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ANCILLARY SCIENTISTS SYMPOSIUM |
USDA, ARS, Growth Biology Laboratory, Beltsville, MD 20705-2350
3 Corresponding author: richards{at}anri.barc.usda.gov
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONSIGNALING PATHWAYSCENTRAL AND PERIPHERAL CIRCUITSADENOSINE MONOPHOSPHATE...HYPOTHALAMIC INTEGRATION OF...CONCLUSIONS AND FUTURE...REFERENCES |
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Key Words: feed intake • energy balance • appetite • adenosine monophosphate-activated protein kinase • regulation
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONSIGNALING PATHWAYSCENTRAL AND PERIPHERAL CIRCUITSADENOSINE MONOPHOSPHATE...HYPOTHALAMIC INTEGRATION OF...CONCLUSIONS AND FUTURE...REFERENCES |
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In poultry species, as in all animals, BW is maintained throughout the lifecycle by adjustments to feed intake and energy expenditure. Both of these processes are controlled by complex and interconnected neuronal and endocrine networks that function to achieve energy homeostasis and maintain BW. Specific mechanisms have evolved to sense nutritional (energy) status. These are coupled with unique signaling pathways that link peripheral tissues with the central nervous system (CNS). Within the CNS, hypothalamic neural circuits play a critical role in integrating peripheral signals conveying information about energy and nutrient status, which is interpreted and used to modulate feeding behavior and energy expenditure to maintain BW and energy stores at a set level.
There have been a number of reviews regarding the regulation of feed intake by CNS and peripheral tissue mechanisms in poultry (Sykes, 1983; Denbow, 1994; Kuenzel, 1994; Kuenzel et al., 1999; Furuse, 2002; Richards, 2003). However, our understanding of the mechanisms that integrate feed intake regulation with control of energy expenditure in poultry remains quite limited, especially concerning the genetic and molecular basis for this regulation. Because feeding behavior and energy homeostasis are basic processes crucial to the survival of all animals, it is logical to assume that the regulatory mechanisms governing these processes in birds and mammals would involve highly conserved neural and endocrine signaling networks as well as similar neuroanatomical sites (Kuenzel, 1994; Kuenzel et al., 1999). In fact, much of what has been discovered recently concerning the genetic basis for the mechanisms regulating appetite and energy expenditure has emerged from studies involving mammalian species. The purpose of this review is to discuss the regulation of feed intake and energy expenditure in poultry including recent genetic and molecular discoveries and some newly emerging concepts.
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SIGNALING PATHWAYS |
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TOPABSTRACTINTRODUCTIONSIGNALING PATHWAYSCENTRAL AND PERIPHERAL CIRCUITSADENOSINE MONOPHOSPHATE...HYPOTHALAMIC INTEGRATION OF...CONCLUSIONS AND FUTURE...REFERENCES |
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Table 1
lists a number of peptides that have been studied in poultry with respect to their effects on feed intake. These signaling molecules function in peripheral or CNS sites, or both, to activate specific neural circuits or serve as endocrine and metabolic modulators that ultimately affect feed intake and energy homeostasis. Specific examples of some well-studied avian signaling molecules include neuropeptide Y (NPY), proopiomelanocortin (POMC) and its processed product alpha-melanocyte stimulating hormone (
MSH), cholecystokinin, and bombesin (Denbow, 1994; Kuenzel, 1994; Jensen, 2001; Furuse, 2002). It is clear that, despite the generally conserved nature of these peptide-signaling molecules in birds and mammals, there are differences in the function of specific peptide signals. For example, peptide YY and pancreatic polypeptide suppress appetite in mammals, whereas they are potent orexigenic agents in birds (Kuenzel et al., 1987; Ando et al., 2001). Although ghrelin stimulates feeding in mammals, it has been found to be anorexigenic in birds (Furuse et al., 2001; Kaiya et al., 2002; Saito et al., 2002, 2005; Geelissen et al., 2005). On the other hand, melanin concentrating hormone, orexins (A and B), galanin, and motilin all are potent orexigenic agents in mammals but are without any apparent effect on feed intake in chickens (Furuse et al., 1999; Ando et al., 2000; Furuse, 2002; Ohkubo et al., 2002). Thus, the fact that birds and mammals utilize common signaling molecules does not necessarily mean that they also share a common function.
