scholarly journals Metabolomics analysis in adults with high bone mass identifies a relationship between bone resorption and circulating citrate which replicates in the general population

2021 ◽  
Author(s):  
April Hartley ◽  
Lavinia Paternoster ◽  
David M Evans ◽  
William D Fraser ◽  
Jonathan Tang ◽  
...  
Keyword(s):  
Bone Resorption ◽  
General Population ◽  
Bone Mass ◽  
High Bone Mass ◽  
High Bone ◽  
Metabolomics Analysis

scholarly journals Metabolomics analysis in adults with high bone mass identifies a relationship between bone resorption and circulating citrate which replicates in the general population

2019 ◽  
Vol 92 (1) ◽  
pp. 29-37 ◽  
Author(s):  
April Hartley ◽  
Lavinia Paternoster ◽  
David M. Evans ◽  
William D. Fraser ◽  
Jonathan Tang ◽  
...  
Keyword(s):  
Bone Resorption ◽  
General Population ◽  
Bone Mass ◽  
High Bone Mass ◽  
High Bone ◽  
Metabolomics Analysis

scholarly journals Cart Overexpression Is the Only Identifiable Cause of High Bone Mass in Melanocortin 4 Receptor Deficiency

Endocrinology ◽  
2006 ◽  
Vol 147 (7) ◽  
pp. 3196-3202 ◽  
Author(s):  
Jong Deok Ahn ◽  
Beatrice Dubern ◽  
Cecile Lubrano-Berthelier ◽  
Karine Clement ◽  
Gerard Karsenty
Keyword(s):  
Energy Metabolism ◽  
Bone Resorption ◽  
Bone Mass ◽  
Bone Remodeling ◽  
Neural Control ◽  
Osteoclast Differentiation ◽  
Serum Levels ◽  
High Bone Mass ◽  
Melanocortin 4 Receptor ◽  
High Bone

The neural regulation of bone remodeling has proven to be increasingly complex at the molecular level because it involves both positive and negative mediators of bone formation and resorption. One of the mediators expressed in hypothalamic neurons that leptin uses to inhibit osteoclast differentiation and thereby bone resorption is cocaine- and amphetamine-regulated transcript (CART). CART expression in the hypothalamus is increased in mice lacking melanocortin 4 receptor (Mc4r−/− mice). Moreover, we show here that humans or mice lacking only one allele of Mc4r display a decrease in bone resorption parameters, high bone mass, and an increase in CART serum levels and/or hypothalamic expression. To demonstrate that the Cart overexpression is the only identifiable cause for the high bone mass observed upon Mc4r inactivation, we removed one allele of Cart from mice either heterozygous or homozygous for Mc4r inactivation. This manipulation sufficed to either significantly improve or normalize bone resorption parameters, without improving the energy metabolism disturbance that characterizes Mc4r-deficient mice. These results identify CART signaling as the main if not only molecular pathway accounting for the decrease in bone resorption leading to high bone mass in mice and humans deficient in Mc4r. As importantly, they also indicate that CART regulates bone resorption independently of the role it may exert in energy metabolism, suggesting that the neural control of appetite and bone remodeling are independent of each other.

scholarly journals Amylin inhibits bone resorption while the calcitonin receptor controls bone formation in vivo

2004 ◽  
Vol 164 (4) ◽  
pp. 509-514 ◽  
Author(s):  
Romain Dacquin ◽  
Rachel A. Davey ◽  
Catherine Laplace ◽  
Régis Levasseur ◽  
Howard A. Morris ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Formation ◽  
Bone Mass ◽  
Dependent Manner ◽  
Calcitonin Receptor ◽  
Low Bone Mass ◽  
High Bone Mass ◽  
High Bone

Amylin is a member of the calcitonin family of hormones cosecreted with insulin by pancreatic β cells. Cell culture assays suggest that amylin could affect bone formation and bone resorption, this latter function after its binding to the calcitonin receptor (CALCR). Here we show that Amylin inactivation leads to a low bone mass due to an increase in bone resorption, whereas bone formation is unaffected. In vitro, amylin inhibits fusion of mononucleated osteoclast precursors into multinucleated osteoclasts in an ERK1/2-dependent manner. Although Amylin +/− mice like Amylin-deficient mice display a low bone mass phenotype and increased bone resorption, Calcr +/− mice display a high bone mass due to an increase in bone formation. Moreover, compound heterozygote mice for Calcr and Amylin inactivation displayed bone abnormalities observed in both Calcr +/− and Amylin +/− mice, thereby ruling out that amylin uses CALCR to inhibit osteoclastogenesis in vivo. Thus, amylin is a physiological regulator of bone resorption that acts through an unidentified receptor.

scholarly journals Monosodium Glutamate-Sensitive Hypothalamic Neurons Contribute to the Control of Bone Mass

Endocrinology ◽  
2003 ◽  
Vol 144 (9) ◽  
pp. 3842-3847 ◽  
Author(s):  
Florent Elefteriou ◽  
Shu Takeda ◽  
Xiuyun Liu ◽  
Dawna Armstrong ◽  
Gerard Karsenty
Keyword(s):  
Bone Resorption ◽  
Bone Formation ◽  
Bone Mass ◽  
Monosodium Glutamate ◽  
Hypothalamic Neurons ◽  
High Bone Mass ◽  
Independent Manner ◽  
Normal Bone ◽  
High Bone ◽  
High Bone Mass Phenotype

Abstract Using chemical lesioning we previously identified hypothalamic neurons that are required for leptin antiosteogenic function. In the course of these studies we observed that destruction of neurons sensitive to monosodium glutamate (MSG) in arcuate nuclei did not affect bone mass. However MSG treatment leads to hypogonadism, a condition inducing bone loss. Therefore the normal bone mass of MSG-treated mice suggested that MSG-sensitive neurons may be implicated in the control of bone mass. To test this hypothesis we assessed bone resorption and bone formation parameters in MSG-treated mice. We show here that MSG-treated mice display the expected increase in bone resorption and that their normal bone mass is due to a concomitant increase in bone formation. Correction of MSG-induced hypogonadism by physiological doses of estradiol corrected the abnormal bone resorptive activity in MSG-treated mice and uncovered their high bone mass phenotype. Because neuropeptide Y (NPY) is highly expressed in MSG-sensitive neurons we tested whether NPY regulates bone formation. Surprisingly, NPY-deficient mice had a normal bone mass. This study reveals that distinct populations of hypothalamic neurons are involved in the control of bone mass and demonstrates that MSG-sensitive neurons control bone formation in a leptin-independent manner. It also indicates that NPY deficiency does not affect bone mass.

Mutations in LRP5 and SOST are a rare cause of high bone mass in the general population

Bone ◽  
2009 ◽  
Vol 44 ◽  
pp. S340-S341 ◽  
Author(s):  
E.L. Duncan ◽  
C.L. Gregson⁎ ◽  
K. Addison ◽  
M. Brugmans ◽  
J.J. Pointon ◽  
...  
Keyword(s):  
General Population ◽  
Bone Mass ◽  
High Bone Mass ◽  
High Bone

scholarly journals Mice lacking DKK1 in T cells exhibit high bone mass and are protected from estrogen deficiency-induced bone loss

iScience ◽  
2021 ◽  
pp. 102224
Author(s):  
Juliane Lehmann ◽  
Sylvia Thiele ◽  
Ulrike Baschant ◽  
Tilman D. Rachner ◽  
Christof Niehrs ◽  
...  
Keyword(s):  
T Cells ◽  
Bone Loss ◽  
Bone Mass ◽  
Estrogen Deficiency ◽  
High Bone Mass ◽  
High Bone
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