Adiponectin Deficiency Triggers Bone Loss by Up-Regulation of Osteoclastogenesis and Down-Regulation of Osteoblastogenesis

Osteoporosis and bone disorders related to the metabolic syndrome are often associated with adipokines secreted by adipocytes in bone. Adiponectin, a type of adipokine, is a regulator of immune responses and metabolic processes, but its role in bone biology remains uncertain. We investigated the rol...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Jihyun Yang [verfasserIn] Ok-Jin Park [verfasserIn] Jiseon Kim [verfasserIn] Sora Han [verfasserIn] Young Yang [verfasserIn] Cheol-Heui Yun [verfasserIn] Seung Hyun Han [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	adiponectin osteoclast osteoblast adipocyte RANKL/OPG ratio

Übergeordnetes Werk:	In: Frontiers in Endocrinology - Frontiers Media S.A., 2011, 10(2019)
Übergeordnetes Werk:	volume:10 ; year:2019

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fendo.2019.00815

Katalog-ID:	DOAJ016687477

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allfields	10.3389/fendo.2019.00815 doi (DE-627)DOAJ016687477 (DE-599)DOAJ07ac15f06d8a4f32b9e5e67a05f9c60e DE-627 ger DE-627 rakwb eng RC648-665 Jihyun Yang verfasserin aut Adiponectin Deficiency Triggers Bone Loss by Up-Regulation of Osteoclastogenesis and Down-Regulation of Osteoblastogenesis 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Osteoporosis and bone disorders related to the metabolic syndrome are often associated with adipokines secreted by adipocytes in bone. Adiponectin, a type of adipokine, is a regulator of immune responses and metabolic processes, but its role in bone biology remains uncertain. We investigated the role of adiponectin in bone metabolism using adiponectin-deficient mice in vivo and in vitro. Adiponectin-deficient mice exhibited reduced bone mass and increased adiposity. Adiponectin-deficient calvarial cells were prone to differentiate into adipocytes rather than osteoblasts. Although bone marrow macrophages (BMMs) from adiponectin-deficient mice had low osteoclastogenic potential as osteoclast precursors with increasing interferon regulatory factor 5 expression, under co-culture conditions of calvarial cells and BMMs, the enhanced receptor activator of nuclear factor κB ligand/osteoprotegerin (RANKL/OPG) ratio of adiponectin-deficient mesenchymal progenitor cells facilitated osteoclast differentiation. In addition, increased RANKL/OPG ratio was observed in the bone marrow extracellular fluid of adiponectin-deficient mice compared to that of wild-type mice. Notably, recombinant adiponectin treatment enhanced RANKL-induced osteoclast differentiation from BMMs but up-regulated OPG production in recombinant adiponectin-exposed calvarial cells, which inhibited osteoclast differentiation. Taken together, these results suggest that adiponectin plays an inhibitory role in bone metabolism through cross talk between precursor cells of both osteoclasts and osteoblasts by regulating RANKL/OPG ratio in the bone marrow microenvironment. adiponectin osteoclast osteoblast adipocyte RANKL/OPG ratio Diseases of the endocrine glands. Clinical endocrinology Jihyun Yang verfasserin aut Ok-Jin Park verfasserin aut Jiseon Kim verfasserin aut Sora Han verfasserin aut Young Yang verfasserin aut Cheol-Heui Yun verfasserin aut Seung Hyun Han verfasserin aut In Frontiers in Endocrinology Frontiers Media S.A., 2011 10(2019) (DE-627)645090948 (DE-600)2592084-4 16642392 nnns volume:10 year:2019 https://doi.org/10.3389/fendo.2019.00815 kostenfrei https://doaj.org/article/07ac15f06d8a4f32b9e5e67a05f9c60e kostenfrei https://www.frontiersin.org/article/10.3389/fendo.2019.00815/full kostenfrei https://doaj.org/toc/1664-2392 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2019
