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Article ; Online: A central regulation of PTH secretion and function.

Ducy, Patricia

2024 Volume 111, Issue 12, Page(s) 1847–1849

Abstract: PTH orchestrates calcium homeostasis and doubles as a potent, clinically important regulator of bone mass. Adding to the known peripheral regulation of PTH secretion and function, a study by Zhang et al. ...

Abstract	PTH orchestrates calcium homeostasis and doubles as a potent, clinically important regulator of bone mass. Adding to the known peripheral regulation of PTH secretion and function, a study by Zhang et al.
MeSH term(s)	Parathyroid Hormone/metabolism ; Calcium/metabolism
Chemical Substances	Parathyroid Hormone ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2024-01-08
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	808167-0
ISSN	1097-4199 ; 0896-6273
ISSN (online)	1097-4199
ISSN	0896-6273
DOI	10.1016/j.neuron.2023.05.018
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Zs.MG 92: Show issues

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Article ; Online: Bone Regulation of Insulin Secretion and Glucose Homeostasis.

Ducy, Patricia

Endocrinology

2020 Volume 161, Issue 10

Abstract: For centuries our image of the skeleton has been one of an inert structure playing a supporting role for muscles and a protective role for inner organs like the brain. Cell biology and physiology modified this view in the 20st century by defining the ... ...

Abstract	For centuries our image of the skeleton has been one of an inert structure playing a supporting role for muscles and a protective role for inner organs like the brain. Cell biology and physiology modified this view in the 20st century by defining the constant interplay between bone-forming and bone resorbing cells that take place during bone growth and remodeling, therefore demonstrating that bone is as alive as any other tissues in the body. During the past 40 years human and, most important, mouse genetics, have allowed not only the refinement of this notion by identifying the many genes and regulatory networks responsible for the crosstalk existing between bone cells, but have redefined the role of bone by showing that its influence goes way beyond its own physiology. Among its newly identified functions is the regulation of energy metabolism by 2 bone-derived hormones, osteocalcin and lipocalin-2. Their biology and respective roles in this process are the topic of this review.
MeSH term(s)	Animals ; Bone Remodeling/physiology ; Bone Resorption/metabolism ; Bone and Bones/metabolism ; Bone and Bones/physiology ; Glucose/metabolism ; Homeostasis/physiology ; Humans ; Insulin/metabolism ; Insulin Secretion/physiology ; Mice ; Signal Transduction/physiology
Chemical Substances	Insulin ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2020-08-21
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqaa149
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Article ; Online: The role of osteocalcin in the endocrine cross-talk between bone remodelling and energy metabolism.

Ducy, P

Diabetologia

2011 Volume 54, Issue 6, Page(s) 1291–1297

Abstract: Bone remodelling, which maintains bone mass constant during adulthood, is an energy-demanding process. This, together with the observation that the adipocyte-derived hormone leptin is a major inhibitor of bone remodelling, led to the hypothesis that bone ...

Abstract	Bone remodelling, which maintains bone mass constant during adulthood, is an energy-demanding process. This, together with the observation that the adipocyte-derived hormone leptin is a major inhibitor of bone remodelling, led to the hypothesis that bone cells regulate energy metabolism through an endocrine mechanism. Studies to test this hypothesis identified osteocalcin, a hormone secreted by osteoblasts, as a positive regulator of insulin secretion, insulin resistance and energy expenditure. Remarkably, insulin signalling in osteoblasts is a positive regulator of osteocalcin production and activation via its ability to indirectly enhance bone resorption by osteoclasts. In contrast, leptin is a potent inhibitor of osteocalcin function through its effect on the sympathetic tone. Hence, osteocalcin is part of a complex signalling network between bone and the organs more classically associated with the regulation of energy homeostasis, such as the pancreas and adipose tissue. This review summarises the molecular and cellular bases of the present knowledge on osteocalcin biology and discusses the potential relevance of osteocalcin to human metabolism and pathology.
MeSH term(s)	Animals ; Bone Remodeling/physiology ; Endocrine System/physiology ; Energy Metabolism/physiology ; Humans ; Insulin Resistance/physiology ; Leptin/physiology ; Mice ; Models, Animal ; Osteocalcin/physiology
Chemical Substances	Leptin ; Osteocalcin (104982-03-8)
Language	English
Publishing date	2011-04-19
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	1694-9
ISSN	1432-0428 ; 0012-186X
ISSN (online)	1432-0428
ISSN	0012-186X
DOI	10.1007/s00125-011-2155-z
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Article ; Online: 5-HT and bone biology.

