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Book ; Conference proceedings: The melanocortin system

Cone, Roger D.

[result of a Meeting entitled the Fifth International Melanocortin Meeting, held on August 25 - 28, 2002 in Sunriver, Oregon]

(Annals of the New York Academy of Sciences ; 994)

2003

Event/congress	International Melanocortin Meeting (5, 2002, SunriverOr.)
Author's details	ed. by Roger D. Cone
Series title	Annals of the New York Academy of Sciences ; 994
Collection
Keywords	MSH (Hormone) ; Proopiomelanocortin/Receptors ; Melanotropin ; Melanocortin-4-Rezeptor
Subject	MSH ; Intermedin ; Melanozyten stimulierendes Hormon
Subject code	573.454
Language	English
Size	XII, 387 S. : Ill., graph. Darst.
Publishing place	New York, NY
Publishing country	Great Britain
Document type	Book ; Conference proceedings
HBZ-ID	HT013819009
ISBN	1-573-31442-0 ; 1-573-31443-9 ; 978-1-573-31442-8 ; 978-1-573-31443-5
Database	Catalogue ZB MED Medicine, Health

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Se 110 -994-	verfügbar in Königswinter	Königswinter

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Article ; Online: Loss of Agrp1 in zebrafish: Effects on the growth and reproductive axis.

Wei, Zehong / Lakshminarasimha, Amrutha Bagivalu / Cone, Roger D / Michel, Maximilian

General and comparative endocrinology

2023 Volume 336, Page(s) 114243

Abstract: Loss of agouti related neuropeptide (AgRP) does not lead to overt phenotypes in mammals unless AgRP neurons are ablated. In contrast, in zebrafish it has been shown that Agrp1 loss of function (LOF) leads to reduced growth in Agrp1 morphant as well as ... ...

Abstract	Loss of agouti related neuropeptide (AgRP) does not lead to overt phenotypes in mammals unless AgRP neurons are ablated. In contrast, in zebrafish it has been shown that Agrp1 loss of function (LOF) leads to reduced growth in Agrp1 morphant as well as Agrp1 mutant larvae. Further, it has been shown that multiple endocrine axes are dysregulated upon Agrp1 LOF in Agrp1 morphant larvae. Here we show that adult Agrp1 LOF zebrafish show normal growth and reproductive behavior in spite of a significant reduction in multiple related endocrine axes namely reduced expression in pituitary growth hormone (gh) follicle stimulating hormone (fshb) as well as luteinizing hormone (lhb). We looked for compensatory changes in candidate gene expression but found no changes in growth hormone and gonadotropin hormone receptors that would explain the lack of phenotype. We further looked at expression in the hepatic and muscular insulin-like growth factor (Igf) axis which appears to be normal. Fecundity as well as ovarian histology also appear largely normal while we do see an increase in mating efficiency specifically in fed but not fasted AgRP1 LOF animals. This data shows that zebrafish can grow and reproduce normally in spite of significant central hormone changes and suggests a peripheral compensatory mechanism additional to previously reported central compensatory mechanisms in other zebrafish neuropeptide LOF lines.
MeSH term(s)	Animals ; Zebrafish/metabolism ; Agouti-Related Protein/genetics ; Agouti-Related Protein/metabolism ; Follicle Stimulating Hormone/genetics ; Luteinizing Hormone ; Gonadotropins ; Growth Hormone/genetics ; Growth Hormone/metabolism ; Mammals/metabolism
Chemical Substances	Agouti-Related Protein ; Follicle Stimulating Hormone (9002-68-0) ; Luteinizing Hormone (9002-67-9) ; Gonadotropins ; Growth Hormone (9002-72-6)
Language	English
Publishing date	2023-02-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1851-x
ISSN	1095-6840 ; 0016-6480
ISSN (online)	1095-6840
ISSN	0016-6480
DOI	10.1016/j.ygcen.2023.114243
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Article ; Online: Targeting the central melanocortin system for the treatment of metabolic disorders.

