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Article ; Online: The NPY system and its neural and neuroendocrine regulation of bone.

Khor, Ee Cheng / Baldock, Paul

2012 Volume 10, Issue 2, Page(s) 160–168

Abstract: The past decade has seen a significant expansion of our understanding of the interaction between the neural system and bone. While innervation of bone was long appreciated, the discovery of central relays from the hypothalamus to the cells of bone has ... ...

Abstract	The past decade has seen a significant expansion of our understanding of the interaction between the neural system and bone. While innervation of bone was long appreciated, the discovery of central relays from the hypothalamus to the cells of bone has seen the identification of a number of efferent neural pathways to bone. The neuropeptide Y (NPY) system has proven to represent a major central pathway, regulating the activity of osteoblasts and osteoclasts, through signaling of central and peripheral ligands, through specific receptors within the hypothalamus and the osteoblast. Moreover, this pathway is now recognized as acting to coordinate both skeletal and energy homeostasis. This review examines the mechanism and actions of the NPY pathway to regulate bone mass and bone cell activity.
MeSH term(s)	Animals ; Bone and Bones/physiology ; Homeostasis/physiology ; Humans ; Mice ; Models, Animal ; Neural Pathways/physiology ; Neuropeptide Y/physiology ; Neurosecretory Systems/physiology ; Signal Transduction/physiology
Chemical Substances	Neuropeptide Y
Language	English
Publishing date	2012-04-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2186581-4
ISSN	1544-2241 ; 1544-1873
ISSN (online)	1544-2241
ISSN	1544-1873
DOI	10.1007/s11914-012-0102-7
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Article ; Online: Influence of hormonal appetite and energy regulators on bone.

Khor, Ee Cheng / Wee, Natalie Kah Yun / Baldock, Paul A

Current osteoporosis reports

2013 Volume 11, Issue 3, Page(s) 194–202

Abstract: Nutritional status is an essential component in determining whole body energy homeostasis. The balance between energy/food intake and metabolism is governed by a range of hormones secreted from various parts of the body. Their subsequent dissemination ... ...

Abstract	Nutritional status is an essential component in determining whole body energy homeostasis. The balance between energy/food intake and metabolism is governed by a range of hormones secreted from various parts of the body. Their subsequent dissemination via the blood results in a wide range of biological responses including satiety, hunger, and glucose uptake. The roles of these systemic hormones also extend to bone regulation with animal and clinical studies establishing a relationship between these regulatory pathways. This review covers the gastrointestinal hormones, ghrelin, PYY, GIP, GLP-1, and GLP-2, and the adipokines, leptin, and adiponectin and their roles in regulating bone homeostasis. Their known actions are reviewed, with an emphasis upon recent advances in understanding. Taken together, this review outlines an expanding appreciation of the interactions between bone mass and the nutritional control of whole body energy balance by gut and adipose tissue.
MeSH term(s)	Adiponectin/physiology ; Animals ; Appetite/physiology ; Bone and Bones/metabolism ; Energy Metabolism/physiology ; Gastric Inhibitory Polypeptide/physiology ; Gastrointestinal Hormones/physiology ; Ghrelin/physiology ; Glucagon-Like Peptide 1/physiology ; Glucagon-Like Peptide 2/physiology ; Homeostasis/physiology ; Humans ; Leptin/physiology ; Peptide YY/physiology
Chemical Substances	Adiponectin ; Gastrointestinal Hormones ; Ghrelin ; Glucagon-Like Peptide 2 ; Leptin ; Peptide YY (106388-42-5) ; Gastric Inhibitory Polypeptide (59392-49-3) ; Glucagon-Like Peptide 1 (89750-14-1)
Language	English
Publishing date	2013-08-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2186581-4
ISSN	1544-2241 ; 1544-1873
ISSN (online)	1544-2241
ISSN	1544-1873
DOI	10.1007/s11914-013-0157-0
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Article ; Online: Diet-induced obesity suppresses cortical bone accrual by a neuropeptide Y-dependent mechanism.

