateral hypothalamic area is the
feeding center that accelerates feed intake, and the ventromedialProofs nucleus of the
hypothalamus is the satiety center that decelerates feed intake. The hypothalamic
arcuate nucleus (ARC) has become the focus of much attention in recent years because
of its critical brain site, which is conveniently located at the floor of the third ventricle in an area without the blood brain barrier. View This facilitates signaling from the peripheral organs/tissues to reach the relevant nuclei via the ARC.
To regulate feeding, caloric intake must equal caloric expenditure over time.
Such an intricate process relies on the interactions of a number of physiological systems.
There is considerable evidence that the regulatory system signals from the peripheries
(e.g., intestines, pancreas and adipose tissue) inform the ARC about the status of
peripheral energy balance. Several observations suggest that the ARC contains neuroendocrineAdvance neurons, the so called melanocortin system which is an essential mediator for the peripheral signals such as leptin and insulin action in the CNS
(Schwartz et al., 2000; Benoit et al., 2002). In an expanded sense, the melanocortin
system consists of pro-opiomelanocortin (POMC) neurons inhibiting feeding, and
neuropeptide-Y (NPY) and/or agouti-related protein (AGRP) neurons stimulating
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feeding.
Previous reviews of the relevant neuropeptides and their comparative functions
in mammals on feeding regulation have discussed the role of the CNS in chicks (Furuse,
2002; Furuse et al., 2007). This review provides an overview of and discusses the role
of the melanocortin system on feeding regulation in birds, especially in chickens.
1. Characteristics of Feeding Regulation in the Melanocortin System
1.1. POMC
POMC is a precursor for the melanocortin peptides, α-, β- and γ-melanocyte
stimulating hormone (MSH) and the endogenous opioid, β-endorphin. To date, five
melanocortin receptors (MC1R to MC5R) have been identified (MounProofstjoy et al., 1992;
Adan and Gispen, 2000). MC3R and MC4R are highly expressed in the CNS, and
α-MSH released by POMC neurons in the ARC plays a key role in the control of feed
intake by acting on these receptors in mammals (Mountjoy et al., 1992, 1994; Roselli-Rehfuss et al., 1993). Central Viewinjection of α-MSH or MTII (a synthetic melanocortin agonist for MC3R and MC4R) inhibits feed intake in rodents, as well as in
primates (Poggioli et al., 1986; Fan et al., 1997; Rossi et al., 1998; Murphy et al., 2000;
Koegler et al., 2001; Wirth et al., 2001), and the intracerebroventricular (ICV)
administration of melanocortin antagonists, SHU9119 (both MC3R and MC4R
antagonists) and HS014 (a selective MC4R antagonist), stimulates feeding behavior in
rats (Seeley et al., 1997; Fan et al., 1997; Kask et al., 1998). α-MSH can also increase energyAdvance expenditure (Poggioli et al., 1986; Brown et al., 1998; Hillebrand et al., 2005). Genetic rodent models indicate the importance of the melanocortin system in the
maintenance of body weight (Huszar et al., 1997; Yaswen et al., 1999; Butler et al.,
2000).
The chicken POMC gene was found to be a single copy gene and shows the
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same structural organization as that of other species of different classes, suggesting that
melanocortins in chickens act in a paracrine and/or autocrine manner to control a variety
of functions in the central and peripheral tissues (Takeuchi et al., 1999). Additionally,
Phillip-Singh et al. (2003) revealed the presence of α-MSH-expressing neurons in the
infundibular nucleus (IN), the avian equivalent of the mammalian ARC (Figure 1). As
for the control of feeding behavior, the central injection of α- and β-MSH, which
non-specifically binds both MC3R and MC4R, suppresses feed intake in chicks
(Kawakami et al., 2000; Smith et al., 2008; Kamisoyama et al., 2009), and HS014
stimulates feed consumption in doves (Strader et al., 2003) and chicks (Bungo et al.,
unpublished data). Although MC3R and MC4R, which have potential roles in the
control of feed intake and body weight in mammals, are highly expressedProofs in mammalian
brains (Grantz et al., 1993; Mountjoy et al., 1994), MC3R expression is not detected by
RT-PCR in the chicken brain (Takeuchi and Takahashi, 1999). However, γ-MSH that
is highly selective for MC3R versus MC4R in chickens (Ling et al., 2004), reduces feed intake in chicks (Smith et al., 2009). Thus,View similar to mammals, the anorexigenic action of melanocortins by POMC neurons in birds seems to be mediated by both
MC3R and MC4R.
