Growth hormone secretagogue receptor: Difference between revisions
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'''Growth hormone secretagogue receptor''' ( | '''Growth hormone secretagogue receptor'''(GHS-R), also known as '''ghrelin receptor''', is a [[G protein–coupled receptor|G protein-coupled receptor]] that binds growth hormone secretagogues (GHSs), such as [[Ghrelin|ghrelin, the "hunger hormone"]].<ref>{{cite journal | vauthors = Davenport AP, Bonner TI, Foord SM, Harmar AJ, Neubig RR, Pin JP, Spedding M, Kojima M, Kangawa K | title = International Union of Pharmacology. LVI. Ghrelin receptor nomenclature, distribution, and function | journal = Pharmacological Reviews | volume = 57 | issue = 4 | pages = 541–6 | date = December 2005 | pmid = 16382107 | doi = 10.1124/pr.57.4.1 }}</ref><ref name="Pradhan_2005">{{cite journal | vauthors = Pradhan G, Samson SL, Sun Y | title = Ghrelin: much more than a hunger hormone | journal = Current Opinion in Clinical Nutrition and Metabolic Care | volume = 16 | issue = 6 | pages = 619–24 | date = November 2013 | pmid = 24100676 | doi = 10.1097/mco.0b013e328365b9be | pmc=4049314}}</ref> The role of GHS-R is thought to be in regulating energy homeostasis and body weight.<ref name="Pazos_2008">{{cite journal | vauthors = Pazos Y, Casanueva FF, Camiña JP | title = Basic aspects of ghrelin action | journal = Vitamins and Hormones | volume = 77 | issue = | pages = 89–119 | year = 2008 | pmid = 17983854 | doi = 10.1016/S0083-6729(06)77005-4 }}</ref> In the brain, they are most highly expressed in the [[hypothalamus]], specifically the [[Ventromedial nucleus of the hypothalamus|ventromedial nucleus]] and [[arcuate nucleus]]. GSH-Rs are also expressed in other areas of the brain, including the [[ventral tegmental area]], [[hippocampus]], and [[substantia nigra]].<ref name="Andrews_2011">{{cite journal | vauthors = Andrews ZB | title = The extra-hypothalamic actions of ghrelin on neuronal function | journal = Trends in Neurosciences | volume = 34 | issue = 1 | pages = 31–40 | date = January 2011 | pmid = 21035199 | doi = 10.1016/j.tins.2010.10.001 }}</ref> Outside the central nervous system, too, GSH-Rs are also found in the [[liver]], in [[skeletal muscle]], and even in the [[Cardiomyocyte|heart]].<ref name="Yin_2014">{{cite journal | vauthors = Yin Y, Li Y, Zhang W | title = The growth hormone secretagogue receptor: its intracellular signaling and regulation | journal = International Journal of Molecular Sciences | volume = 15 | issue = 3 | pages = 4837–55 | date = March 2014 | pmid = 24651458 | doi = 10.3390/ijms15034837 | pmc=3975427}}</ref> | ||
==Structure== | |||
Two identified transcript variants are expressed in several tissues and are evolutionary conserved in fish and swine. One transcript, 1a, excises an intron and encodes the functional protein; this protein is the receptor for the ghrelin ligand and defines a neuroendocrine pathway for growth hormone release. The second transcript (1b) retains the intron and does not function as a receptor for ghrelin; however, it may function to attenuate activity of isoform 1a.<ref name="entrez">{{cite web|url=https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=2693|title=Entrez Gene: GHS-R growth hormone secretagogue receptor|accessdate=}}</ref> | |||
GHS-R1a falls into [[G protein–coupled receptor|G-protein-coupled receptor (GPCR)]] family. Previous studies have shown that GPCRs can form [[heterodimers]], or functional receptor pairs with other types of G-protein coupled receptors (GPCRs). Various studies suggest that GHS-R1a specifically forms [[Protein dimer|dimer]]s with the following hormone and neurotransmitter receptors: [[somatostatin receptor 5]],<ref name="Pradhan_2005" /> [[Dopamine receptor D2|dopamine receptor type 2 (DRD2)]],<ref name="Schellekens_2013">{{cite journal | vauthors = Schellekens H, Dinan TG, Cryan JF | title = Taking two to tango: a role for ghrelin receptor heterodimerization in stress and reward | journal = Frontiers in Neuroscience | volume = 7 | pages = 148 | date = August 2013 | pmid = 24009547 | doi = 10.3389/fnins.2013.00148 | pmc=3757321}}</ref> [[Melanocortin 3 receptor|melanocortin-3 receptor (MC3R)]], and [[5-HT2C receptor|serotonin receptor type 2C (5-HT<sub>2c</sub> receptor)]].<ref name="Schellekens_2013" /> See "Function" section below for details on the purported functions of these heterodimers. | |||