Wee, Natalie K Y / Enriquez, Ronaldo F / Nguyen, Amy D / Horsnell, Harry / Kulkarni, Rishikesh / Khor, Ee Cheng / Herzog, Herbert / Baldock, Paul A

International journal of obesity (2005)

2018 Volume 42, Issue 11, Page(s) 1925–1938

Abstract: Objective: To determine whether age and neuropeptide Y (NPY) were involved in the skeletal response to extended periods of diet-induced obesity.: Methods: Male wild-type (WT) and NPY null (NPYKO) mice were fed a mild (23% fat) high-fat diet for 10 ... ...

Abstract	Objective: To determine whether age and neuropeptide Y (NPY) were involved in the skeletal response to extended periods of diet-induced obesity. Methods: Male wild-type (WT) and NPY null (NPYKO) mice were fed a mild (23% fat) high-fat diet for 10 weeks from 6 or 16 weeks of age. Metabolism and bone density were assessed during feeding. Skeletal changes were assessed by microCT and histomorphometry. Results: High-fat feeding in 6-week-old WT mice led to significantly increased body weight, adiposity and serum leptin levels, accompanied with markedly suppressed cortical bone accrual. NPYKO mice were less susceptible to fat accrual but, importantly, displayed a complete lack of suppression of bone accrual or cortical bone loss. In contrast, when skeletally mature (16 week old) mice underwent 10 weeks of fat feeding, the metabolic response to HFD was similar to younger mice, however bone mass was not affected in either WT or NPYKO. Thus, growing mice are particularly susceptible to the detrimental effects of HFD on bone mass, through suppression of bone accrual involving NPY signalling. Conclusion: This study provides new insights into the relationship between the opposing processes of a positive weight/bone relationship and the negative 'metabolic' effect of obesity on bone mass. This negative effect is particularly active in growing skeletons, which have heightened sensitivity to changes in obesity. In addition, NPY is identified as a fundamental driver of this negative 'metabolic' pathway to bone.
MeSH term(s)	Animals ; Bone Density ; Bone Remodeling/physiology ; Cortical Bone/pathology ; Diet, High-Fat/adverse effects ; Disease Models, Animal ; Mice ; Mice, Inbred Strains ; Neuropeptide Y/deficiency ; Neuropeptide Y/physiology ; Obesity/metabolism ; Obesity/pathology ; Weight Gain/physiology
Chemical Substances	Neuropeptide Y
Language	English
Publishing date	2018-03-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	752409-2
ISSN	1476-5497 ; 0307-0565
ISSN (online)	1476-5497
ISSN	0307-0565
DOI	10.1038/s41366-018-0028-y
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Article ; Online: Uncoupling protein-1 is protective of bone mass under mild cold stress conditions.

Nguyen, Amy D / Lee, Nicola J / Wee, Natalie K Y / Zhang, Lei / Enriquez, Ronaldo F / Khor, Ee Cheng / Nie, Tao / Wu, Donghai / Sainsbury, Amanda / Baldock, Paul A / Herzog, Herbert

Bone

2018 Volume 106, Page(s) 167–178

Abstract: Brown adipose tissue (BAT), largely controlled by the sympathetic nervous system (SNS), has the ability to dissipate energy in the form of heat through the actions of uncoupling protein-1 (UCP-1), thereby critically influencing energy expenditure. ... ...

Abstract	Brown adipose tissue (BAT), largely controlled by the sympathetic nervous system (SNS), has the ability to dissipate energy in the form of heat through the actions of uncoupling protein-1 (UCP-1), thereby critically influencing energy expenditure. Besides BAT, the SNS also strongly influences bone, and recent studies have demonstrated a positive correlation between BAT activity and bone mass, albeit the interactions between BAT and bone remain unclear. Here we show that UCP-1 is critical for protecting bone mass in mice under conditions of permanent mild cold stress for this species (22°C). UCP-1
MeSH term(s)	Adipose Tissue, Brown/metabolism ; Animals ; Blotting, Western ; Body Composition/physiology ; Body Weight/physiology ; Calorimetry, Indirect ; Cold Temperature ; Energy Metabolism/physiology ; In Situ Hybridization ; Male ; Mice ; Mice, Knockout ; Neuropeptide Y/metabolism ; Uncoupling Protein 1/genetics ; Uncoupling Protein 1/metabolism ; X-Ray Microtomography
Chemical Substances	Neuropeptide Y ; Uncoupling Protein 1
Language	English
Publishing date	2018-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	632515-4
ISSN	1873-2763 ; 8756-3282
ISSN (online)	1873-2763
ISSN	8756-3282
DOI	10.1016/j.bone.2015.05.037
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Article ; Online: Neuropeptide Y is a critical modulator of leptin's regulation of cortical bone.