1.2. AGRP
AGRP is a 132 amino acid peptide with 25% homology to agouti (Fong et al.,
1997), and is produced in the ARC as a biologically active fragment of the endogenous
antagonist of α-MSH at the MC3R and MC4R (Ollman et al., 1997). In rodents, centralAdvance injection of AGRP potently increases feed intake (Hagan et al., 2000; Kim et al., 2000; Lu et al., 2001), and the anorexic effects of α-MSH and MTII can be blocked by
co-administration of AGRP (Rossi et al., 1998). In good agreement with these
pharmacological findings, genetic manipulations resulting in over expression of AGRP
lead to hyperphagia and obesity in mammals (Ollmann et al., 1997; Marks and Cone,
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2001). Marsh et al. (1999) reported that a targeted disruption of the MC4R gene in
mice eliminates the anorexic effects of MTII, suggesting that the anorexigenic effect of
α-MSH and the orexigenic effect of AGRP are integrated by MC4R. Taken together,
this system is unique in neuroendocrinology in having both agonistic and antagonistic
endogenous ligands that regulate stimulation and inhibition of feed intake depending on
the state of energy balance.
The chicken AGRP gene was found to encode a 154 or 165 amino acid protein
with its C-terminal region showing high homology to mammalian counterparts, and
PT-PCR analysis detected the AGRP mRNA in the brain, liver and so on (Takeuchi et al., 2000). Administration of AGRP into the lateral ventricleProofs of chicks enhances feeding behavior and inhibits the anorexigenic action of α-MSH (Tachibana et al.,
2001). Collectively, α-MSH and AGRP produce opposing effects on feeding behavior
in chicks, comparable to those in mammals. In mammals, several pharmacological
studies have suggested a role for the central melanocortin system in the regulation of the activity of the hypothalamo-pituitary-adrenalView (HPA) axis (Calogero et al., 1988; Ludwig et al., 1998; Dhillo et al., 2002). In avians, ICV injection of α-MSH increases the
level of plasma corticosterone in chicks but the effect is not blocked by
co-administration of AGRP (Tachibana et al., 2007), suggesting that MCs related to the
feeding regulation or HPA axis might be different in the chick CNS. AGRP gene
expression in avians closely resembles that in mammals both in its exclusive
localization in the IN and also in the fact that the majority of neurons that express AGRPAdvance also co-express NPY, a potent appetite neuropeptide as mentioned below (Boswell et al., 2002; Phillips-Singh et al., 2003).