== Function == | == Function == | ||
== | === Growth hormone release === | ||
The binding of ghrelin to GHS-R1a in pituitary cells stimulates the secretion of [[Growth hormone|growth hormone (GH)]] by the [[pituitary gland]].<ref name="Andrews_2011" /><ref>{{cite journal | vauthors = Wren AM, Small CJ, Ward HL, Murphy KG, Dakin CL, Taheri S, Kennedy AR, Roberts GH, Morgan DG, Ghatei MA, Bloom SR | title = The novel hypothalamic peptide ghrelin stimulates food intake and growth hormone secretion | journal = Endocrinology | volume = 141 | issue = 11 | pages = 4325–8 | date = November 2000 | pmid = 11089570 | doi = 10.1210/endo.141.11.7873 }}</ref> | |||
=== Constitutive activity === | |||
One important feature of GHS-R1a is that there is still some activity in the receptor even when it is not actively being stimulated. This is called [[constitutive activity]], and it means that the receptor is always "on," unless acted on by an [[inverse agonist]]. This constitutive activity seems to provide a tonic signal required for the development of normal height, probably through an effect on the GH axis.<ref>{{cite journal | vauthors = Pantel J, Legendre M, Cabrol S, Hilal L, Hajaji Y, Morisset S, Nivot S, Vie-Luton MP, Grouselle D, de Kerdanet M, Kadiri A, Epelbaum J, Le Bouc Y, Amselem S | title = Loss of constitutive activity of the growth hormone secretagogue receptor in familial short stature | journal = The Journal of Clinical Investigation | volume = 116 | issue = 3 | pages = 760–8 | date = March 2006 | pmid = 16511605 | doi = 10.1172/jci25303 | pmc=1386106}}</ref> In fact, some genetic variations, or [[Single-nucleotide polymorphism|single nucleotide polymorphisms (SNPs)]], in growth hormone secretagogue receptor, have been found to be associated with hereditary obesity and others with hereditary short stature.<ref name="Wang_2016">{{cite journal | vauthors = Wang W, Tao YX | title = Ghrelin Receptor Mutations and Human Obesity | journal = Progress in Molecular Biology and Translational Science | volume = 140 | issue = | pages = 131–50 | year = 2016 | pmid = 27288828 | doi = 10.1016/bs.pmbts.2016.02.001 }}</ref> It was also found that, when GHS-R1A constitutive activity, was diminished, there were decreased levels of hunger-inducing hormone [[Neuropeptide Y|neuropeptide Y (NPY)]] as well as in food intake and body weight.<ref>{{cite journal | vauthors = Holst B, Cygankiewicz A, Jensen TH, Ankersen M, Schwartz TW | title = High constitutive signaling of the ghrelin receptor--identification of a potent inverse agonist | journal = Molecular Endocrinology | volume = 17 | issue = 11 | pages = 2201–10 | date = November 2003 | pmid = 12907757 | doi = 10.1210/me.2003-0069 }}</ref><ref>{{cite journal | vauthors = Petersen PS, Woldbye DP, Madsen AN, Egerod KL, Jin C, Lang M, Rasmussen M, Beck-Sickinger AG, Holst B | title = In vivo characterization of high Basal signaling from the ghrelin receptor | journal = Endocrinology | volume = 150 | issue = 11 | pages = 4920–30 | date = November 2009 | pmid = 19819980 | doi = 10.1210/en.2008-1638 }}</ref> | |||
=== Intracellular signaling mechanisms === | |||
When growth hormone secretagogue receptor is activated, a variety of different intracellular signaling cascades can result, depending on the cell type in which the receptor is expressed. These intracellular signaling cascades include [[Mitogen-activated protein kinase|mitogen-activated protein kinase (MAPK)]]<ref name="Yin_2014" />[[Mitogen-activated protein kinase|)]], [[Protein kinase A|protein kinase A (PKA)]],<ref name="Yin_2014" /> [[Protein kinase B|protein kinase B (PKB)]], also known as [[AKT]]<ref name="Yin_2014" />), and [[AMP-activated protein kinase|AMP Activated Protein Kinase (AMPK)]] cascades.<ref name="Yin_2014" /> | |||
=== Behavioral reinforcement of food intake === | |||