Sweeney, Patrick / Gimenez, Luis E / Hernandez, Ciria C / Cone, Roger D

Nature reviews. Endocrinology

2023 Volume 19, Issue 9, Page(s) 507–519

Abstract: A large body of preclinical and clinical data shows that the central melanocortin system is a promising therapeutic target for treating various metabolic disorders such as obesity and cachexia, as well as anorexia nervosa. Setmelanotide, which functions ... ...

Abstract	A large body of preclinical and clinical data shows that the central melanocortin system is a promising therapeutic target for treating various metabolic disorders such as obesity and cachexia, as well as anorexia nervosa. Setmelanotide, which functions by engaging the central melanocortin circuitry, was approved by the FDA in 2020 for use in certain forms of syndromic obesity. Furthermore, the FDA approvals in 2019 of two peptide drugs targeting melanocortin receptors for the treatment of generalized hypoactive sexual desire disorder (bremelanotide) and erythropoietic protoporphyria-associated phototoxicity (afamelanotide) demonstrate the safety of this class of peptides. These approvals have also renewed excitement in the development of therapeutics targeting the melanocortin system. Here, we review the anatomy and function of the melanocortin system, discuss progress and challenges in developing melanocortin receptor-based therapeutics, and outline potential metabolic and behavioural disorders that could be addressed using pharmacological agents targeting these receptors.
MeSH term(s)	Humans ; Melanocortins/therapeutic use ; Sexual Dysfunctions, Psychological/drug therapy ; Sexual Dysfunctions, Psychological/metabolism ; Obesity/drug therapy ; Cachexia ; Metabolic Diseases/drug therapy
Chemical Substances	Melanocortins
Language	English
Publishing date	2023-06-26
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2489381-X
ISSN	1759-5037 ; 1759-5029
ISSN (online)	1759-5037
ISSN	1759-5029
DOI	10.1038/s41574-023-00855-y
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Article ; Online: Melanocortin-3 receptor expression in AgRP neurons is required for normal activation of the neurons in response to energy deficiency.

Gui, Yijun / Dahir, Naima S / Wu, Yanan / Downing, Griffin / Sweeney, Patrick / Cone, Roger D

Cell reports

2023 Volume 42, Issue 10, Page(s) 113188

Abstract: The melanocortin-3 receptor (MC3R) is a negative regulator of the central melanocortin circuitry via presynaptic expression on agouti-related protein (AgRP) nerve terminals, from where it regulates GABA release onto secondary MC4R-expressing neurons. ... ...

Abstract	The melanocortin-3 receptor (MC3R) is a negative regulator of the central melanocortin circuitry via presynaptic expression on agouti-related protein (AgRP) nerve terminals, from where it regulates GABA release onto secondary MC4R-expressing neurons. However, MC3R knockout (KO) mice also exhibit defective behavioral and neuroendocrine responses to fasting. Here, we demonstrate that MC3R KO mice exhibit defective activation of AgRP neurons in response to fasting, cold exposure, or ghrelin while exhibiting normal inhibition of AgRP neurons by sensory detection of food in the ad libitum-fed state. Using a conditional MC3R KO model, we show that the control of AgRP neuron activation by fasting and ghrelin requires the specific presence of MC3R within AgRP neurons. Thus, MC3R is a crucial player in the responsiveness of the AgRP soma to both hormonal and neuronal signals of energy need.
MeSH term(s)	Mice ; Animals ; Agouti-Related Protein/metabolism ; Receptor, Melanocortin, Type 3/genetics ; Receptor, Melanocortin, Type 3/metabolism ; Ghrelin ; Neurons/metabolism ; Mice, Knockout
Chemical Substances	Agouti-Related Protein ; Receptor, Melanocortin, Type 3 ; Ghrelin
Language	English
Publishing date	2023-10-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.113188
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Article: Cell autonomous regulation of the activation of AgRP neurons by the melanocortin-3 receptor.