spelling	10.3389/fendo.2019.00815 doi (DE-627)DOAJ016687477 (DE-599)DOAJ07ac15f06d8a4f32b9e5e67a05f9c60e DE-627 ger DE-627 rakwb eng RC648-665 Jihyun Yang verfasserin aut Adiponectin Deficiency Triggers Bone Loss by Up-Regulation of Osteoclastogenesis and Down-Regulation of Osteoblastogenesis 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Osteoporosis and bone disorders related to the metabolic syndrome are often associated with adipokines secreted by adipocytes in bone. Adiponectin, a type of adipokine, is a regulator of immune responses and metabolic processes, but its role in bone biology remains uncertain. We investigated the role of adiponectin in bone metabolism using adiponectin-deficient mice in vivo and in vitro. Adiponectin-deficient mice exhibited reduced bone mass and increased adiposity. Adiponectin-deficient calvarial cells were prone to differentiate into adipocytes rather than osteoblasts. Although bone marrow macrophages (BMMs) from adiponectin-deficient mice had low osteoclastogenic potential as osteoclast precursors with increasing interferon regulatory factor 5 expression, under co-culture conditions of calvarial cells and BMMs, the enhanced receptor activator of nuclear factor κB ligand/osteoprotegerin (RANKL/OPG) ratio of adiponectin-deficient mesenchymal progenitor cells facilitated osteoclast differentiation. In addition, increased RANKL/OPG ratio was observed in the bone marrow extracellular fluid of adiponectin-deficient mice compared to that of wild-type mice. Notably, recombinant adiponectin treatment enhanced RANKL-induced osteoclast differentiation from BMMs but up-regulated OPG production in recombinant adiponectin-exposed calvarial cells, which inhibited osteoclast differentiation. Taken together, these results suggest that adiponectin plays an inhibitory role in bone metabolism through cross talk between precursor cells of both osteoclasts and osteoblasts by regulating RANKL/OPG ratio in the bone marrow microenvironment. adiponectin osteoclast osteoblast adipocyte RANKL/OPG ratio Diseases of the endocrine glands. Clinical endocrinology Jihyun Yang verfasserin aut Ok-Jin Park verfasserin aut Jiseon Kim verfasserin aut Sora Han verfasserin aut Young Yang verfasserin aut Cheol-Heui Yun verfasserin aut Seung Hyun Han verfasserin aut In Frontiers in Endocrinology Frontiers Media S.A., 2011 10(2019) (DE-627)645090948 (DE-600)2592084-4 16642392 nnns volume:10 year:2019 https://doi.org/10.3389/fendo.2019.00815 kostenfrei https://doaj.org/article/07ac15f06d8a4f32b9e5e67a05f9c60e kostenfrei https://www.frontiersin.org/article/10.3389/fendo.2019.00815/full kostenfrei https://doaj.org/toc/1664-2392 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2019
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allfieldsGer	10.3389/fendo.2019.00815 doi (DE-627)DOAJ016687477 (DE-599)DOAJ07ac15f06d8a4f32b9e5e67a05f9c60e DE-627 ger DE-627 rakwb eng RC648-665 Jihyun Yang verfasserin aut Adiponectin Deficiency Triggers Bone Loss by Up-Regulation of Osteoclastogenesis and Down-Regulation of Osteoblastogenesis 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Osteoporosis and bone disorders related to the metabolic syndrome are often associated with adipokines secreted by adipocytes in bone. Adiponectin, a type of adipokine, is a regulator of immune responses and metabolic processes, but its role in bone biology remains uncertain. We investigated the role of adiponectin in bone metabolism using adiponectin-deficient mice in vivo and in vitro. Adiponectin-deficient mice exhibited reduced bone mass and increased adiposity. Adiponectin-deficient calvarial cells were prone to differentiate into adipocytes rather than osteoblasts. Although bone marrow macrophages (BMMs) from adiponectin-deficient mice had low osteoclastogenic potential as osteoclast precursors with increasing interferon regulatory factor 5 expression, under co-culture conditions of calvarial cells and BMMs, the enhanced receptor activator of nuclear factor κB ligand/osteoprotegerin (RANKL/OPG) ratio of adiponectin-deficient mesenchymal progenitor cells facilitated osteoclast differentiation. In addition, increased RANKL/OPG ratio was observed in the