It is well-characterized that activating the growth hormone secretagogue receptor with ghrelin induces an [[orexigenic]] state, or general feeling of hunger.<ref name="Pradhan_2005" /> However, ghrelin may also play a role in behavioral reinforcement. Studies in animal models, found that food intake increased when ghrelin was specifically administered to just the ventral tegmental area (VTA), a brain area that uses dopamine signaling to reinforce behavior.<ref name="Andrews_2011" /> In fact, the more ghrelin administered, the more food the rodent consumed.<ref name="Andrews_2011" /> This is called a [[Dose–response relationship|dose-dependent effect]]. Building on this, it was found that there are growth hormone secretagogue receptors in the VTA and that ghrelin acts on the VTA through these receptors.<ref name="Andrews_2011" /> Current studies, furthermore, suggest that the VTA may contain dimers of GHS-R1a and dopamine receptor type 2 (DRD2). If these two receptors do indeed form dimers, this would somehow link ghrelin signaling to dopaminergic signaling.<ref name="Andrews_2011" /> | |||
=== Enhancement of learning and memory === | |||
The growth hormone secretagogue receptor may also be linked to learning and memory. First of all, the receptor is found in the [[hippocampus]], the brain region responsible for long-term memory.<ref name="Lutter_2009">{{cite journal | vauthors = Lutter M, Elmquist J | title = Depression and metabolism: linking changes in leptin and ghrelin to mood | journal = F1000 Biology Reports | volume = 1 | issue = 63 | pages = 63 | date = August 2009 | pmid = 20948621 | doi = 10.3410/b1-63 | pmc=2948264}}</ref> Second, it was found that specifically activating the receptor in just the hippocampus increased both [[long-term potentiation]] (LTP) and [[dendritic spine]] density, two cellular phenomena thought to be involved in learning.<ref name="Andrews_2011" /> Third, short-term calorie restriction, defined as a 30% reduction in caloric intake for two weeks, which naturally increases ghrelin levels and thus activates the receptor, was found to both increase both performance on [[Spatial memory|spatial learning]] tasks as well as [[Adult neurogenesis|neurogenesis in the adult hippocampus]].<ref name="Lutter_2009" /> | |||
== Selective ligands == | == Selective ligands == | ||
| Line 15: | Line 36: | ||
{{div col|colwidth=20em}} | {{div col|colwidth=20em}} | ||
* [[Adenosine]]<ref name="KordonRobinson2012">{{cite book|first1=Claude | last1 = Kordon | first2 = I. | last2 = Robinson | first3=Jacques | last3 = Hanoune | first4 = R. | last4 = Dantzer | title = Brain Somatic Cross-Talk and the Central Control of Metabolism|url=https://books.google.com/books?id=Ml7vCAAAQBAJ&pg=PA42|date=6 December 2012|publisher=Springer Science & Business Media|isbn=978-3-642-18999-9|pages=42– | * [[Adenosine]]<ref name="KordonRobinson2012">{{cite book|first1=Claude | last1 = Kordon | first2 = I. | last2 = Robinson | first3=Jacques | last3 = Hanoune | first4 = R. | last4 = Dantzer | name-list-format = vanc | title = Brain Somatic Cross-Talk and the Central Control of Metabolism|url=https://books.google.com/books?id=Ml7vCAAAQBAJ&pg=PA42|date=6 December 2012|publisher=Springer Science & Business Media|isbn=978-3-642-18999-9|pages=42– }}</ref> | ||
* [[Alexamorelin]] | * [[Alexamorelin]] | ||
* [[Anamorelin]] | * [[Anamorelin]] | ||
| Line 43: | Line 64: | ||
===Antagonists=== | ===Antagonists=== | ||
* [[A-778,193]] | * [[A-778,193]] | ||
* [[PF-5190457]] <ref>{{cite journal | vauthors = Bhattacharya SK, Andrews K, Beveridge R, Cameron KO, Chen C, Dunn M, Fernando D, Gao H, Hepworth D, Jackson VM, Khot V, Kong J, Kosa RE, Lapham K, Loria PM, Londregan AT, McClure KF, Orr ST, Patel J, Rose C, Saenz J, Stock IA, Storer G, VanVolkenburg M, Vrieze D, Wang G, Xiao J, Zhang Y | display-authors = 6 | title = Discovery of PF-5190457, a Potent, Selective, and Orally Bioavailable Ghrelin Receptor Inverse Agonist Clinical Candidate | journal = ACS Medicinal Chemistry Letters | volume = 5 | issue = 5 | pages = 474–9 | date = May 2014 | pmid = 24900864 | pmc = 4027753 | doi = 10.1021/ml400473x }}</ref> | |||
