Adiponectin signaling and its role in bone metabolism
Adiponectin, the most prevalent adipo-cytokine in plasma plays critical metabolic and anti-inflammatory roles is fast emerging as an important molecular target for the treatment of metabolic disorders. Adiponectin action is critical in multiple organs including cardio-vascular system, muscle, liver,...
Ausführliche Beschreibung
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| Autor*in: |
Pal China, Shyamsundar [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2018transfer abstract |
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| Schlagwörter: |
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| Umfang: |
16 |
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| Übergeordnetes Werk: |
Enthalten in: The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types - McLaughlin, Richard J. ELSEVIER, 2022, the official journal of the International Cytokine Society, Oxford [u.a.] |
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| Übergeordnetes Werk: |
volume:112 ; year:2018 ; pages:116-131 ; extent:16 |
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| DOI / URN: |
10.1016/j.cyto.2018.06.012 |
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| 520 | |a Adiponectin, the most prevalent adipo-cytokine in plasma plays critical metabolic and anti-inflammatory roles is fast emerging as an important molecular target for the treatment of metabolic disorders. Adiponectin action is critical in multiple organs including cardio-vascular system, muscle, liver, adipose tissue, brain and bone. Adiponectin signaling in bone has been a topic of active investigation lately. Human association studies and multiple mice models of gene deletion/modification failed to define a clear cause and effect of adiponectin signaling in bone. The most plausible reason could be the multimeric forms of adiponectin that display differential binding to receptors (adipoR1 and adipoR2) with cell-specific receptor variants in bone. Discovery of small molecule agonist of adipoR1 suggested a salutary role of this receptor in bone metabolism. The downstream signaling of adipoR1 in osteoblasts involves stimulation of oxidative phosphorylation leading to increased differentiation via the likely suppression of wnt inhibitor, sclerostin. On the other hand, the inflammation modulatory effect of adiponectin signaling suppresses the RANKL (receptor activator of nuclear factor κ-B ligand) – to – OPG (osteprotegerin) ratio in osteoblasts leading to the suppression of osteoclastogenic response. This review will discuss the adiponectin signaling and its role in skeletal homeostasis and critically assess whether adipoR1 could be a therapeutic target for the treatment of metabolic bone diseases. | ||
| 520 | |a Adiponectin, the most prevalent adipo-cytokine in plasma plays critical metabolic and anti-inflammatory roles is fast emerging as an important molecular target for the treatment of metabolic disorders. Adiponectin action is critical in multiple organs including cardio-vascular system, muscle, liver, adipose tissue, brain and bone. Adiponectin signaling in bone has been a topic of active investigation lately. Human association studies and multiple mice models of gene deletion/modification failed to define a clear cause and effect of adiponectin signaling in bone. The most plausible reason could be the multimeric forms of adiponectin that display differential binding to receptors (adipoR1 and adipoR2) with cell-specific receptor variants in bone. Discovery of small molecule agonist of adipoR1 suggested a salutary role of this receptor in bone metabolism. The downstream signaling of adipoR1 in osteoblasts involves stimulation of oxidative phosphorylation leading to increased differentiation via the likely suppression of wnt inhibitor, sclerostin. On the other hand, the inflammation modulatory effect of adiponectin signaling suppresses the RANKL (receptor activator of nuclear factor κ-B ligand) – to – OPG (osteprotegerin) ratio in osteoblasts leading to the suppression of osteoclastogenic response. This review will discuss the adiponectin signaling and its role in skeletal homeostasis and critically assess whether adipoR1 could be a therapeutic target for the treatment of metabolic bone diseases. | ||
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10.1016/j.cyto.2018.06.012 doi GBV00000000000453.pica (DE-627)ELV045182361 (ELSEVIER)S1043-4666(18)30260-6 DE-627 ger DE-627 rakwb eng 610 VZ 44.83 bkl Pal China, Shyamsundar verfasserin aut Adiponectin signaling and its role in bone metabolism 2018transfer abstract 16 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Adiponectin, the most prevalent adipo-cytokine in plasma plays critical metabolic and anti-inflammatory roles is fast emerging as an important molecular target for the treatment of metabolic disorders. Adiponectin action is critical in multiple organs including cardio-vascular system, muscle, liver, adipose tissue, brain and bone. Adiponectin signaling in bone has been a topic of active investigation lately. Human association studies and multiple mice models of gene deletion/modification failed to define a clear cause and effect of adiponectin signaling in bone. The most plausible reason could be the multimeric forms of adiponectin that display differential binding to receptors (adipoR1 and adipoR2) with cell-specific receptor variants in bone. Discovery of small molecule agonist of adipoR1 suggested a salutary role of this receptor in