Gui, Yijun / Dahir, Naima S / Downing, Griffin / Sweeney, Patrick / Cone, Roger D

bioRxiv : the preprint server for biology

2023

Abstract: The melanocortin-3 receptor (MC3R) is a negative regulator of the central melanocortin circuitry via presynaptic expression on AgRP nerve terminals, from where it regulates GABA release onto secondary MC4R-expressing neurons. Hence, animals lacking MC3R ( ...

Abstract	The melanocortin-3 receptor (MC3R) is a negative regulator of the central melanocortin circuitry via presynaptic expression on AgRP nerve terminals, from where it regulates GABA release onto secondary MC4R-expressing neurons. Hence, animals lacking MC3R (MC3R KO) exhibit hypersensitivity to MC4R agonists. However, MC3R KO mice also exhibit defective behavioral and neuroendocrine responses to fasting. Here, we demonstrate that MC3R KO mice exhibit defective activation of AgRP neurons in response to fasting and cold exposure, while exhibiting normal inhibition of AgRP neurons by sensory detection of food. Further, using an AgRP-specific MC3R knockout model, we show that the control of AgRP neuron activation by MC3R is cell-autonomous. One mechanism underlying this involves the response to ghrelin, which is also blunted in mice with AgRP-specific deletion of the MC3R. Thus, MC3R is a crucial player in the control of energy homeostasis by the central melanocortin system, not only acting presynaptically on AgRP neurons, but via AgRP cell-autonomous regulation of fasting- and cold-induced neuronal activation as well.
Language	English
Publishing date	2023-06-29
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.06.28.546874
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Article ; Online: The unique structural characteristics of the Kir 7.1 inward rectifier potassium channel: a novel player in energy homeostasis control.

Hernandez, Ciria C / Gimenez, Luis E / Dahir, Naima S / Peisley, Alys / Cone, Roger D

American journal of physiology. Cell physiology

2023 Volume 324, Issue 3, Page(s) C694–C706

Abstract: The inward rectifier potassium channel Kir7.1, encoded by ... ...

Abstract	The inward rectifier potassium channel Kir7.1, encoded by the
MeSH term(s)	Humans ; Mutation ; Neurons/metabolism ; Potassium/metabolism ; Potassium Channels, Inwardly Rectifying/genetics ; Potassium Channels, Inwardly Rectifying/metabolism ; Protein Domains
Chemical Substances	Potassium (RWP5GA015D) ; Potassium Channels, Inwardly Rectifying ; KCNJ13 protein, human
Language	English
Publishing date	2023-01-30
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00335.2022
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Article ; Online: Aqueous remote loading of setmelanotide in poly(lactic-co-glycolic acid) microspheres for long-term obesity treatment.

Wang, Shuying / Downing, Griffin / Olsen, Karl F / Sawyer, Tomi K / Cone, Roger D / Schwendeman, Steven P

Journal of controlled release : official journal of the Controlled Release Society

2023 Volume 364, Page(s) 589–600

Abstract: Setmelanotide (Imcivree™) was developed as a daily injectable therapeutic peptide for the treatment of rare forms of syndromic obesity, such as POMC deficiency and leptin receptor deficiency. The important option of poly(lactic-co-glycolic acid) (PLGA) ... ...