bone marrow extracellular fluid of adiponectin-deficient mice compared to that of wild-type mice. Notably, recombinant adiponectin treatment enhanced RANKL-induced osteoclast differentiation from BMMs but up-regulated OPG production in recombinant adiponectin-exposed calvarial cells, which inhibited osteoclast differentiation. Taken together, these results suggest that adiponectin plays an inhibitory role in bone metabolism through cross talk between precursor cells of both osteoclasts and osteoblasts by regulating RANKL/OPG ratio in the bone marrow microenvironment. adiponectin osteoclast osteoblast adipocyte RANKL/OPG ratio Diseases of the endocrine glands. Clinical endocrinology Jihyun Yang verfasserin aut Ok-Jin Park verfasserin aut Jiseon Kim verfasserin aut Sora Han verfasserin aut Young Yang verfasserin aut Cheol-Heui Yun verfasserin aut Seung Hyun Han verfasserin aut In Frontiers in Endocrinology Frontiers Media S.A., 2011 10(2019) (DE-627)645090948 (DE-600)2592084-4 16642392 nnns volume:10 year:2019 https://doi.org/10.3389/fendo.2019.00815 kostenfrei https://doaj.org/article/07ac15f06d8a4f32b9e5e67a05f9c60e kostenfrei https://www.frontiersin.org/article/10.3389/fendo.2019.00815/full kostenfrei https://doaj.org/toc/1664-2392 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2019
allfieldsSound	10.3389/fendo.2019.00815 doi (DE-627)DOAJ016687477 (DE-599)DOAJ07ac15f06d8a4f32b9e5e67a05f9c60e DE-627 ger DE-627 rakwb eng RC648-665 Jihyun Yang verfasserin aut Adiponectin Deficiency Triggers Bone Loss by Up-Regulation of Osteoclastogenesis and Down-Regulation of Osteoblastogenesis 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Osteoporosis and bone disorders related to the metabolic syndrome are often associated with adipokines secreted by adipocytes in bone. Adiponectin, a type of adipokine, is a regulator of immune responses and metabolic processes, but its role in bone biology remains uncertain. We investigated the role of adiponectin in bone metabolism using adiponectin-deficient mice in vivo and in vitro. Adiponectin-deficient mice exhibited reduced bone mass and increased adiposity. Adiponectin-deficient calvarial cells were prone to differentiate into adipocytes rather than osteoblasts. Although bone marrow macrophages (BMMs) from adiponectin-deficient mice had low osteoclastogenic potential as osteoclast precursors with increasing interferon regulatory factor 5 expression, under co-culture conditions of calvarial cells and BMMs, the enhanced receptor activator of nuclear factor κB ligand/osteoprotegerin (RANKL/OPG) ratio of adiponectin-deficient mesenchymal progenitor cells facilitated osteoclast differentiation. In addition, increased RANKL/OPG ratio was observed in the bone marrow extracellular fluid of adiponectin-deficient mice compared to that of wild-type mice. Notably, recombinant adiponectin treatment enhanced RANKL-induced osteoclast differentiation from BMMs but up-regulated OPG production in recombinant adiponectin-exposed calvarial cells, which inhibited osteoclast differentiation. Taken together, these results suggest that adiponectin plays an inhibitory role in bone metabolism through cross talk between precursor cells of both osteoclasts and osteoblasts by regulating RANKL/OPG ratio in the bone marrow microenvironment. adiponectin osteoclast osteoblast adipocyte RANKL/OPG ratio Diseases of the endocrine glands. Clinical endocrinology Jihyun Yang verfasserin aut Ok-Jin Park verfasserin aut Jiseon Kim verfasserin aut Sora Han verfasserin aut Young Yang verfasserin aut Cheol-Heui Yun verfasserin aut Seung Hyun Han verfasserin aut In Frontiers in Endocrinology Frontiers Media S.A., 2011 10(2019) (DE-627)645090948 (DE-600)2592084-4 16642392 nnns volume:10 year:2019 https://doi.org/10.3389/fendo.2019.00815 kostenfrei https://doaj.org/article/07ac15f06d8a4f32b9e5e67a05f9c60e kostenfrei https://www.frontiersin.org/article/10.3389/fendo.2019.00815/full kostenfrei https://doaj.org/toc/1664-2392 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2019