1.3. NPY
NPY contains 36 amino acid residues belonging to the pancreatic polypeptide
family (Tatemoto, 1982), and is one of the most abundant peptides in the brain of rats
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(Allen et al., 1983). In mammals, NPY is the most potent stimulator of feed intake
(Edwards et al., 1999) and NPY producing neurons are present in the hypothalamus and
brainstem (Gray and Morley, 1986). The ARC is the major site of expression for NPY
within neurons in the hypothalamus that projects to the paraventricular nucleus, the
ventromedial nucleus and other sites, facilitating the interaction of NPY with other
orexigenic and anorexigenic signals in the hypothalamus (Sahu et al., 1988). For
example, NPY and AGRP co-express in the ARC neurons and simultaneously repress
anorexigenic melanocortin signaling in the ARC (Kalra and Kalra, 2004). ICV
injection of NPY produces a powerful and prolonged increase in feed intake in rats
(Clark et al., 1984), while long-term administration results in decreased thermogenesis
and obesity (Stanley et al., 1986). The NPY stimulationProofs of feeding is in a
dose-dependent manner, although at higher doses feeding stimulation is less marked
(Clark et al., 1987). As for the receptors for NPY, fasting increases NPY Y1 mRNA
expression in the rat hypothalamus (Wyss et al., 1998), and Y1 receptor deficient mice show significant reduction of daily, fasting-View and NPY-induced feed intake (Pedrazzini et al., 1998; Kanatani et al., 2000). Mice lacking the Y5 receptor eat normally with
normal responses to exogenous NPY but demonstrate late onset of weight gain (Marsh
et al., 1988). Consistent with these findings, pharmacological studies prove that
appetite stimulation by NPY in mammals is mediated by receptors Y1 and Y5 (Kask et
al., 1998; Lecklin et al., 2002; 2003). In addition to Y1 and Y5, Y2 is also an
important receptor in the melanocortin system: POMC neurons in the ARC are inhibited by Advancethe administration of the Y2 receptor agonist PYY3-36 (Ghamari-Langroudi et al., 2005), and mice without Y2 receptors in the NPY neurons show increased NPY and
decreased POMC mRNA expression in the ARC (Shi et al., 2010).
The presence of NPY in the CNS of chickens was first demonstrated by the
NPY-like immunohistochemical study using antibodies against porcine NPY and avian
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pancreatic polypeptide (Kuenzel and McMurtry, 1988). Thereafter, the chicken NPY
gene was cloned (Blomqvist et al., 1992), and NPY was found to be synthesized within
the avian brain by in situ hybridization studies (Boswell et al., 1998; Wang et al., 2001;
Boswell et al., 2002). Similar to mammals, central administration of NPY robustly
stimulates feeding behavior in chickens and chicks in a dose-dependent manner
(Kuenzel et al., 1987; Kuenzel and McMurtry, 1988; Furuse et al., 1997; Bungo et al.,
2000). Fasting leads to increased NPY mRNA levels in the IN hypothalamus of birds
(Boswell et al., 2002). Six NPY receptors (Y1, Y2, Y4, Y5, Y6 and Y7) have been
identified in chickens and their binding characteristics have been investigated (Salaneck
et al., 2000; Holmberg et al., 2002; Lundell et al., 2002; Bromée et al., 2006).
Although these reports demonstrate that the Y1 and Y5 receptorsProofs are expressed in the
hypothalamus containing the IN (Holmberg et al., 2002), in vivo pharmacological
studies have shown contradictory results: the Y1 receptor antagonist did not prevent
fasting- and NPY-induced feeding (Kawakami et al., 2001), while [Leu31, Pro34]-NPY, with a high affinity to the chicken NPY ViewY2 and Y4 receptors (Salaneck et al., 2000; Lundell et al., 2002), increased feed intake, comparable to NPY (Ando et al., 2001).
Because there are conflicting data between the receptor expressions and
pharmacological effects, further studies will be needed to understand the role of NPY
and its receptor subtypes in the melanocortin system.
1.4. Simplified Correlation between the Components on the Feeding Behavior
Based on the above-mentioned mammalian results, a schematic illustration of the hypothalamicAdvance melanocortin system for regulating feed intake is shown in Figure 2. Briefly, increased signals of a fasting condition (negative energy balance) from the
peripheries (intestines, pancreas and adipose tissue) to the ARC inhibits the POMC
catabolic pathway and stimulates the NPY/AGRP anabolic pathway, resulting in
accelerated feed intake (left diagram in Figure 2), while increased satiety signals inhibit
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the NPY/AGRP pathway and stimulate the POMC pathway, resulting in decelerated
feed intake (right diagram in Figure 2). As described above, the melanocortin system
in the IN of chickens resembles that in mammals, and the system has been
neuroanatomically and functionally conserved during long periods of vertebrate
evolution (Lin et al., 2000; Phillips-Singh et al., 2003; Boswell, 2005).