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In the following text, 2 signaling molecules, ghrelin and leptin, are discussed in greater detail to illustrate examples of specific signaling axes. The gut-brain axis involves communication of information about the presence or absence of feed or specific nutrients in the gut to the brain and ghrelin falls into this category. The connection between adipose tissue (fat) and the brain involves communication of the level of peripheral tissue energy storage to the CNS, and leptin exemplifies this form of signaling.
Ghrelin, a peptide hormone produced by the stomach, has been reported to stimulate feeding in mammals (Wren et al., 2000). In birds, ghrelin is produced by the proventriculus, and it modulates feeding behavior in addition to functioning as a potent pituitary releasing factor for growth hormone mediated through the GHS-R (Furuse et al., 2001; Ahmed and Harvey, 2002; Kaiya et al., 2002; Baudet and Harvey, 2003; Wada et al., 2003). Interestingly, ghrelin has been shown to inhibit feed intake when administered centrally to chickens (Furuse et al., 2001; Saito et al., 2002). Ghrelin genes have been identified and characterized in chickens and turkeys (Kaiya et al., 2002; Richards et al., 2006). The predicted amino acid sequence of ghrelin in birds shows significant conservation especially in the amino-terminal region of the mature peptide hormone that contains an important site (serine 3) that is modified by esterification with a fatty acid (Kaiya et al., 2002). Expression and tissue localization of GHS-R transcripts have been reported in chickens and the widespread expression of the receptor is consistent with potential pleotropic effects of ghrelin (Tanaka et al., 2003; Geelissen et al., 2003, Richards et al., 2006). The discrepancy in function between avian and mammalian ghrelin peptides with respect to feed intake regulation is not readily apparent from the structure of ghrelin or its receptor (gene or protein). However, it has recently been reported that the inhibitory effect of ghrelin on feed intake in chickens may be mediated by the corticotrophin-releasing factor (CRF) system in the hypothalamus which is known to suppress feed intake (Saito et al., 2005).
Recently, it was reported that the preproghrelin precursor molecule in rats contained an additional 23 amino acid peptide hormone molecule that was named obestatin (Zhang et al., 2005). Obestatin, unlike ghrelin, was found to inhibit feed intake and decrease BW in rats. Like ghrelin which requires an amino-terminal fatty acylation modification for bioactivity, obestatin has been reported to require a carboxy-terminal modification (amidation) to bind to the orphan receptor GPR39, a member of the GPCR family (Zhang et al., 2005). However, subsequent investigations by a number of groups have failed to find any effect of obestatin on feed intake, BW, body composition, energy expenditure, or hypothalamic neuropeptides involved in energy balance regulation in rodents following central or peripheral administration of the hormone (Nogueiras et al., 2007). Moreover, it has recently been reported that obestatin does not bind to GPR39 or activate GPR39 signaling as originally indicated (Lauwers et al., 2006; Holst et al., 2007). Finally, targeted disruption of the GPR39 gene in mice had no effect on feed intake or BW (Tremblay et al., 2007). Together, these recent findings cast doubt on the role of the obestatin/GPR39 system in the regulation of BW and energy balance (Nogueiras et al., 2007).
Figure 1 shows different avian preproghrelins and demonstrates the presence of the 2 regulatory peptides (ghrelin and obestatin) derived from the same precursor in the chicken, turkey, duck and goose. There is uncertainty surrounding the posttranslational amidation of avain obestatin peptides because they all lack a terminal glycine residue that is highly conserved in mammalian obestatin peptides and required for carboxy-terminal amidation (Zhang et al., 2005). The chicken GPR39 gene has now been identified on chromosome 7 and, like its mammalian counterpart, codes for a protein that is a GPCR. The GPR39 gene is widely expressed in broiler chickens, in peripheral and CNS (including the hypothalamus) tissue sites (M. Proszkowiec-Weglarz and M. P. Richards, unpublished findings). Nothing is currently known about the role, if any, of the avian obestatin/GPR39 system in regulating feed intake and BW in birds or if it produces effects opposite those of ghrelin (i.e., stimulates feed intake and BW gain) as would be predicted from mammalian findings (Zhang et al., 2005). However, in light of the recent evidence obtained from mammalian models, it is entirely possible that this system will have no role in energy balance and BW regulation in birds. Perhaps, further study of the avian preproghrelin precursor and the 2 peptides derived from it will provide some additional insight into a possible function for the obestatin peptide and any unique physiological role(s) that it might play specifically in birds.