language	English
source	In Frontiers in Endocrinology 10(2019) volume:10 year:2019
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topic_facet	adiponectin osteoclast osteoblast adipocyte RANKL/OPG ratio Diseases of the endocrine glands. Clinical endocrinology
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container_title	Frontiers in Endocrinology
authorswithroles_txt_mv	Jihyun Yang @@aut@@ Ok-Jin Park @@aut@@ Jiseon Kim @@aut@@ Sora Han @@aut@@ Young Yang @@aut@@ Cheol-Heui Yun @@aut@@ Seung Hyun Han @@aut@@
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callnumber-first	R - Medicine
author	Jihyun Yang
spellingShingle	Jihyun Yang misc RC648-665 misc adiponectin misc osteoclast misc osteoblast misc adipocyte misc RANKL/OPG ratio misc Diseases of the endocrine glands. Clinical endocrinology Adiponectin Deficiency Triggers Bone Loss by Up-Regulation of Osteoclastogenesis and Down-Regulation of Osteoblastogenesis
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topic_title	RC648-665 Adiponectin Deficiency Triggers Bone Loss by Up-Regulation of Osteoclastogenesis and Down-Regulation of Osteoblastogenesis adiponectin osteoclast osteoblast adipocyte RANKL/OPG ratio
topic	misc RC648-665 misc adiponectin misc osteoclast misc osteoblast misc adipocyte misc RANKL/OPG ratio misc Diseases of the endocrine glands. Clinical endocrinology
topic_unstemmed	misc RC648-665 misc adiponectin misc osteoclast misc osteoblast misc adipocyte misc RANKL/OPG ratio misc Diseases of the endocrine glands. Clinical endocrinology
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title	Adiponectin Deficiency Triggers Bone Loss by Up-Regulation of Osteoclastogenesis and Down-Regulation of Osteoblastogenesis
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title_full	Adiponectin Deficiency Triggers Bone Loss by Up-Regulation of Osteoclastogenesis and Down-Regulation of Osteoblastogenesis
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title_sort	adiponectin deficiency triggers bone loss by up-regulation of osteoclastogenesis and down-regulation of osteoblastogenesis
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title_auth	Adiponectin Deficiency Triggers Bone Loss by Up-Regulation of Osteoclastogenesis and Down-Regulation of Osteoblastogenesis
abstract	Osteoporosis and bone disorders related to the metabolic syndrome are often associated with adipokines secreted by adipocytes in bone. Adiponectin, a type of adipokine, is a regulator of immune responses and metabolic processes, but its role in bone biology remains uncertain. We investigated the role of adiponectin in bone metabolism using adiponectin-deficient mice in vivo and in vitro. Adiponectin-deficient mice exhibited reduced bone mass and increased adiposity. Adiponectin-deficient calvarial cells were prone to differentiate into adipocytes rather than osteoblasts. Although bone marrow macrophages (BMMs) from adiponectin-deficient mice had low osteoclastogenic potential as osteoclast precursors with increasing interferon regulatory factor 5 expression, under co-culture conditions of calvarial cells and BMMs, the enhanced receptor activator of nuclear factor κB ligand/osteoprotegerin (RANKL/OPG) ratio of adiponectin-deficient mesenchymal progenitor cells facilitated osteoclast differentiation. In addition, increased RANKL/OPG ratio was observed in the bone marrow extracellular fluid of adiponectin-deficient mice compared to that of wild-type mice. Notably, recombinant adiponectin treatment enhanced RANKL-induced osteoclast differentiation from BMMs but up-regulated OPG production in recombinant adiponectin-exposed calvarial cells, which inhibited osteoclast differentiation. Taken together, these results suggest that adiponectin plays an inhibitory role in bone metabolism through cross talk between precursor cells of both osteoclasts and osteoblasts by regulating RANKL/OPG ratio in the bone marrow microenvironment.