2. Factors Affecting the Melanocortin System
Increasing evidence suggests that peripheral signals from adipose tissue, the
pancreas and the intestines may communicate with the centers of feeding regulation in
the CNS through the melanocortin pathway. There have been a number of reviews
regarding the network in the mammalian melanocortin systemProofs (e.g., Schwartz et al.,
2000; Seeley et al., 2004; Cone, 2005; Garfield et al., 2009). However, it should be
noted that the network in the avian melanocortin system remains to be fully explored.
This section is a summary of the characteristics of major factors, which regulate the network in the hypothalamus of chicks, coViewmpared with the results in mammals. 2.1. Hypothalamic Signals
2.1.1. Cocaine- and Amphetamine-Regulated Transcript (CART)
CART was first identified as a major brain mRNA up-regulated by cocaine and
amphetamine and found to be co-localized with POMC, and expressed in the
hypothalamus (Douglass et al., 1995; Kuhar and Dall Vechia, 1999). In rodents, ICV
injection of CART fragments has been shown to suppress both normal and fasting-inducedAdvance feeding, and completely blocks the feeding response induced by NPY (Kristensen et al., 1998; Lambert et al., 1998). While CART antiserum administration
increases nighttime feeding, suggesting the role of CART as an endogenous satiety
factor (Lambert et al., 1998). There is a decrease in the ARC CART mRNA following
feed deprivation, demonstrating that CART mRNA regulation is related to the fuel
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availability and peripheral hormone status (Li et al., 2002).
Like mammals, central infusion of human CART induces anorexia in chicks
(Tachibana et al., 2003), and the CART mRNA expressions are changed by
anorexigenic and orexigenic peptide treatments (Honda et al., 2007; Bungo et al., 2009).
Although the chicken CART gene has not yet been fully identified, it can be predicted
that POMC neurons in the IN also resemble their mammalian counterparts in
co-expressing CART mRNA. Studies are therefore required to clone and characterize
the chicken CART gene.
2.1.2. μ-Opioid Receptor Agonists and β-Endorphin Fragments
The opioid system, β-endorphin, dynorphin and enkephalins are the three
biologically active peptides described in the hypothalamus (LevineProofs and Billington,
1989). Opioid peptides mediate the hunger component in the control of feed intake
(Baile et al., 1986), but in contrast to NPY-induced feeding, their effect is relatively
modest and short-lived. Among opioid peptides, β-endorphin (and its receptor) is one of the essential modulators in the melanocViewortin system because it is derived from β-lipotropin, which in turn is derived from POMC (Mains et al., 1977). β-Endorphin
has affinity for both the μ- and δ-opioid receptors (MOR and DOR) in rats (Raynor et
al., 1994), but opioid antagonist analyses of β-endorphin feeding have shown reductions
induced by MOR, but not by DOR antagonists in mammals (Silva et al., 2001). It has
been recognized that β-endorphin acts in an autoreceptor manner to the MOR on POMC
neurons, diminishing the ARC POMC neuronal activity in response to elevated POMC-derivedAdvance melanocortin peptides that inhibit feed intake in mammals (Wardlaw et al., 1996; Cowley et al., 2001). NPY stimulates β-endorphin release in the
hypothalamus (Horvath et al., 1992), indicating a functional link between NPY and
β-endorphin in mammals. These results suggest that NPY may induce feeding directly
on its own and also by stimulating β-endorphin. The immediate actions of AGRP are
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blocked by non-specific opioid receptor antagonists but not the long-term effects
(Hagan et al., 2001). These findings suggest that the endogenous MOR ligands are an
important “system” modulator which may regulate not only the POMC but also
NPY/AGRP neuron activities.