== References == | == References == | ||
| Line 49: | Line 71: | ||
== Further reading == | == Further reading == | ||
* {{cite journal | vauthors = Portelli J, Thielemans L, Ver Donck L, Loyens E, Coppens J, Aourz N, Aerssens J, Vermoesen K, Clinckers R, Schallier A, Michotte Y, Moechars D, Collingridge GL, Bortolotto ZA, Smolders I | title = Inactivation of the constitutively active ghrelin receptor attenuates limbic seizure activity in rodents | journal = Neurotherapeutics | volume = 9 | issue = 3 | pages = 658–72 | | * {{cite journal | vauthors = Portelli J, Thielemans L, Ver Donck L, Loyens E, Coppens J, Aourz N, Aerssens J, Vermoesen K, Clinckers R, Schallier A, Michotte Y, Moechars D, Collingridge GL, Bortolotto ZA, Smolders I | title = Inactivation of the constitutively active ghrelin receptor attenuates limbic seizure activity in rodents | journal = Neurotherapeutics | volume = 9 | issue = 3 | pages = 658–72 | date = July 2012 | pmid = 22669710 | pmc = 3441926 | doi = 10.1007/s13311-012-0125-x }} | ||
== External links == | == External links == | ||
*{{cite web | url = http://www.iuphar-db.org/GPCR/ChapterMenuForward?chapterID=1335 | title = Ghrelin Receptor | accessdate = | date = | format = | work = IUPHAR Database of Receptors and Ion Channels | publisher = International Union of Basic and Clinical Pharmacology | pages = | archiveurl = | archivedate = | quote = }} | * {{cite web | url = http://www.iuphar-db.org/GPCR/ChapterMenuForward?chapterID=1335 | title = Ghrelin Receptor | accessdate = | date = | format = | work = IUPHAR Database of Receptors and Ion Channels | publisher = International Union of Basic and Clinical Pharmacology | pages = | archiveurl = | archivedate = | quote = }} | ||
* {{MeshName|growth+hormone+secretagogue+receptor}} | * {{MeshName|growth+hormone+secretagogue+receptor}} | ||
* [http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/gi/ghrelin.html Ghrelin] at [[Colorado State University]] | * [http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/gi/ghrelin.html Ghrelin] at [[Colorado State University]] | ||
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{{GH/IGF-1 axis signaling modulators}} | {{GH/IGF-1 axis signaling modulators}} | ||
[[Category:G protein coupled receptors]] | [[Category:G protein-coupled receptors]] | ||
Latest revision as of 03:37, 8 October 2018
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Growth hormone secretagogue receptor(GHS-R), also known as ghrelin receptor, is a G protein-coupled receptor that binds growth hormone secretagogues (GHSs), such as ghrelin, the "hunger hormone".[1][2] The role of GHS-R is thought to be in regulating energy homeostasis and body weight.[3] In the brain, they are most highly expressed in the hypothalamus, specifically the ventromedial nucleus and arcuate nucleus. GSH-Rs are also expressed in other areas of the brain, including the ventral tegmental area, hippocampus, and substantia nigra.[4] Outside the central nervous system, too, GSH-Rs are also found in the liver, in skeletal muscle, and even in the heart.[5]
Structure
Two identified transcript variants are expressed in several tissues and are evolutionary conserved in fish and swine. One transcript, 1a, excises an intron and encodes the functional protein; this protein is the receptor for the ghrelin ligand and defines a neuroendocrine pathway for growth hormone release. The second transcript (1b) retains the intron and does not function as a receptor for ghrelin; however, it may function to attenuate activity of isoform 1a.[6]
GHS-R1a falls into G-protein-coupled receptor (GPCR) family. Previous studies have shown that GPCRs can form heterodimers, or functional receptor pairs with other types of G-protein coupled receptors (GPCRs). Various studies suggest that GHS-R1a specifically forms dimers with the following hormone and neurotransmitter receptors: somatostatin receptor 5,[2] dopamine receptor type 2 (DRD2),[7] melanocortin-3 receptor (MC3R), and serotonin receptor type 2C (5-HT2c receptor).[7] See "Function" section below for details on the purported functions of these heterodimers.