abstractGer	Osteoporosis and bone disorders related to the metabolic syndrome are often associated with adipokines secreted by adipocytes in bone. Adiponectin, a type of adipokine, is a regulator of immune responses and metabolic processes, but its role in bone biology remains uncertain. We investigated the role of adiponectin in bone metabolism using adiponectin-deficient mice in vivo and in vitro. Adiponectin-deficient mice exhibited reduced bone mass and increased adiposity. Adiponectin-deficient calvarial cells were prone to differentiate into adipocytes rather than osteoblasts. Although bone marrow macrophages (BMMs) from adiponectin-deficient mice had low osteoclastogenic potential as osteoclast precursors with increasing interferon regulatory factor 5 expression, under co-culture conditions of calvarial cells and BMMs, the enhanced receptor activator of nuclear factor κB ligand/osteoprotegerin (RANKL/OPG) ratio of adiponectin-deficient mesenchymal progenitor cells facilitated osteoclast differentiation. In addition, increased RANKL/OPG ratio was observed in the bone marrow extracellular fluid of adiponectin-deficient mice compared to that of wild-type mice. Notably, recombinant adiponectin treatment enhanced RANKL-induced osteoclast differentiation from BMMs but up-regulated OPG production in recombinant adiponectin-exposed calvarial cells, which inhibited osteoclast differentiation. Taken together, these results suggest that adiponectin plays an inhibitory role in bone metabolism through cross talk between precursor cells of both osteoclasts and osteoblasts by regulating RANKL/OPG ratio in the bone marrow microenvironment.
abstract_unstemmed	Osteoporosis and bone disorders related to the metabolic syndrome are often associated with adipokines secreted by adipocytes in bone. Adiponectin, a type of adipokine, is a regulator of immune responses and metabolic processes, but its role in bone biology remains uncertain. We investigated the role of adiponectin in bone metabolism using adiponectin-deficient mice in vivo and in vitro. Adiponectin-deficient mice exhibited reduced bone mass and increased adiposity. Adiponectin-deficient calvarial cells were prone to differentiate into adipocytes rather than osteoblasts. Although bone marrow macrophages (BMMs) from adiponectin-deficient mice had low osteoclastogenic potential as osteoclast precursors with increasing interferon regulatory factor 5 expression, under co-culture conditions of calvarial cells and BMMs, the enhanced receptor activator of nuclear factor κB ligand/osteoprotegerin (RANKL/OPG) ratio of adiponectin-deficient mesenchymal progenitor cells facilitated osteoclast differentiation. In addition, increased RANKL/OPG ratio was observed in the bone marrow extracellular fluid of adiponectin-deficient mice compared to that of wild-type mice. Notably, recombinant adiponectin treatment enhanced RANKL-induced osteoclast differentiation from BMMs but up-regulated OPG production in recombinant adiponectin-exposed calvarial cells, which inhibited osteoclast differentiation. Taken together, these results suggest that adiponectin plays an inhibitory role in bone metabolism through cross talk between precursor cells of both osteoclasts and osteoblasts by regulating RANKL/OPG ratio in the bone marrow microenvironment.
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title_short	Adiponectin Deficiency Triggers Bone Loss by Up-Regulation of Osteoclastogenesis and Down-Regulation of Osteoblastogenesis
url	https://doi.org/10.3389/fendo.2019.00815 https://doaj.org/article/07ac15f06d8a4f32b9e5e67a05f9c60e https://www.frontiersin.org/article/10.3389/fendo.2019.00815/full https://doaj.org/toc/1664-2392
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author2	Jihyun Yang Ok-Jin Park Jiseon Kim Sora Han Young Yang Cheol-Heui Yun Seung Hyun Han
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up_date	2024-07-03T22:27:27.758Z
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Adiponectin Deficiency Triggers Bone Loss by Up-Regulation of Osteoclastogenesis and Down-Regulation of Osteoblastogenesis

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