Similar to that in mammals, central infusion of MOR agonist enhances feeding
behavior in chicks (Bungo et al., 2004; 2005; 2007), and the orexigenic effect is
abolished by MOR, but not by DOR antagonists (Yanagita et al., 2008a). Co-injection
of MOR antagonists are effective in reducing NPY-induced feeding, whereas DOR
antagonists had little effect, suggesting NPY stimulates β-endorphin release in the
hypothalamus in chicks (Dodo et al., 2005). Central MOR agonist infusion with
insulin prevents insulin-induced hypophagia, and attenuates increasingProofs POMC mRNA
expression in the brain of chicks (refer to “2.2.2 Insulin” below). β-Endorphin is
processed into N-terminal fragment peptides by enzyme, and its fragments having low
potency, attenuate β-endorphin-induced action in mammals (Hammonds et al., 1984; Suh et al., 1987; Plum et al., 2009).View In chicks, the fragment abolishes β-endorphin-induced feeding (Yanagita et al., 2008b), and accelerates insulin-induced
anorexia (Shiraishi et al., 2010). These findings imply that β-endorphin acts in an
autoreceptor manner to the MOR on POMC neurons in the IN of chicks, as in mammals.
Further histochemical studies will be needed to understand the role of MOR and MOR
ligands in the melanocortin system of chicks.
2.1.3. Nociceptin/orphanin FQ (N/OFQ) AdvanceNociceptin/orphanin FQ (N/OFQ) is an opioid-related heptadecapeptide identified as the endogenous ligand for the orphan Gi/Go-coupled opioid receptor-like 1
receptor (NOP1) (Meunier et al., 1995; Reinscheid et al., 1995). N/OFQ and NOP1 are
widely distributed in the brain (Mollereau and Mouledous, 2000; Reinscheid et al.,
2000), consistent with involvement in the control of a variety of biological functions
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including feeding regulation: N/OFQ has been shown to stimulate feeding behavior in
rats following ICV administration (Pomonis et al., 1996; Polidori et al., 2000;
Economidou et al., 2006). The ARC has been shown to be the most sensitive brain site
of action for N/OFQ in rats (Polidori et al., 2000). The orexigenic effects of N/OFQ in
the CNS are associated with changes in the hypothalamic AGRP, CART, catecholamines
and excitatory and inhibitory amino acids (Murphy et al., 1996; Murphy and Maidment,
1999; Schlicker and Morari, 2000; Marti et al., 2004; Bewick et al., 2005).
As in mammals, ICV injection of N/OFQ increases feed intake in chickens
(Abbasnejad et al., 2005; Tajalli et al., 2006). It also induces the increased AGRP and decreased CART mRNA expression in the CNS of chicks,Proofs and simultaneous administration of α-MSH completely blocks its orexigenic effect (Bungo et al., 2009),
suggesting that N/OFQ functions in chickens as one of the modulators in the
melanocortin system, as in mammals.
2.1.4. Gamma-Aminobutyric Acid (GABA) It should be emphasized that in Viewthe hypothalamus, the key chemical mode of communication between neurons is via GABA. GABA, the most widely distributed
inhibitory neurotransmitter in the vertebrate central nervous system (Sivilotti and Nistri,
1991), is found in high concentrations in brain areas known to be involved in the control
of ingestive behavior (Decavel and Van den Pol, 1990). Hence, rather than functioning
as a directly acting facilitatory orexigenic agent, it is possible that GABA may exert an
inhibitory effect on an existing anorexigenic tone in the CNS, thus indirectly facilitating feedingAdvance behavior. This might be mediated by decreasing α-MSH release (Jegou et al., 1993) or by rendering crucial target sites highly responsive to NPY. Concerning the
melanocortin system, histochemical studies suggest that NPY neurons in the ARC
largely contain GABA (Horvath et al., 1997), and NPY/AGRP neurons contact and
inhibit adjacent POMC neurons by releasing the inhibitory neurotransmitter GABA
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(Acuna-Goycolea et al., 2005).