Wong, Iris P L / Nguyen, Amy D / Khor, Ee Cheng / Enriquez, Ronaldo F / Eisman, John A / Sainsbury, Amanda / Herzog, Herbert / Baldock, Paul A

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

2013 Volume 28, Issue 4, Page(s) 886–898

Abstract: Leptin signaling is required for normal bone homeostasis; however, loss of leptin results in differing effects on cortical and cancellous bone, as well as altered responses between the axial and appendicular regions. Local β-adrenergic actions are ... ...

Abstract	Leptin signaling is required for normal bone homeostasis; however, loss of leptin results in differing effects on cortical and cancellous bone, as well as altered responses between the axial and appendicular regions. Local β-adrenergic actions are responsible for the greater cancellous bone volume in leptin-deficient (ob/ob) mice; however, the mechanism responsible for the opposing reduction in cortical bone in ob/ob mice is not known. Here we show that blocking the leptin-deficient increase in neuropeptide Y (NPY) expression reverses the cortical bone loss in ob/ob mice. Mice null for both NPY and leptin (NPY(-/-) ob/ob), display greater cortical bone mass in both long-bones and vertebra, with NPY(-/-) ob/ob mice exhibiting thicker and denser cortical bone, associated with greater endocortical and periosteal mineral apposition rate (MAR), compared to ob/ob animals. Importantly, these cortical changes occurred without significant increases in body weight, with NPY(-/-) ob/ob mice showing significantly reduced adiposity compared to ob/ob controls, most likely due to the reduced respiratory exchange ratio seen in these animals. Interestingly, cancellous bone volume was not different between NPY(-/-) ob/ob and ob/ob, suggesting that NPY is not influencing the adrenergic axis. Taken together, this work demonstrates the critical role of NPY signaling in the regulation of bone and energy homeostasis, and more importantly, suggests that reduced leptin levels or leptin resistance, which occurs in obesity, could potentially inhibit cortical bone formation via increased central NPY signaling.
MeSH term(s)	Absorptiometry, Photon ; Adiposity ; Animals ; Bone Density ; Bone and Bones/anatomy & histology ; Bone and Bones/diagnostic imaging ; Bone and Bones/metabolism ; Corticosterone/blood ; Fasting/blood ; Feeding Behavior ; Femur/diagnostic imaging ; Femur/metabolism ; Fertility ; Gene Deletion ; Leptin/metabolism ; Male ; Mice, Inbred C57BL ; Mice, Obese ; Minerals/metabolism ; Neuropeptide Y/deficiency ; Neuropeptide Y/metabolism ; Organ Size ; Phenotype ; Spine/anatomy & histology ; Spine/diagnostic imaging ; Spine/metabolism
Chemical Substances	Leptin ; Minerals ; Neuropeptide Y ; Corticosterone (W980KJ009P)
Language	English
Publishing date	2013-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	632783-7
ISSN	1523-4681 ; 0884-0431
ISSN (online)	1523-4681
ISSN	0884-0431
DOI	10.1002/jbmr.1786
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Article ; Online: Prader-Willi Critical Region, a Non-Translated, Imprinted Central Regulator of Bone Mass: Possible Role in Skeletal Abnormalities in Prader-Willi Syndrome.

Khor, Ee-Cheng / Fanshawe, Bruce / Qi, Yue / Zolotukhin, Sergei / Kulkarni, Rishikesh N / Enriquez, Ronaldo F / Purtell, Louise / Lee, Nicola J / Wee, Natalie K / Croucher, Peter I / Campbell, Lesley / Herzog, Herbert / Baldock, Paul A

PloS one

2016 Volume 11, Issue 1, Page(s) e0148155

Abstract: Prader-Willi Syndrome (PWS), a maternally imprinted disorder and leading cause of obesity, is characterised by insatiable appetite, poor muscle development, cognitive impairment, endocrine disturbance, short stature and osteoporosis. A number of ... ...