Ducy, Patricia

Current opinion in pharmacology

2011 Volume 11, Issue 1, Page(s) 34–38

Abstract: Bone formation and bone resorption, the two processes occurring constantly and in a balanced fashion throughout the skeleton, are regulated by signals as various as local and low range growth factors, hormones, and neuronal outputs. Adding to the long ... ...

Abstract	Bone formation and bone resorption, the two processes occurring constantly and in a balanced fashion throughout the skeleton, are regulated by signals as various as local and low range growth factors, hormones, and neuronal outputs. Adding to the long list of molecules involved in these regulations, gut-derived and brain-derived serotonin were recently shown to control one or both of these processes. They do so, however, by targeting different cells, respectively acting as a hormone and as a neuromediator. Moreover, while brain serotonin positively regulates bone mass accrual peripheral serotonin is a potent inhibitor of bone formation. These findings raise the prospect that pharmacologically manipulating serotonin production could therefore become a novel strategy to treat bone loss disorders.
MeSH term(s)	Animals ; Bone Resorption/metabolism ; Bone and Bones/metabolism ; Humans ; Osteogenesis/physiology ; Serotonin/metabolism ; Signal Transduction
Chemical Substances	Serotonin (333DO1RDJY)
Language	English
Publishing date	2011-02
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2037057-X
ISSN	1471-4973 ; 1471-4892
ISSN (online)	1471-4973
ISSN	1471-4892
DOI	10.1016/j.coph.2011.01.007
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Article: 5-HT and bone biology

Ducy, Patricia

Current opinion in pharmacology. 2011 Feb., v. 11, no. 1

2011

Abstract	Bone formation and bone resorption, the two processes occurring constantly and in a balanced fashion throughout the skeleton, are regulated by signals as various as local and low range growth factors, hormones, and neuronal outputs. Adding to the long list of molecules involved in these regulations, gut-derived and brain-derived serotonin were recently shown to control one or both of these processes. They do so, however, by targeting different cells, respectively acting as a hormone and as a neuromediator. Moreover, while brain serotonin positively regulates bone mass accrual peripheral serotonin is a potent inhibitor of bone formation. These findings raise the prospect that pharmacologically manipulating serotonin production could therefore become a novel strategy to treat bone loss disorders.
Keywords	bone density ; bone formation ; bone resorption ; brain ; growth factors ; hormones ; serotonin ; skeleton
Language	English
Dates of publication	2011-02
Size	p. 34-38.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	2037057-X
ISSN	1471-4973 ; 1471-4892
ISSN (online)	1471-4973
ISSN	1471-4892
DOI	10.1016/j.coph.2011.01.007
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Osteocalcin of maternal and embryonic origins synergize to establish homeostasis in offspring.

Correa Pinto Junior, Danilo / Canal Delgado, Isabella / Yang, Haiyang / Clemenceau, Alisson / Corvelo, André / Narzisi, Giuseppe / Musunuri, Rajeeva / Meyer Berger, Julian / Hendricks, Lauren E / Tokumura, Kazuya / Luo, Na / Li, Hongchao / Oury, Franck / Ducy, Patricia / Yadav, Vijay K / Li, Xiang / Karsenty, Gerard

EMBO reports

2024 Volume 25, Issue 2, Page(s) 593–615

Abstract: Many physiological osteocalcin-regulated functions are affected in adult offspring of mothers experiencing unhealthy pregnancy. Furthermore, osteocalcin signaling during gestation influences cognition and adrenal steroidogenesis in adult mice. Together ... ...