Function
Growth hormone release
The binding of ghrelin to GHS-R1a in pituitary cells stimulates the secretion of growth hormone (GH) by the pituitary gland.[4][8]
Constitutive activity
One important feature of GHS-R1a is that there is still some activity in the receptor even when it is not actively being stimulated. This is called constitutive activity, and it means that the receptor is always "on," unless acted on by an inverse agonist. This constitutive activity seems to provide a tonic signal required for the development of normal height, probably through an effect on the GH axis.[9] In fact, some genetic variations, or single nucleotide polymorphisms (SNPs), in growth hormone secretagogue receptor, have been found to be associated with hereditary obesity and others with hereditary short stature.[10] It was also found that, when GHS-R1A constitutive activity, was diminished, there were decreased levels of hunger-inducing hormone neuropeptide Y (NPY) as well as in food intake and body weight.[11][12]
Intracellular signaling mechanisms
When growth hormone secretagogue receptor is activated, a variety of different intracellular signaling cascades can result, depending on the cell type in which the receptor is expressed. These intracellular signaling cascades include mitogen-activated protein kinase (MAPK)[5]), protein kinase A (PKA),[5] protein kinase B (PKB), also known as AKT[5]), and AMP Activated Protein Kinase (AMPK) cascades.[5]
Behavioral reinforcement of food intake
It is well-characterized that activating the growth hormone secretagogue receptor with ghrelin induces an orexigenic state, or general feeling of hunger.[2] However, ghrelin may also play a role in behavioral reinforcement. Studies in animal models, found that food intake increased when ghrelin was specifically administered to just the ventral tegmental area (VTA), a brain area that uses dopamine signaling to reinforce behavior.[4] In fact, the more ghrelin administered, the more food the rodent consumed.[4] This is called a dose-dependent effect. Building on this, it was found that there are growth hormone secretagogue receptors in the VTA and that ghrelin acts on the VTA through these receptors.[4] Current studies, furthermore, suggest that the VTA may contain dimers of GHS-R1a and dopamine receptor type 2 (DRD2). If these two receptors do indeed form dimers, this would somehow link ghrelin signaling to dopaminergic signaling.[4]
Enhancement of learning and memory
The growth hormone secretagogue receptor may also be linked to learning and memory. First of all, the receptor is found in the hippocampus, the brain region responsible for long-term memory.[13] Second, it was found that specifically activating the receptor in just the hippocampus increased both long-term potentiation (LTP) and dendritic spine density, two cellular phenomena thought to be involved in learning.[4] Third, short-term calorie restriction, defined as a 30% reduction in caloric intake for two weeks, which naturally increases ghrelin levels and thus activates the receptor, was found to both increase both performance on spatial learning tasks as well as neurogenesis in the adult hippocampus.[13]
Selective ligands
A range of selective ligands for the GHS-R receptor are now available and are being developed for several clinical applications. GHS-R agonists have appetite-stimulating and growth hormone-releasing effects, and are likely to be useful for the treatment of muscle wasting and frailty associated with old-age and degenerative diseases. On the other hand, GHS-R antagonists have anorectic effects and are likely to be useful for the treatment of obesity.
Agonists
Antagonists
References
- ↑ Davenport AP, Bonner TI, Foord SM, Harmar AJ, Neubig RR, Pin JP, Spedding M, Kojima M, Kangawa K (December 2005). "International Union of Pharmacology. LVI. Ghrelin receptor nomenclature, distribution, and function". Pharmacological Reviews. 57 (4): 541–6. doi:10.1124/pr.57.4.1. PMID 16382107.
- ↑ 2.0 2.1 2.2 Pradhan G, Samson SL, Sun Y (November 2013). "Ghrelin: much more than a hunger hormone". Current Opinion in Clinical Nutrition and Metabolic Care. 16 (6): 619–24. doi:10.1097/mco.0b013e328365b9be. PMC 4049314. PMID 24100676.
- ↑ Pazos Y, Casanueva FF, Camiña JP (2008). "Basic aspects of ghrelin action". Vitamins and Hormones. 77: 89–119. doi:10.1016/S0083-6729(06)77005-4. PMID 17983854.
- ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 Andrews ZB (January 2011). "The extra-hypothalamic actions of ghrelin on neuronal function". Trends in Neurosciences. 34 (1): 31–40. doi:10.1016/j.tins.2010.10.001. PMID 21035199.