Abstract	Prader-Willi Syndrome (PWS), a maternally imprinted disorder and leading cause of obesity, is characterised by insatiable appetite, poor muscle development, cognitive impairment, endocrine disturbance, short stature and osteoporosis. A number of causative loci have been located within the imprinted Prader-Willi Critical Region (PWCR), including a set of small non-translated nucleolar RNA's (snoRNA). Recently, micro-deletions in humans identified the snoRNA Snord116 as a critical contributor to the development of PWS exhibiting many of the classical symptoms of PWS. Here we show that loss of the PWCR which includes Snord116 in mice leads to a reduced bone mass phenotype, similar to that observed in humans. Consistent with reduced stature in PWS, PWCR KO mice showed delayed skeletal development, with shorter femurs and vertebrae, reduced bone size and mass in both sexes. The reduction in bone mass in PWCR KO mice was associated with deficiencies in cortical bone volume and cortical mineral apposition rate, with no change in cancellous bone. Importantly, while the length difference was corrected in aged mice, consistent with continued growth in rodents, reduced cortical bone formation was still evident, indicating continued osteoblastic suppression by loss of PWCR expression in skeletally mature mice. Interestingly, deletion of this region included deletion of the exclusively brain expressed Snord116 cluster and resulted in an upregulation in expression of both NPY and POMC mRNA in the arcuate nucleus. Importantly, the selective deletion of the PWCR only in NPY expressing neurons replicated the bone phenotype of PWCR KO mice. Taken together, PWCR deletion in mice, and specifically in NPY neurons, recapitulates the short stature and low BMD and aspects of the hormonal imbalance of PWS individuals. Moreover, it demonstrates for the first time, that a region encoding non-translated RNAs, expressed solely within the brain, can regulate bone mass in health and disease.
MeSH term(s)	Animals ; Base Sequence ; Bone Density ; Bone and Bones/abnormalities ; Bone and Bones/metabolism ; Disease Models, Animal ; Female ; Gene Expression Regulation, Developmental ; Genomic Imprinting ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Neurons/metabolism ; Neurons/pathology ; Neuropeptide Y/genetics ; Neuropeptide Y/metabolism ; Prader-Willi Syndrome/genetics ; Prader-Willi Syndrome/metabolism ; Prader-Willi Syndrome/pathology ; Proprotein Convertases/genetics ; Proprotein Convertases/metabolism ; RNA, Small Nucleolar/genetics ; RNA, Small Nucleolar/metabolism ; Sequence Deletion ; Signal Transduction
Chemical Substances	Neuropeptide Y ; RNA, Small Nucleolar ; Proprotein Convertases (EC 3.4.21.-)
Language	English
Publishing date	2016-01-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0148155
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Article ; Online: The y6 receptor suppresses bone resorption and stimulates bone formation in mice via a suprachiasmatic nucleus relay.

Khor, Ee-Cheng / Yulyaningsih, Ernie / Driessler, Frank / Kovaĉić, Natasha / Wee, Natalie K Y / Kulkarni, Rishikesh N / Lee, Nicola J / Enriquez, Ronaldo F / Xu, Jiake / Zhang, Lei / Herzog, Herbert / Baldock, Paul A

Bone

2016 Volume 84, Page(s) 139–147

Abstract: The neuropeptide Y system is known to play an important role in the regulation of bone homeostasis and while the functions of its major receptors, Y1R and Y2R, in this process have become clearer, the contributions of other Y-receptors, like the y6 ... ...