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Leptin receptor genes have been cloned and sequenced for chickens and turkeys (Horev et al., 2000; Ohkubo et al., 2000; Richards and Poch, 2003; Liu et al., 2007). Based on the deduced amino acid sequence, it appears that the avian leptin receptor is quite similar to the mammalian receptor in its structure and binding properties. In addition, short form gene transcripts (coding for proteins truncated at their carboxy-terminal ends) have recently been identified and characterized in chickens (Liu et al., 2007), demonstrating that avian leptin receptor gene primary transcripts are subject to similar alternative splicing events as observed previously in mammals. The long form of the receptor is presumed to be capable of full signaling in response to bound leptin, while the physiological functions of truncated (short) forms, if any, remain to be determined (Liu et al., 2007). Sequence analysis of the putative leptin-binding domain indicates that avian leptin receptors are capable of binding mammalian leptin proteins because of their conserved structure (Richards and Poch, 2003; Niv-Spector et al., 2005). Similarly, the leptin-binding domain of the human leptin receptor has recently been shown to bind nonhuman leptin proteins, including recombinant chicken leptin (Sandowski et al., 2002). This may help explain the reported effectiveness of mammalian recombinant leptin proteins (viz., human and sheep) in reducing feed intake when administered to chickens (Denbow et al., 2000; Taouis et al., 2001). Based on these findings, it is clear that birds express a functional leptin receptor in CNS and peripheral tissue sites.
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CENTRAL AND PERIPHERAL CIRCUITS |
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TOPABSTRACTINTRODUCTIONSIGNALING PATHWAYSCENTRAL AND PERIPHERAL CIRCUITSADENOSINE MONOPHOSPHATE...HYPOTHALAMIC INTEGRATION OF...CONCLUSIONS AND FUTURE...REFERENCES |
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Figure 2 depicts a proposed regulatory system for birds that integrates signals from peripheral tissues with specific brain centers to bring about short-term changes in appetite and long-term changes in energy expenditure that work together to maintain BW. Signals coming from the periphery include peptide hormones secreted by the gastrointestinal tract, adipose tissue, liver and pancreas, as well as neural inputs (e.g., vagal afferents). Within the brain, the brainstem contains regions, such as the so-called satiety center, that receive and process signals from vagal afferent nerves and relay signals back to the gastrointestinal tract via vagal efferents that control peripheral tissue functions and produce a sense of satiety. Cholecystokinin, a potent inhibitor of feeding, has been well studied in birds, as has bombesin and its related peptides (Denbow, 1994; Kuenzel, 1994; Jensen, 2001; Furuse, 2002). Not only does cholecystokinin stimulate gastric emptying and the release of pancreatic enzymes to aid in the digestion of feed, but it also functions as a satiety signal to the brainstem capable of depressing appetite. The importance of the gut-brain axis is reflected in a dual role demonstrated by many of the gut-derived peptide signals acting as hormones and as neuropeptides (Chaudhri et al., 2006). Their effects are relatively short-lived, and components of these signaling systems are expressed in the gut and in the brain. Moreover, because their effects on appetite generally are short-lived, gut peptide signals are not thought to play a significant role in mediating long-term changes in energy balance and BW.