In chicks, GABA has been shown to exist in various regions of the brain
(Csillag et al., 1987; Stewart et al., 1988; Granda and Grossland, 1989), as it does in
mammals. Although there is considerable evidence that GABA in the CNS directly
and indirectly induces hyperphagia in chickens (Jonaidi et al., 2002; Takagi et al., 2003;
Bungo et al., 2003), little is known concerning the relationship with the components in
the hypothalamic melanocortin system. Further histochemical and mRNA expression
studies will be needed to understand the role of GABA in the melanocortin system.
2.1.5. Fatty Acid Synthase (FAS)
FAS, a critical enzyme in de novo lipogenesis, catalyzes the seven steps in the
conversion of malonyl-CoA and acetyl-CoA to palmitate in Proofsthe cytoplasm. FAS
inhibition has been shown to facilitate weight loss through increased peripheral
utilization of fat as well as reduction of feed intake in mammals (Ronnett et al., 2005).
Additionally, FAS is expressed in various sites of the brain, and co-localized with NPY in neurons in the ARC. ViewInhibitor experiments revealed that 3-Carboxy-4-alkyl-2-methylenebutyrolactone (C75), a specific inhibitor of FAS, alters
feed intake via interactions within the ARC-PVN pathway mediated by NPY in mice.
(Kim et al., 2002). C75 also prevents the hypophagia-induced increases in mRNA for
AGRP in the ARC of rodents (Aja et al., 2006), suggesting that FAS may be involved in
the mammalian melanocortin system.
Similar to mammals, FAS is found in a number of brain regions, including the IN, Advanceand peripheral administration of FAS inhibitor significantly reduces feed intake in chickens (Dridi et al., 2006). Dridi et al. (2006) also revealed that the inhibitor
decreased gene expressions of the MC1, MC4 and MC5 receptors, but not NPY, AGRP
and POMC in the brain of chickens. These results suggest that the central FAS in
chickens may participate in the regulation of feeding behavior through the melanocortin
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system. Although experiments aimed at determining the role of FAS in the
melanocortin system of neonatal chicks have not been performed, our recent research
shows that ICV injection of C75 reduces feed intake in chicks (Bungo et al.,
unpublished data), suggesting the central FAS in neonatal chicks may also be involved
in the melanocortin system, comparable to mammals.
2.1. Peripheral Signals to the CNS
2.2.1. Leptin
The discovery of leptin, the adipocyte-derived protein hormone providing this
signal (Zhang et al., 1994), plays an important role in defining the neuronal circuitry in
the hypothalamic controlling feed intake in mammals (Schwartz et al., 2000; Horvath et
al., 2004). Peripheral leptin administration results in activationProofs of hypothalamic
neurons expressing the leptin receptor (Håkansson et al., 1998), suggesting a
hypothalamic mediation of leptin effects on satiety. In the hypothalamic ARC, leptin
facilitates satiety through inhibition of the NPY/AGRP neurons while stimulating POMC neurons (Sahu, 2003) and CARTView (Kristensen et al., 1998). Leptin acutely suppresses NPY-induced feeding and on a long term basis in rats (Xu et al., 1998).
NPY-deficient mice demonstrated leptin-induced suppression of feeding, suggesting the
importance of other pathways in the action of leptin (Erickson et al., 1996). Blockade
of MC4R reduces the ability of leptin to inhibit feed intake, suggesting that the
melanocortin pathway has a major role in mediating leptin effects (Seeley et al., 1997).