Abstract	Many physiological osteocalcin-regulated functions are affected in adult offspring of mothers experiencing unhealthy pregnancy. Furthermore, osteocalcin signaling during gestation influences cognition and adrenal steroidogenesis in adult mice. Together these observations suggest that osteocalcin may broadly function during pregnancy to determine organismal homeostasis in adult mammals. To test this hypothesis, we analyzed in unchallenged wildtype and Osteocalcin-deficient, newborn and adult mice of various genotypes and origin maintained on different genetic backgrounds, the functions of osteocalcin in the pancreas, liver and testes and their molecular underpinnings. This analysis revealed that providing mothers are Osteocalcin-deficient, Osteocalcin haploinsufficiency in embryos hampers insulin secretion, liver gluconeogenesis, glucose homeostasis, testes steroidogenesis in adult offspring; inhibits cell proliferation in developing pancreatic islets and testes; and disrupts distinct programs of gene expression in these organs and in the brain. This study indicates that osteocalcin exerts dominant functions in most organs it influences. Furthermore, through their synergistic regulation of multiple physiological functions, osteocalcin of maternal and embryonic origins contributes to the establishment and maintenance of organismal homeostasis in newborn and adult offspring.
MeSH term(s)	Animals ; Female ; Humans ; Mice ; Pregnancy ; Blood Glucose/analysis ; Blood Glucose/metabolism ; Homeostasis ; Insulin/metabolism ; Insulin Secretion ; Mammals/metabolism ; Osteocalcin/genetics ; Osteocalcin/metabolism ; Prenatal Exposure Delayed Effects/metabolism
Chemical Substances	Blood Glucose ; Insulin ; Osteocalcin (104982-03-8) ; Ceacam2 protein, mouse
Language	English
Publishing date	2024-01-16
Publishing country	England
Document type	Journal Article
ZDB-ID	2020896-0
ISSN	1469-3178 ; 1469-221X
ISSN (online)	1469-3178
ISSN	1469-221X
DOI	10.1038/s44319-023-00031-3
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Article ; Online: How understanding gut serotonin secretion could potentially lead to new treatments for osteoporosis.

Ortuño, María José / Ducy, Patricia

Expert review of endocrinology & metabolism

2014 Volume 8, Issue 2, Page(s) 93–95

Language	English
Publishing date	2014-03-29
Publishing country	England
Document type	Journal Article
ISSN	1744-8417
ISSN (online)	1744-8417
DOI	10.1586/eem.12.80
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Article ; Online: Melanocortin 4 receptor stimulation prevents antidepressant-associated weight gain in mice caused by long-term fluoxetine exposure.

Ortuño, María José / Schneeberger, Marc / Ilanges, Anoj / Marchildon, François / Pellegrino, Kyle / Friedman, Jeffrey M / Ducy, Patricia

The Journal of clinical investigation

2021 Volume 131, Issue 24

Abstract: Contrasting with the predicted anorexigenic effect of increasing brain serotonin signaling, long-term use of selective serotonin reuptake inhibitor (SSRI) antidepressants correlates with body weight (BW) gain. This adverse outcome increases the risk of ... ...

Abstract	Contrasting with the predicted anorexigenic effect of increasing brain serotonin signaling, long-term use of selective serotonin reuptake inhibitor (SSRI) antidepressants correlates with body weight (BW) gain. This adverse outcome increases the risk of transitioning to obesity and interferes with treatment compliance. Here, we show that orally administered fluoxetine (Flx), a widely prescribed SSRI, increased BW by enhancing food intake in healthy mice at 2 different time points and through 2 distinct mechanisms. Within hours, Flx decreased the activity of a subset of brainstem serotonergic neurons by triggering autoinhibitory signaling through 5-hydroxytryptamine receptor 1a (Htr1a). Following a longer treatment period, Flx blunted 5-hydroxytryptamine receptor 2c (Htr2c) expression and signaling, decreased the phosphorylation of cAMP response element-binding protein (CREB) and STAT3, and dampened the production of pro-opiomelanocortin (POMC, the precursor of α-melanocyte stimulating hormone [α-MSH]) in hypothalamic neurons, thereby increasing food intake. Accordingly, exogenous stimulation of the melanocortin 4 receptor (Mc4r) by cotreating mice with Flx and lipocalin 2, an anorexigenic hormone signaling through this receptor, normalized feeding and BW. Flx and other SSRIs also inhibited CREB and STAT3 phosphorylation in a human neuronal cell line, suggesting that these noncanonical effects could also occur in individuals treated long term with SSRIs. By defining the molecular basis of long-term SSRI-associated weight gain, we propose a therapeutic strategy to counter this effect.
MeSH term(s)	Animals ; Antidepressive Agents/adverse effects ; Antidepressive Agents/pharmacology ; Cell Line ; Fluoxetine/adverse effects ; Fluoxetine/pharmacology ; Humans ; Mice ; Mice, Knockout ; Pro-Opiomelanocortin/genetics ; Pro-Opiomelanocortin/metabolism ; Receptor, Melanocortin, Type 4/genetics ; Receptor, Melanocortin, Type 4/metabolism ; Receptor, Serotonin, 5-HT1A/genetics ; Receptor, Serotonin, 5-HT1A/metabolism ; Receptor, Serotonin, 5-HT2C/genetics ; Receptor, Serotonin, 5-HT2C/metabolism ; Time Factors ; Weight Gain/drug effects ; Weight Gain/genetics
Chemical Substances	5-hydroxytryptamine2C receptor, mouse ; Antidepressive Agents ; Htr1a protein, mouse ; MC4R protein, mouse ; Receptor, Melanocortin, Type 4 ; Receptor, Serotonin, 5-HT2C ; Fluoxetine (01K63SUP8D) ; Receptor, Serotonin, 5-HT1A (112692-38-3) ; Pro-Opiomelanocortin (66796-54-1)
Language	English
Publishing date	2021-10-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI151976
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Article: Molecular signaling.