Abstract	Setmelanotide (Imcivree™) was developed as a daily injectable therapeutic peptide for the treatment of rare forms of syndromic obesity, such as POMC deficiency and leptin receptor deficiency. The important option of poly(lactic-co-glycolic acid) (PLGA) controlled release microspheres has become more attractive for this class of drugs upon the discovery that net positively charged peptides can be remote-loaded rapidly from aqueous peptide solution into blank microspheres at high loading and encapsulation efficiency. Here we sought to remote-load setmelanotide in PLGA microspheres and examine its potential for long-term controlled release and body weight control. The influence of PLGA microsphere porosity was investigated with respect to morphology, drug loading, and in vitro release profiles. Increased density of the microspheres inhibited the progress of encapsulation of the dicationic peptide. A diet-induced obese murine model was then used to determine the pharmacokinetic profile and to evaluate long-term efficacy of an optimal formulation. Remote loaded PLGA formulations encapsulated setmelanotide as high as ∼63% (∼6.3% w/w loading) and exhibited slow and continuous peptide release over ∼6 weeks in vitro largely independent of microsphere porosity. The obtained in vivo release pattern from deconvolution of the pharmacokinetics after subcutaneous microsphere injection was consistent with the in vitro release profile but with a lower initial burst release and overall slightly faster release rate. After a single injection of remote-loaded setmelanotide, continuous long-term inhibition of food intake and body weight control was observed over 17 and 30 days, respectively. The improvement in body weight control over drug-free microsphere vehicle-treated control groups matched the observed PK profile. This study provides the first report of long-acting release formulation for 1-month controlled release of setmelanotide and body weight control in a diet induced obese murine model, and supports the further development of long-acting treatment options for obese patients.
MeSH term(s)	Humans ; Mice ; Animals ; Polylactic Acid-Polyglycolic Acid Copolymer ; Polyglycolic Acid ; Lactic Acid ; Microspheres ; Drug Carriers ; Delayed-Action Preparations ; Glycols ; Disease Models, Animal ; alpha-MSH ; Obesity/drug therapy ; Body Weight ; Particle Size
Chemical Substances	Polylactic Acid-Polyglycolic Acid Copolymer (1SIA8062RS) ; Polyglycolic Acid (26009-03-0) ; Lactic Acid (33X04XA5AT) ; Drug Carriers ; Delayed-Action Preparations ; Glycols ; setmelanotide ; alpha-MSH (581-05-5)
Language	English
Publishing date	2023-11-15
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	632533-6
ISSN	1873-4995 ; 0168-3659
ISSN (online)	1873-4995
ISSN	0168-3659
DOI	10.1016/j.jconrel.2023.09.015
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Article ; Online: QnAs with Roger D. Cone.

Cone, Roger D

Proceedings of the National Academy of Sciences of the United States of America

2013 Volume 110, Issue 24, Page(s) 9618

MeSH term(s)	Animals ; Eating/genetics ; Eating/physiology ; Humans ; Larva/genetics ; Larva/physiology ; Mice ; Models, Animal ; Obesity/genetics ; Obesity/physiopathology ; Receptor, Melanocortin, Type 4/genetics ; Receptor, Melanocortin, Type 4/physiology ; Zebrafish/genetics ; Zebrafish/physiology
Chemical Substances	Receptor, Melanocortin, Type 4
Language	English
Publishing date	2013-05-28
Publishing country	United States
Document type	Interview ; Portrait
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1308417110
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Article ; Online: Network dynamics of hypothalamic feeding neurons.

Sweeney, Patrick / Chen, Can / Rajapakse, Indika / Cone, Roger D

Proceedings of the National Academy of Sciences of the United States of America

2021 Volume 118, Issue 14

Abstract: Mutations in the melanocortin 4 receptor (MC4R) result in hyperphagia and obesity and are the most common cause of monogenic obesity in humans. Preclinical rodent studies have determined that the critical role of the MC4R in controlling feeding can be ... ...

Abstract	Mutations in the melanocortin 4 receptor (MC4R) result in hyperphagia and obesity and are the most common cause of monogenic obesity in humans. Preclinical rodent studies have determined that the critical role of the MC4R in controlling feeding can be mapped in part to its expression in the paraventricular nucleus of the hypothalamus (paraventricular nucleus [PVN]), where it regulates the activity of anorexic neural circuits. Despite the critical role of PVN MC4R neurons in regulating feeding, the in vivo neuronal activity of these cells remains largely unstudied, and the network activity of PVN MC4R neurons has not been determined. Here, we utilize in vivo single-cell endomicroscopic and mathematical approaches to determine the activity and network dynamics of PVN MC4R neurons in response to changes in energy state and pharmacological manipulation of central melanocortin receptors. We determine that PVN MC4R neurons exhibit both quantitative and qualitative changes in response to fasting and refeeding. Pharmacological stimulation of MC4R with the therapeutic MC4R agonist setmelanotide rapidly increases basal PVN MC4R activity, while stimulation of melanocortin 3 receptor (MC3R) inhibits PVN MC4R activity. Finally, we find that distinct PVN MC4R neuronal ensembles encode energy deficit and energy surfeit and that energy surfeit is associated with enhanced network connections within PVN MC4R neurons. These findings provide valuable insight into the neural dynamics underlying hunger and energy surfeit.
MeSH term(s)	Animals ; Feeding Behavior/physiology ; Male ; Mice ; Microscopy, Fluorescence ; Nerve Net ; Optical Imaging ; Paraventricular Hypothalamic Nucleus/cytology ; Paraventricular Hypothalamic Nucleus/physiology ; Receptor, Melanocortin, Type 3/agonists ; Receptor, Melanocortin, Type 4/metabolism ; Single-Cell Analysis
Chemical Substances	MC4R protein, mouse ; Mc3r protein, mouse ; Receptor, Melanocortin, Type 3 ; Receptor, Melanocortin, Type 4
Language	English
Publishing date	2021-08-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2011140118
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Article ; Online: Deletion of the Feeding-Induced Hepatokine TSK Ameliorates the Melanocortin Obesity Syndrome.