Abstract	The neuropeptide Y system is known to play an important role in the regulation of bone homeostasis and while the functions of its major receptors, Y1R and Y2R, in this process have become clearer, the contributions of other Y-receptors, like the y6 receptor (y6R), are unknown. Y6R expression is restricted to the suprachiasmatic nucleus (SCN) of the hypothalamus, an area known to regulate circadian rhythms, and the testis. Here we show that lack of y6R signalling, results in significant reduction in bone mass, but no changes in bone length. Male and female y6R knockout (KO) mice display reduced cortical and cancellous bone volume in axial and appendicular bones. Mechanistically, the reduction in cancellous bone is the result of an uncoupling of bone remodelling, leading to an increase in osteoclast surface and number, and a reduction in osteoblast number, osteoid surface, mineralizing surface and bone formation rate. y6R KO mice displayed increased numbers of osteoclast precursors and produced greater numbers of osteoclasts in RANKL-treated cultures. They also produced fewer CFU-ALP osteoblast precursors in the marrow and showed reduced mineralization in primary osteoblastic cultures, as well as reduced expression for the osteoblast lineage marker, alkaline phosphatase, in bone isolates. The almost exclusive location of y6Rs in the hypothalamus suggests a critical role of central neuronal pathways controlling this uncoupling of bone remodelling which is in line with known actions or other Y-receptors in the brain. In conclusion, y6R signalling is required for maintenance of bone mass, with loss of y6R uncoupling bone remodelling and resulting in a negative bone balance. This study expands the scope of hypothalamic regulation of bone, highlighting the importance for neural/endocrine coordination and their marked effect upon skeletal homeostasis.
MeSH term(s)	Aging/metabolism ; Animals ; Bone Marrow/metabolism ; Bone Resorption/metabolism ; Bone Resorption/pathology ; Calcification, Physiologic ; Cell Count ; Cell Differentiation ; Female ; Gene Expression Regulation ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Osteoblasts/metabolism ; Osteoblasts/pathology ; Osteoclasts/pathology ; Osteocytes/metabolism ; Osteocytes/pathology ; Osteogenesis/genetics ; Receptors, Neuropeptide Y/deficiency ; Receptors, Neuropeptide Y/genetics ; Receptors, Neuropeptide Y/metabolism ; Signal Transduction ; Suprachiasmatic Nucleus/metabolism ; Suprachiasmatic Nucleus/pathology
Chemical Substances	Receptors, Neuropeptide Y ; neuropeptide Y6 receptor
Language	English
Publishing date	2016-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	632515-4
ISSN	1873-2763 ; 8756-3282
ISSN (online)	1873-2763
ISSN	8756-3282
DOI	10.1016/j.bone.2015.12.011
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Article ; Online: Pancreatic polypeptide controls energy homeostasis via Npy6r signaling in the suprachiasmatic nucleus in mice.

Yulyaningsih, Ernie / Loh, Kim / Lin, Shu / Lau, Jackie / Zhang, Lei / Shi, Yanchuan / Berning, Britt A / Enriquez, Ronaldo / Driessler, Frank / Macia, Laurence / Khor, Ee Cheng / Qi, Yue / Baldock, Paul / Sainsbury, Amanda / Herzog, Herbert

Cell metabolism

2014 Volume 19, Issue 1, Page(s) 58–72

Abstract: Y-receptors control energy homeostasis, but the role of Npy6 receptors (Npy6r) is largely unknown. Young Npy6r-deficient (Npy6r(-/-)) mice have reduced body weight, lean mass, and adiposity, while older and high-fat-fed Npy6r(-/-) mice have low lean mass ...