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In mammals, changes in the circulating level of leptin and most likely insulin signal the hypothalamus to effect long-term changes in energy balance by activating and/or inhibiting specific anabolic and catabolic pathways (Schwartz et al., 2000; Woods et al., 2006). It has been suggested that MSH acting through the melanocortin-4 receptor subtype (MC4-R) serves as an important central mediator for leptin action on feed intake and energy expenditure (Forbes et al., 2001). Leptin, signaling through the leptin receptor, enlists the response of POMC-expressing hypothalamic neurons that produce MSH, which signals through MC4-R. Dridi et al. (2005) reported that leptin acts on the melanocortin system within the hypothalamus, directly or indirectly, to regulate feed intake in chickens. It is not known if circulating insulin levels reflect adipose tissue size (i.e., energy stores) in birds as seems to be the case in mammals (Woods et al., 1998; McMinn et al., 2000; Blevins et al., 2002; Woods et al., 2006). Although insulin receptors have been identified in the brain of chickens (Simon and Leroith, 1986), there are no reports of the effects of central administration of insulin on feed intake in birds (Kuenzel, 1994). However, there is evidence for elevated circulating insulin levels in fed or feed-deprived chickens with lesions of the ventromedial hypothalamus, suggesting the production of metabolic obesity (Sonoda, 1983). Because plasma levels of leptin and insulin rise and fall with increases and decreases in energy state in chickens such as during fasting and refeeding (Figure 3A), it is possible that these 2 key metabolic hormones could serve as peripheral signals of energy state in birds as they have been postulated to do in mammals (Niswender et al., 2004; Woods et al., 2006). In doing so, they would be expected to modulate hypothalamic melanocortin neural circuits that produce appropriate changes in feed intake and energy expenditure to achieve energy balance and maintain BW (Figure 3B).
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MSH that appears to play an important role in regulating feed intake in chickens (Takeuchi et al., 1999; Gerets et al., 2000; Kawakami et al., 2000). Central administration of MSH strongly inhibits feed intake in chickens (Kawakami et al., 2000). Not only are melanocortin receptors expressed in central sites, but they are also widely expressed in peripheral tissues of chickens as well (Takeuchi and Takahashi, 1998; Boswell and Takeuchi, 2005). The AgRP gene homologue has been identified, cloned, and sequenced in chickens, and expression of this naturally occurring antagonist of melanocortin action was reported to be widespread in central and peripheral tissues (Takeuchi et al., 2000). The AgRP serves as an antagonist of MSH in chickens, as it does in mammals, by binding to specific melanocortin receptor subtypes (MC3-R and MC4-R). Furthermore, AgRP is upregulated, like NPY, in response to fasting (Phillips-Singh et al., 2003). The AgRP is orexigenic in layer-type chickens, but not broilers, when administered centrally (Tachibana et al., 2001). Based on these observations, it was concluded that the MC4-R might function in the regulation of feed intake and energy expenditure in chickens (Tachibana et al., 2001; Boswell and Takeuchi, 2005) as this particular receptor subtype has been postulated to do in mammals and that the central melanocortin system appears to be well conserved between birds and mammals (Phillips-Singh et al., 2003). |
ADENOSINE MONOPHOSPHATE-ACTIVATED PROTEIN KINASE: AN ENERGY SENSOR |
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TOPABSTRACTINTRODUCTIONSIGNALING PATHWAYSCENTRAL AND PERIPHERAL CIRCUITSADENOSINE MONOPHOSPHATE...HYPOTHALAMIC INTEGRATION OF...CONCLUSIONS AND FUTURE...REFERENCES |
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). This is accomplished by regulating the activity and expression levels of key metabolic enzymes involved in lipid, carbohydrate, and protein metabolism, as well as other related cellular pathways.
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The hormones leptin and insulin inhibit AMPK in the hypothalamus (Minokoshi et al., 2004; Carling, 2005). This leads to increased activity of acetyl-CoA carboxylase, which results in an increased level of malynoyl-CoA. Elevated malonyl-CoA promotes anorexigenic signaling, which reduces feed intake and increases energy expenditure (Wolfgang and Lane, 2006). The AMPK also functions in peripheral tissues such as liver and skeletal muscle to bring about changes in energy balance (Carling, 2004; Kahn et al., 2005). Thus, the coordinated regulation of hypothalamic AMPK and its downstream actions on metabolic pathways plays a critical role in integrating hormonal and nutrient signaling that affects feed intake and whole-body energy homeostasis.
Recently, we have begun to explore aspects of the AMPK signaling pathway in chickens (Proszkowiec-Weglarz et al., 2006a,b). Seven AMPK subunit genes have been identified and their expression studied in different tissues including the hypothalamus. Genes for 2 upstream AMPK kinases, LKB1 and calcium/calmodulin-dependent protein kinase kinase, have also been identified in chickens and their expression investigated (Proszkowiec-Weglarz et al., 2006b; Proszkowiec-Weglarz and Richards, unpublished findings). Active (phosphorylated) AMPK has been detected in peripheral tissues as well as in hypothalamic feeding centers, suggesting the existence of a functional AMPK pathway in birds with similar characteristics to mammals (Proszkowiec-Weglarz et al., 2006b). However, the precise role(s) of the AMPK pathway in regulating feed intake and energy expenditure in birds and the specific signaling mechanisms involved remain to be fully elucidated.