Wang, Qiuyu / Zhang, Peng / Cakir, Isin / Mi, Lin / Cone, Roger D / Lin, Jiandie D

Diabetes

2021 Volume 70, Issue 9, Page(s) 2081–2091

Abstract: Work in recent decades has established that metabolic hormones released by endocrine cells and diverse other cell types serve to regulate nutrient intake and energy homeostasis. Tsukushi (TSK) is a leucine-rich repeat-containing protein secreted ... ...

Abstract	Work in recent decades has established that metabolic hormones released by endocrine cells and diverse other cell types serve to regulate nutrient intake and energy homeostasis. Tsukushi (TSK) is a leucine-rich repeat-containing protein secreted primarily by the liver that exerts an inhibitory effect on brown fat sympathetic innervation and thermogenesis. Despite this, physiological regulation of TSK and the mechanisms underlying its effects on energy balance remain poorly understood. Here we show that hepatic expression and plasma concentrations of TSK are induced by feeding and regulated by melanocortin-4 receptor (MC4R) signaling. We generated TSK and MC4R-double-knockout mice to elucidate the nature of cross talk between TSK and the central regulatory circuit of energy balance. Remarkably, TSK inactivation restores energy balance, ameliorates hyperphagia, and improves metabolic health in MC4R-deficient mice. TSK ablation enhances thermogenic gene expression in brown fat, dampens obesity-association inflammation in the liver and adipose tissue, and protects MC4R-null mice from diet-induced nonalcoholic steatohepatitis. At the cellular level, TSK deficiency augments feeding-induced c-Fos expression in the paraventricular nucleus of the hypothalamus. These results illustrate physiological cross talk between TSK and the central regulatory circuit in maintaining energy balance and metabolic homeostasis.
MeSH term(s)	Adipose Tissue, Brown/drug effects ; Adipose Tissue, Brown/metabolism ; Adipose Tissue, White/drug effects ; Adipose Tissue, White/metabolism ; Animals ; Anti-Obesity Agents/pharmacology ; Energy Metabolism/physiology ; Hypothalamus/drug effects ; Hypothalamus/metabolism ; Liver/drug effects ; Liver/metabolism ; Mice ; Mice, Knockout ; Non-alcoholic Fatty Liver Disease/genetics ; Non-alcoholic Fatty Liver Disease/metabolism ; Obesity/genetics ; Obesity/metabolism ; Proteoglycans/genetics ; Proteoglycans/metabolism ; Receptor, Melanocortin, Type 4/genetics ; Receptor, Melanocortin, Type 4/metabolism ; Signal Transduction/physiology ; Thermogenesis/physiology ; alpha-MSH/analogs & derivatives ; alpha-MSH/pharmacology
Chemical Substances	Anti-Obesity Agents ; Proteoglycans ; Receptor, Melanocortin, Type 4 ; setmelanotide ; tsukushi protein, mouse ; alpha-MSH (581-05-5)
Language	English
Publishing date	2021-06-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db21-0161
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