Ducy, Patricia

Annals of the New York Academy of Sciences

2002 Volume 961, Page(s) 161

MeSH term(s)	Animals ; Cell Differentiation ; Genetic Therapy/methods ; Humans ; Signal Transduction
Language	English
Publishing date	2002-06
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	211003-9
ISSN	1749-6632 ; 0077-8923
ISSN (online)	1749-6632
ISSN	0077-8923
DOI	10.1111/j.1749-6632.2002.tb03073.x
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Article: Cbfa1: a molecular switch in osteoblast biology.

Ducy, P

Developmental dynamics : an official publication of the American Association of Anatomists

2000 Volume 219, Issue 4, Page(s) 461–471

Abstract: During the past 4 years, our molecular understanding of osteoblast biology has made rapid progress due to the characterization of the function of one molecule, Cbfa1. This member of the runt/Cbfa family of transcription factors was first identified as ... ...

Abstract	During the past 4 years, our molecular understanding of osteoblast biology has made rapid progress due to the characterization of the function of one molecule, Cbfa1. This member of the runt/Cbfa family of transcription factors was first identified as the nuclear protein binding to an osteoblast-specific cis-acting element activating the expression of Osteocalcin, the most osteoblast-specific gene. Cbfa1 was then shown to regulate the expression of all the major genes expressed by osteoblasts. Consistent with this ability, genetic experiments identified Cbfa1 as a key regulator of osteoblast differentiation in vivo. Indeed, analysis of Cbfa1-deficient mice revealed that osteoblast differentiation is arrested in absence of Cbfa1, demonstrating both that it is required for this process and that no parallel pathway can overcome its absence. The importance of Cbfa1 in controlling osteoblast differentiation was further emphasized by the identification of Cbfa1 haploinsufficiency as the cause of cleidocranial dysplasia in humans and mice, a syndrome characterized by generalized bone defects. Lastly, Cbfa1 was shown to have a role beyond development and differentiation, regulating the rate of bone matrix deposition by differentiated osteoblasts. Thus, Cbfa1 is a critical gene not only for osteoblast differentiation but also for osteoblast function. These aspects, as well as the more recent progresses in understanding Cbfa1 biology, are the focuses of this review.
MeSH term(s)	Animals ; Bone Development ; Cell Differentiation ; Chondrocytes/cytology ; Chondrocytes/physiology ; Cleidocranial Dysplasia/genetics ; Collagen/genetics ; Collagen/metabolism ; Core Binding Factor Alpha 1 Subunit ; Gene Expression Regulation, Developmental ; Mice ; Neoplasm Proteins ; Osteoblasts/cytology ; Osteoblasts/physiology ; Osteocalcin/genetics ; Osteogenesis ; Protein Structure, Tertiary ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	Core Binding Factor Alpha 1 Subunit ; Neoplasm Proteins ; Transcription Factors ; Osteocalcin (104982-03-8) ; Collagen (9007-34-5)
Language	English
Publishing date	2000-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	1102541-4
ISSN	1097-0177 ; 1058-8388
ISSN (online)	1097-0177
ISSN	1058-8388
DOI	10.1002/1097-0177(2000)9999:9999<::AID-DVDY1074>3.0.CO;2-C
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