The chicken leptin cDNA sequence that shares 95% and 97% sequence identity withAdvance mouse leptin at the nucleotide and amino acid level, was cloned (Taouis et al., 1998; Ashwell et al., 1999). The effect of central administration of mammalian or
recombinant chicken leptin is consistent with an inhibitory influence of the hormone on
feed intake in chickens (Denbow et al., 2000; Dridi et al., 2000). Continuous infusion
of chicken leptin down-regulates the expression of the MC4R, MC5R, leptin and NPY
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receptors but does not affect POMC or AGRP mRNA expression in the hypothalamus
(Dridi et al., 2005). There is evidence that the cloned chicken leptin receptor shows
conservation of the key motifs in the long form (Horev et al., 2000; Ohkubo et al.,
2000) and short form (Liu et al., 2007), and a leptin-like signaling system is present
(Adachi et al., 2008). On the other hand, several independent laboratories have been
unable to amplify the reported sequence by PCR (Friedman-Einat et al., 1999; Pitel et
al., 2000; Amills et al., 2003), and infusion of mouse leptin is ineffective in feeding
behavior in chicks (Bungo et al., 1999). Thus, the existence of a natural chicken leptin
gene and its encoded protein should be unequivocally established before progress can
be made in understanding the effects of leptin on energy balance in birds (Sharp et al.,
2008). Proofs
2.2.2. Insulin
Insulin is well recognized as the key glucostatic regulator. Recent data show
that in addition to the control of glucose uptake in peripheral areas, this role also encompasses powerful central effects, inView synergy with leptin. Insulin receptors and components of the insulin-signaling pathway are also widely distributed in the CNS,
and regulate vital physiological processes in mammals (Pagotto, 2009). Recently, it
has been suggested that impairment in brain insulin availability or signaling results in
serious problems such as metabolic, mental or reproductive disorders (Saltiel and Kahan,
2001; Obici et al., 2002; Gerozissis, 2004). Tschritter et al. (2006) reported that CNS
insulin resistance contributes to human obesity. It has been proposed that insulin resistanceAdvance may not only be a consequen ce of, but also involved in the etiology of obesity in humans (Pagotto, 2009). Insulin has been suggested to have anorexic
effects centrally (Woods et al., 1979), and notably, the ARC is one of the prominent
sites of insulin receptor expression in mammals (Corp et al., 1986; Marks et al., 1990).
Insulin down-regulates NPY and AGRP gene expression and increases POMC gene
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expression in the mammalian ARC (Schwartz et al., 1992; Benoit et al., 2002),
suggesting that the anorexigenic effects of insulin are associated with the melanocortin
system.
Like mammals, the insulin receptor is present in the CNS of chickens (Simon
and Le Roith, 1986). Injection of insulin into the lateral ventricle of chicks inhibits
feed intake, and increases expression of POMC mRNA and decreases that of NPY
mRNA (Shiraishi et al., 2008a; 2008b; 2009). Also, the melanocortin antagonists
prevent the anorexic effect of insulin. Recently, we found that the expression of
chicken insulin receptors in the CNS by nutrient conditions (Shiraishi et al., in press), to
be localized in the IN (Shiraishi et al., unpublished data). These findings suggest that
the central melanocortin system mediates the anorexia by central Proofsinsulin, as in mammals.
Further studies are therefore required for the insulin receptor to be co-localized with the
POMC or NPY neurons in the chicken IN.
2.2.3. Ghrelin Ghrelin, identified from rat stomachView as an endogenous ligand for the growth hormone secretagogue receptor, is unique as the first gut hormone (Kojima et al., 1999),
and is shown to stimulate feeding behavior (Strader and Woods, 2005). It further
stimulates feeding by its action on NPY/AGRP neurons and inhibition on POMC
neurons in the CNS (Cowley et al., 2003a; Greenman et al., 2004), suggesting the role
of the melanocortin pathway in transmitting gut hunger signals to the mammalian brain.
Ghrelin increases c-fos activity in the NPY/AGRP neurons but not in the POMC neuronsAdvance (Wang et al., 2002), and the hyperpolarization of POMC neurons thus induced by ghrelin might be mediated through GABA release by NPY/AGRP neuron
depolarization (Cowley et al., 2003b). While leptin might transmit energy balance
signals over a long term, the gut hormones might mediate short term signaling due to
rapid fluctuation with meals.