- ↑ 5.0 5.1 5.2 5.3 5.4 Yin Y, Li Y, Zhang W (March 2014). "The growth hormone secretagogue receptor: its intracellular signaling and regulation". International Journal of Molecular Sciences. 15 (3): 4837–55. doi:10.3390/ijms15034837. PMC 3975427. PMID 24651458.
- ↑ "Entrez Gene: GHS-R growth hormone secretagogue receptor".
- ↑ 7.0 7.1 Schellekens H, Dinan TG, Cryan JF (August 2013). "Taking two to tango: a role for ghrelin receptor heterodimerization in stress and reward". Frontiers in Neuroscience. 7: 148. doi:10.3389/fnins.2013.00148. PMC 3757321. PMID 24009547.
- ↑ Wren AM, Small CJ, Ward HL, Murphy KG, Dakin CL, Taheri S, Kennedy AR, Roberts GH, Morgan DG, Ghatei MA, Bloom SR (November 2000). "The novel hypothalamic peptide ghrelin stimulates food intake and growth hormone secretion". Endocrinology. 141 (11): 4325–8. doi:10.1210/endo.141.11.7873. PMID 11089570.
- ↑ Pantel J, Legendre M, Cabrol S, Hilal L, Hajaji Y, Morisset S, Nivot S, Vie-Luton MP, Grouselle D, de Kerdanet M, Kadiri A, Epelbaum J, Le Bouc Y, Amselem S (March 2006). "Loss of constitutive activity of the growth hormone secretagogue receptor in familial short stature". The Journal of Clinical Investigation. 116 (3): 760–8. doi:10.1172/jci25303. PMC 1386106. PMID 16511605.
- ↑ Wang W, Tao YX (2016). "Ghrelin Receptor Mutations and Human Obesity". Progress in Molecular Biology and Translational Science. 140: 131–50. doi:10.1016/bs.pmbts.2016.02.001. PMID 27288828.
- ↑ Holst B, Cygankiewicz A, Jensen TH, Ankersen M, Schwartz TW (November 2003). "High constitutive signaling of the ghrelin receptor--identification of a potent inverse agonist". Molecular Endocrinology. 17 (11): 2201–10. doi:10.1210/me.2003-0069. PMID 12907757.
- ↑ Petersen PS, Woldbye DP, Madsen AN, Egerod KL, Jin C, Lang M, Rasmussen M, Beck-Sickinger AG, Holst B (November 2009). "In vivo characterization of high Basal signaling from the ghrelin receptor". Endocrinology. 150 (11): 4920–30. doi:10.1210/en.2008-1638. PMID 19819980.
- ↑ 13.0 13.1 Lutter M, Elmquist J (August 2009). "Depression and metabolism: linking changes in leptin and ghrelin to mood". F1000 Biology Reports. 1 (63): 63. doi:10.3410/b1-63. PMC 2948264. PMID 20948621.
- ↑ Kordon C, Robinson I, Hanoune J, Dantzer R (6 December 2012). Brain Somatic Cross-Talk and the Central Control of Metabolism. Springer Science & Business Media. pp. 42–. ISBN 978-3-642-18999-9.
- ↑ Bhattacharya SK, Andrews K, Beveridge R, Cameron KO, Chen C, Dunn M, et al. (May 2014). "Discovery of PF-5190457, a Potent, Selective, and Orally Bioavailable Ghrelin Receptor Inverse Agonist Clinical Candidate". ACS Medicinal Chemistry Letters. 5 (5): 474–9. doi:10.1021/ml400473x. PMC 4027753. PMID 24900864.
Further reading
- Portelli J, Thielemans L, Ver Donck L, Loyens E, Coppens J, Aourz N, Aerssens J, Vermoesen K, Clinckers R, Schallier A, Michotte Y, Moechars D, Collingridge GL, Bortolotto ZA, Smolders I (July 2012). "Inactivation of the constitutively active ghrelin receptor attenuates limbic seizure activity in rodents". Neurotherapeutics. 9 (3): 658–72. doi:10.1007/s13311-012-0125-x. PMC 3441926. PMID 22669710.
External links
- "Ghrelin Receptor". IUPHAR Database of Receptors and Ion Channels. International Union of Basic and Clinical Pharmacology.
- growth+hormone+secretagogue+receptor at the US National Library of Medicine Medical Subject Headings (MeSH)
- Ghrelin at Colorado State University
This article incorporates text from the United States National Library of Medicine, which is in the public domain.