bone metabolism. The downstream signaling of adipoR1 in osteoblasts involves stimulation of oxidative phosphorylation leading to increased differentiation via the likely suppression of wnt inhibitor, sclerostin. On the other hand, the inflammation modulatory effect of adiponectin signaling suppresses the RANKL (receptor activator of nuclear factor κ-B ligand) – to – OPG (osteprotegerin) ratio in osteoblasts leading to the suppression of osteoclastogenic response. This review will discuss the adiponectin signaling and its role in skeletal homeostasis and critically assess whether adipoR1 could be a therapeutic target for the treatment of metabolic bone diseases. Adiponectin, the most prevalent adipo-cytokine in plasma plays critical metabolic and anti-inflammatory roles is fast emerging as an important molecular target for the treatment of metabolic disorders. Adiponectin action is critical in multiple organs including cardio-vascular system, muscle, liver, adipose tissue, brain and bone. Adiponectin signaling in bone has been a topic of active investigation lately. Human association studies and multiple mice models of gene deletion/modification failed to define a clear cause and effect of adiponectin signaling in bone. The most plausible reason could be the multimeric forms of adiponectin that display differential binding to receptors (adipoR1 and adipoR2) with cell-specific receptor variants in bone. Discovery of small molecule agonist of adipoR1 suggested a salutary role of this receptor in bone metabolism. The downstream signaling of adipoR1 in osteoblasts involves stimulation of oxidative phosphorylation leading to increased differentiation via the likely suppression of wnt inhibitor, sclerostin. On the other hand, the inflammation modulatory effect of adiponectin signaling suppresses the RANKL (receptor activator of nuclear factor κ-B ligand) – to – OPG (osteprotegerin) ratio in osteoblasts leading to the suppression of osteoclastogenic response. This review will discuss the adiponectin signaling and its role in skeletal homeostasis and critically assess whether adipoR1 could be a therapeutic target for the treatment of metabolic bone diseases. Catabolic Elsevier Mitochondrial biogenesis Elsevier Inflammatory cytokines Elsevier Therapeutics Elsevier Osteoanabolic Elsevier Sanyal, Sabyasachi oth Chattopadhyay, Naibedya oth Enthalten in Elsevier McLaughlin, Richard J. ELSEVIER The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types 2022 the official journal of the International Cytokine Society Oxford [u.a.] (DE-627)ELV008219540 volume:112 year:2018 pages:116-131 extent:16 https://doi.org/10.1016/j.cyto.2018.06.012 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.83 Rheumatologie Orthopädie VZ AR 112 2018 116-131 16 |
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10.1016/j.cyto.2018.06.012 doi GBV00000000000453.pica (DE-627)ELV045182361 (ELSEVIER)S1043-4666(18)30260-6 DE-627 ger DE-627 rakwb eng 610 VZ 44.83 bkl Pal China, Shyamsundar verfasserin aut Adiponectin signaling and its role in bone metabolism 2018transfer abstract 16 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Adiponectin, the most prevalent adipo-cytokine in plasma plays critical metabolic and anti-inflammatory roles is fast emerging as an important molecular target for the treatment of metabolic disorders. Adiponectin action is critical in multiple organs including cardio-vascular system, muscle, liver, adipose tissue, brain and bone. Adiponectin signaling in bone has been a topic of active investigation lately. Human association studies and multiple mice models of gene deletion/modification failed to define a clear cause and effect of adiponectin signaling in bone. The most plausible reason could be the multimeric forms of adiponectin that display differential binding to receptors (adipoR1 and adipoR2) with cell-specific receptor variants in bone. Discovery of small molecule agonist of adipoR1 suggested a salutary role of this receptor in bone metabolism. The downstream signaling of adipoR1 in osteoblasts involves stimulation of oxidative phosphorylation leading to increased differentiation via the likely suppression of wnt inhibitor, sclerostin. On the other hand, the inflammation modulatory effect of adiponectin signaling suppresses the RANKL (receptor activator of nuclear factor κ-B ligand) – to – OPG (osteprotegerin) ratio in osteoblasts leading to the suppression of osteoclastogenic response. This review will discuss the adiponectin signaling and its role in skeletal homeostasis and critically assess whether adipoR1 could be a therapeutic target for the treatment of metabolic bone diseases. Adiponectin, the most prevalent adipo-cytokine in plasma plays critical metabolic and anti-inflammatory roles is fast emerging as an important molecular target for the treatment of metabolic disorders. Adiponectin action is critical in multiple organs including cardio-vascular system, muscle, liver, adipose tissue, brain and bone. Adiponectin signaling in bone has been a topic of active investigation lately. Human association studies and multiple mice models of gene deletion/modification failed to define a clear cause and effect of adiponectin signaling in bone. The most plausible reason could be the multimeric forms of adiponectin that display differential binding to receptors (adipoR1 and adipoR2) with cell-specific receptor variants in bone. Discovery of small molecule agonist of adipoR1 suggested a salutary role of this receptor in bone