Abstract	Y-receptors control energy homeostasis, but the role of Npy6 receptors (Npy6r) is largely unknown. Young Npy6r-deficient (Npy6r(-/-)) mice have reduced body weight, lean mass, and adiposity, while older and high-fat-fed Npy6r(-/-) mice have low lean mass with increased adiposity. Npy6r(-/-) mice showed reduced hypothalamic growth hormone releasing hormone (Ghrh) expression and serum insulin-like growth factor-1 (IGF-1) levels relative to WT. This is likely due to impaired vasoactive intestinal peptide (VIP) signaling in the suprachiasmatic nucleus (SCN), where we found Npy6r coexpressed in VIP neurons. Peripheral administration of pancreatic polypeptide (PP) increased Fos expression in the SCN, increased energy expenditure, and reduced food intake in WT, but not Npy6r(-/-), mice. Moreover, intraperitoneal (i.p.) PP injection increased hypothalamic Ghrh mRNA expression and serum IGF-1 levels in WT, but not Npy6r(-/-), mice, an effect blocked by intracerebroventricular (i.c.v.) Vasoactive Intestinal Peptide (VPAC) receptors antagonism. Thus, PP-initiated signaling through Npy6r in VIP neurons regulates the growth hormone axis and body composition.
MeSH term(s)	Adiposity ; Animals ; Body Weight ; Corticosterone/metabolism ; Diet ; Energy Metabolism ; Feeding Behavior ; Fertility ; Homeostasis ; Insulin-Like Growth Factor I/metabolism ; Ligands ; Mice ; Mice, Inbred C57BL ; Obesity/blood ; Obesity/pathology ; Pancreatic Polypeptide/metabolism ; Receptors, Gastrointestinal Hormone/deficiency ; Receptors, Gastrointestinal Hormone/metabolism ; Receptors, Neuropeptide Y/deficiency ; Receptors, Neuropeptide Y/metabolism ; Signal Transduction ; Suprachiasmatic Nucleus/metabolism ; Suprachiasmatic Nucleus/pathology ; Thinness/blood ; Thinness/pathology ; Vasoactive Intestinal Peptide/metabolism
Chemical Substances	Ligands ; Npy6r protein, mouse ; Receptors, Gastrointestinal Hormone ; Receptors, Neuropeptide Y ; Vasoactive Intestinal Peptide (37221-79-7) ; Pancreatic Polypeptide (59763-91-6) ; Insulin-Like Growth Factor I (67763-96-6) ; Corticosterone (W980KJ009P)
Language	English
Publishing date	2014-01-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2013.11.019
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Article ; Online: Disruption of the dynein-dynactin complex unveils motor-specific functions in osteoclast formation and bone resorption.

Ng, Pei Ying / Cheng, Tak Sum / Zhao, Haibo / Ye, Shiqiao / Sm Ang, Estabelle / Khor, Ee Cheng / Feng, Hao-Tian / Xu, Jiake / Zheng, Ming H / Pavlos, Nathan J

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

2013 Volume 28, Issue 1, Page(s) 119–134

Abstract: Osteoclastic bone resorption requires strict interplay between acidified carrier vesicles, motor proteins, and the underlying cytoskeleton in order to sustain the specialized structural and functional polarization of the ruffled border. Cytoplasmic ... ...

Abstract	Osteoclastic bone resorption requires strict interplay between acidified carrier vesicles, motor proteins, and the underlying cytoskeleton in order to sustain the specialized structural and functional polarization of the ruffled border. Cytoplasmic dynein, a large processive mechanochemical motor comprising heavy, intermediate, and light chains coupled to the dynactin cofactor complex, powers unilateral motility of diverse cargos to microtubule minus-ends. We have recently shown that regulators of the dynein motor complex constitute critical components of the osteoclastic bone resorptive machinery. Here, by selectively modulating endogenous dynein activity, we show that the integrity of the dynein-dynactin motor complex is an essential requirement for both osteoclast formation and function. Systematic dissection of the osteoclast dynein-dynactin complex revealed that it is differentially localized throughout RANKL-induced osteoclast formation and activation, undergoing microtubule-coupled reorganization upon the establishment of cellular polarization. In osteoclasts actively resorbing bone, dynein-dynactin intimately co-localizes with the CAP-Gly domain-containing microtubule plus-end protein CLIP-170 at the resorptive front, thus orientating the ruffled border as a microtubule plus-end domain. Unexpectedly, disruption of the dynein-dynactin complex by exogenous p50/dynamitin expression retards osteoclast formation in vitro, owing largely to prolonged mitotic stasis of osteoclast progenitor cells. More importantly, loss of osteoclastic dynein activity results in a drastic redistribution of key intracellular organelles, including the Golgi and lysosomes, an effect that coincides with impaired cathepsin K secretion and diminished bone resorptive function. Collectively, these data unveil a previously unrecognized role for the dynein-dynactin motor complex in osteoclast formation and function, serving not only to regulate their timely maturation but also the delivery of osteolytic cargo that is essential to the bone resorptive process.
MeSH term(s)	Animals ; Bone Resorption/enzymology ; Bone Resorption/metabolism ; Bone Resorption/pathology ; Cathepsin K/metabolism ; Cell Differentiation/drug effects ; Cell Polarity/drug effects ; Dynactin Complex ; Dyneins/metabolism ; Endosomes/drug effects ; Endosomes/metabolism ; Golgi Apparatus/drug effects ; Golgi Apparatus/metabolism ; Humans ; Lysosomes/drug effects ; Lysosomes/metabolism ; Mice ; Mice, Inbred C57BL ; Microtubule-Associated Proteins/metabolism ; Microtubules/drug effects ; Microtubules/metabolism ; Neoplasm Proteins/metabolism ; Osteoclasts/drug effects ; Osteoclasts/enzymology ; Osteoclasts/pathology ; Osteogenesis/drug effects ; Protein Binding/drug effects ; Protein Transport/drug effects ; RANK Ligand/pharmacology ; Subcellular Fractions/drug effects ; Subcellular Fractions/metabolism
Chemical Substances	DCTN2 protein, human ; Dctn2 protein, mouse ; Dynactin Complex ; Microtubule-Associated Proteins ; Neoplasm Proteins ; RANK Ligand ; cytoplasmic linker protein 170 (148349-95-5) ; Cathepsin K (EC 3.4.22.38) ; Dyneins (EC 3.6.4.2)
Language	English
Publishing date	2013-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	632783-7
ISSN	1523-4681 ; 0884-0431
ISSN (online)	1523-4681
ISSN	0884-0431
DOI	10.1002/jbmr.1725
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Article ; Online: Peptide YY regulates bone remodeling in mice: a link between gut and skeletal biology.