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HYPOTHALAMIC INTEGRATION OF NUTRIENT AND HORMONAL SIGNALING |
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TOPABSTRACTINTRODUCTIONSIGNALING PATHWAYSCENTRAL AND PERIPHERAL CIRCUITSADENOSINE MONOPHOSPHATE...HYPOTHALAMIC INTEGRATION OF...CONCLUSIONS AND FUTURE...REFERENCES |
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A number of hormones and cytokines linked to energy signaling pathways mediate their effects through mTOR (Wullschleger et al., 2006). Leptin was found to increase hypothalamic mTOR activity via the signal transducer STAT3, a product of signaling through the leptin receptor (Cota et al., 2006). Conversely, inhibition of mTOR signaling by administration of rapamycin antagonizes leptin’s inhibitory effect on feed intake. Moreover, mTOR activity is increased in response to insulin and insulin-like growth factor binding to their respective receptors that, in turn, activate the PI3K/Akt signal transduction pathway (Wullschleger et al., 2006). Thus, mTOR serves as a fuel sensor and, when active in the hypothalamus, this signaling pathway has direct effects on reducing feed intake and BW while increasing energy expenditure (Cota et al., 2006).
Like AMPK, mTOR responds to changes in energy status; however, unlike AMPK, mTOR is activated (phosphorylated) in response to elevated energy status (Wullschleger et al., 2006; Cota et al., 2006). Activation of AMPK-dependent pathways leads to the inactivation of mTOR (Hardie, 2004). Thus, in the hypothalamus, as well as in peripheral tissues, AMPK and mTOR have overlapping but reciprocal functions (Cota et al., 2006). Figure 5 depicts a proposed hypothalamic regulatory model that involves input signaling from nutrients and hormones that influence AMPK activity, which affects malonyl-CoA levels (malonyl-CoA hypothesis) and TOR signaling via its effects on protein synthesis and cell growth to bring about changes in the expression of orexigenic and anorexigenic neuropeptides and thus modulate the activity of melanocortin system neural circuits. The net activity of these 2 opposing pathways ultimately determines a metabolic balance that leads to changes in feed intake and energy expenditure mediated by the actions of orexigenic and anorexigenic neural circuits. The TOR gene homologue, located on chromosome 21, is widely expressed in chicken tissues, including in the hypothalamus (M. Proszkowiec-Weglarz and M. P. Richards, unpublished findings). Although the existence and functioning of a hypothalamic TOR signaling pathway in birds has yet to be demonstrated, the Akt/TOR/p70S6K pathway has recently been characterized in chicken muscle that is stimulated by insulin and refeeding and was found to function in the nutritional regulation of mRNA translation and protein synthesis (Duchene et al., 2006; Tesseraud et al., 2006).
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CONCLUSIONS AND FUTURE DIRECTIONS |
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TOPABSTRACTINTRODUCTIONSIGNALING PATHWAYSCENTRAL AND PERIPHERAL CIRCUITSADENOSINE MONOPHOSPHATE...HYPOTHALAMIC INTEGRATION OF...CONCLUSIONS AND FUTURE...REFERENCES |
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FOOTNOTES |
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2 Presented as part of the Ancillary Scientists Symposium, Functional Genomics: Building the Bridge between the Genome and Phenome, Poultry Science Association Annual Meeting, Sunday, July 16, 2006.
Received for publication February 6, 2007. Accepted for publication February 10, 2007.
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denotes the site of a terminal glycine residue (G), conserved in all mammalian obestatin peptides, that is changed to a glutamic acid residue (E) in avian peptides. GPR39 (?) denotes the current uncertainty concerning the binding and activation by obestatin of the orphan G protein-coupled receptor, GPR39. Amino acid sequences shown for broiler, White Leghorn, turkey, goose, and duck preproghrelin precursor proteins were obtained from GenBank accession No. BAC24980, AAP56234, AAP93133, AAQ56122, and AAQ56123, respectively.