J-STAGE Advance Publication Date: December 25, 2010 The Journal of Poultry Science doi: 10.2141/jpsa.010117
Chicken ghrelin, containing a 26 amino acid peptide, has been cloned and
identified (Kaiya et al., 2002; Geelissen et al., 2003; Tanaka et al., 2003), and has a
various physiological functions, as in mammals (see Review, Kaiya et al., 2007a). The
levels of ghrelin and its mRNA in chicks are changed by nutritional condition, like in
mammals (Kaiya et al., 2007b). However, dissimilar to mammalian results, central
administration of ghrelin or its agonist has the opposite effect on feeding: it prevents
fasting- and NPY-induced hyperphagia (Saito et al., 2002; 2005; Khan et al., 2006).
Also the expression of NPY mRNA in the CNS is not altered by ghrelin infusion (Saito
et al., 2005). Interestingly, recent data show that peripheral injection of chicken
ghrelin has a short acting orexigenic effect, and acutely up-regulated hypothalamic FAS
mRNA levels in chicks (Buyse et al., 2009). This finding indicatesProofs that the effects of
ghrelin in the melanocortin system in chicks remain to be fully explored.
3. Conclusion Figure 3 shows a schematic diagramView for the predicted melanocortin system in the IN of chickens. Population of first-order NPY/AGRP and POMC neurons, which
are mutually connected with synapses, are regulated by peripheral hormonal and
nutrient/metabolic signals, and project to second-order hypothalamic neuropeptide
neurons involved in the regulation of feed intake. Although details for the receptors
are not indicated, some receptors for the numbers of hormones, neuropeptides and
neurotransmitters (e.g., MOR, NPY Y1, and GABA receptors) known to regulate the networkAdvance are assumed to exist in the hypothala mic melanocortin system, as in mammals. Furthermore, detailed second-order hypothalamic neuropeptide neurons (e.g.,
corticotropin-releasing hormone, galanin, melanin-concentrating hormone and so on)
are not described in this review due to lack of space. Some of the studies described in
the present review are only initial studies, and more work remains to be carried out with
J-STAGE Advance Publication Date: December 25, 2010 The Journal of Poultry Science doi: 10.2141/jpsa.010117
regard to the precise mapping in the CNS of the synthesis and release of neuropeptides
related to their feeding regulatory activities, and the innervation and localization of their
receptors in the CNS. A better understanding of feeding regulation may aid the
selection of chickens for production and animal welfare.
Acknowledgements
The authors are deeply indebted to K. Yanagita for his great help in preparation
of the manuscript. The authors further wish to thank M. Fujita, M. Tsudzuki and Y.
Yoshimura for their encouragement. The author, T. Bungo, was awarded the 2009
Scientist Prize of Japan Poultry Science Association for central feeding regulation in
chicks. Proofs
View
Advance
J-STAGE Advance Publication Date: December 25, 2010 The Journal of Poultry Science doi: 10.2141/jpsa.010117
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Legends
Figure 1. Location of the hypothalamic infundibular nucleus (IN) in which the
melanocortin system may exist in the chick brain. Coronal (transverse)
sections through the chick brain are depicted.
Figure 2. Schematic illustration of hypothalamic melanocortin system for regulating
feed intake. See text for details. NPY, neuropeptide Y; AGRP, agouti-related
protein; POMC, pro-opiomelanocortin; α-MSH, α-melanocyte-stimulating
hormone; ARC, arcuate nucleus; (+); activate; (-), inhibit.
Proofs
Figure 3. Schematic diagram depicting the predicted hypothalamic infundibular
nucleus (IN) neuronal network. See text for details. NPY, neuropeptide Y; AGRP, agouti-related protein; POMC,View pro-opiomelanocortin
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