Wong, Iris P L / Driessler, Frank / Khor, Ee Cheng / Shi, Yan-Chuan / Hörmer, Birgit / Nguyen, Amy D / Enriquez, Ronaldo F / Eisman, John A / Sainsbury, Amanda / Herzog, Herbert / Baldock, Paul A

PloS one

2012 Volume 7, Issue 7, Page(s) e40038

Abstract: Background & aims: Gastrointestinal peptides are increasingly being linked to processes controlling the maintenance of bone mass. Peptide YY (PYY), a gut-derived satiety peptide of the neuropeptide Y family, is upregulated in some states that also ... ...

Abstract	Background & aims: Gastrointestinal peptides are increasingly being linked to processes controlling the maintenance of bone mass. Peptide YY (PYY), a gut-derived satiety peptide of the neuropeptide Y family, is upregulated in some states that also display low bone mass. Importantly, PYY has high affinity for Y-receptors, particularly Y1R and Y2R, which are known to regulate bone mass. Anorexic conditions and bariatric surgery for obesity influence circulating levels of PYY and have a negative impact on bone mass, but the precise mechanism behind this is unclear. We thus examined whether alterations in PYY expression affect bone mass. Methods: Bone microstructure and cellular activity were analyzed in germline PYY knockout and conditional adult-onset PYY over-expressing mice at lumbar and femoral sites using histomorphometry and micro-computed tomography. Results: PYY displayed a negative relationship with osteoblast activity. Male and female PYY knockout mice showed enhanced osteoblast activity, with greater cancellous bone mass. Conversely, PYY over-expression lowered osteoblast activity in vivo, via a direct Y1 receptor mediated mechanism involving MAPK stimulation evident in vitro. In contrast to PYY knockout mice, PYY over expression also altered bone resorption, as indicated by greater osteoclast surface, despite the lack of Y-receptor expression in osteoclastic cells. While evident in both sexes, cellular changes were generally more pronounced in females. Conclusions: These data demonstrate that the gut peptide PYY is critical for the control of bone remodeling. This regulatory axis from the intestine to bone has the potential to contribute to the marked bone loss observed in situations of extreme weight loss and higher circulating PYY levels, such as anorexia and bariatric obesity surgery, and may be important in the maintenance of bone mass in the general population.
MeSH term(s)	Animals ; Bone Density/genetics ; Bone Remodeling/physiology ; Bone Resorption/genetics ; Bone and Bones/physiology ; Female ; Gastrointestinal Tract/metabolism ; Gene Expression ; Gene Order ; Gene Targeting ; Male ; Mice ; Mice, Transgenic ; Organ Size/genetics ; Osteoblasts/metabolism ; Osteogenesis/genetics ; Peptide YY/genetics ; Peptide YY/metabolism ; Signal Transduction
Chemical Substances	Peptide YY (106388-42-5)
Language	English
Publishing date	2012-07-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0040038
Database	MEDical Literature Analysis and Retrieval System OnLINE

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