metabolism. The downstream signaling of adipoR1 in osteoblasts involves stimulation of oxidative phosphorylation leading to increased differentiation via the likely suppression of wnt inhibitor, sclerostin. On the other hand, the inflammation modulatory effect of adiponectin signaling suppresses the RANKL (receptor activator of nuclear factor κ-B ligand) – to – OPG (osteprotegerin) ratio in osteoblasts leading to the suppression of osteoclastogenic response. This review will discuss the adiponectin signaling and its role in skeletal homeostasis and critically assess whether adipoR1 could be a therapeutic target for the treatment of metabolic bone diseases. Catabolic Elsevier Mitochondrial biogenesis Elsevier Inflammatory cytokines Elsevier Therapeutics Elsevier Osteoanabolic Elsevier Sanyal, Sabyasachi oth Chattopadhyay, Naibedya oth Enthalten in Elsevier McLaughlin, Richard J. ELSEVIER The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types 2022 the official journal of the International Cytokine Society Oxford [u.a.] (DE-627)ELV008219540 volume:112 year:2018 pages:116-131 extent:16 https://doi.org/10.1016/j.cyto.2018.06.012 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.83 Rheumatologie Orthopädie VZ AR 112 2018 116-131 16 |
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10.1016/j.cyto.2018.06.012 doi GBV00000000000453.pica (DE-627)ELV045182361 (ELSEVIER)S1043-4666(18)30260-6 DE-627 ger DE-627 rakwb eng 610 VZ 44.83 bkl Pal China, Shyamsundar verfasserin aut Adiponectin signaling and its role in bone metabolism 2018transfer abstract 16 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Adiponectin, the most prevalent adipo-cytokine in plasma plays critical metabolic and anti-inflammatory roles is fast emerging as an important molecular target for the treatment of metabolic disorders. Adiponectin action is critical in multiple organs including cardio-vascular system, muscle, liver, adipose tissue, brain and bone. Adiponectin signaling in bone has been a topic of active investigation lately. Human association studies and multiple mice models of gene deletion/modification failed to define a clear cause and effect of adiponectin signaling in bone. The most plausible reason could be the multimeric forms of adiponectin that display differential binding to receptors (adipoR1 and adipoR2) with cell-specific receptor variants in bone. Discovery of small molecule agonist of adipoR1 suggested a salutary role of this receptor in bone metabolism. The downstream signaling of adipoR1 in osteoblasts involves stimulation of oxidative phosphorylation leading to increased differentiation via the likely suppression of wnt inhibitor, sclerostin. On the other hand, the inflammation modulatory effect of adiponectin signaling suppresses the RANKL (receptor activator of nuclear factor κ-B ligand) – to – OPG (osteprotegerin) ratio in osteoblasts leading to the suppression of osteoclastogenic response. This review will discuss the adiponectin signaling and its role in skeletal homeostasis and critically assess whether adipoR1 could be a therapeutic target for the treatment of metabolic bone diseases. Adiponectin, the most prevalent adipo-cytokine in plasma plays critical metabolic and anti-inflammatory roles is fast emerging as an important molecular target for the treatment of metabolic disorders. Adiponectin action is critical in multiple organs including cardio-vascular system, muscle, liver, adipose tissue, brain and bone. Adiponectin signaling in bone has been a topic of active investigation lately. Human association studies and multiple mice models of gene deletion/modification failed to define a clear cause and effect of adiponectin signaling in bone. The most plausible reason could be the multimeric forms of adiponectin that display differential binding to receptors (adipoR1 and adipoR2) with cell-specific receptor variants in bone. Discovery of small molecule agonist of adipoR1 suggested a salutary role of this receptor in bone metabolism. The downstream signaling of adipoR1 in osteoblasts involves stimulation of oxidative phosphorylation leading to increased differentiation via the likely suppression of wnt inhibitor, sclerostin. On the other hand, the inflammation modulatory effect of adiponectin signaling suppresses the RANKL (receptor activator of nuclear factor κ-B ligand) – to – OPG (osteprotegerin) ratio in osteoblasts leading to the suppression of osteoclastogenic response. This review will discuss the adiponectin signaling and its role in skeletal homeostasis and critically assess whether adipoR1 could be a therapeutic target for the treatment of metabolic bone diseases. Catabolic Elsevier Mitochondrial biogenesis Elsevier Inflammatory cytokines Elsevier Therapeutics Elsevier Osteoanabolic Elsevier Sanyal, Sabyasachi oth Chattopadhyay, Naibedya oth Enthalten in Elsevier McLaughlin, Richard J. ELSEVIER The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types 2022 the official journal of the International Cytokine Society Oxford [u.a.] (DE-627)ELV008219540 volume:112 year:2018 pages:116-131 extent:16 https://doi.org/10.1016/j.cyto.2018.06.012 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.83 Rheumatologie Orthopädie VZ AR 112 2018 116-131 16 |
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10.1016/j.cyto.2018.06.012 doi GBV00000000000453.pica (DE-627)ELV045182361 (ELSEVIER)S1043-4666(18)30260-6 DE-627 ger DE-627 rakwb eng 610 VZ 44.83 bkl Pal China, Shyamsundar verfasserin aut Adiponectin signaling and its role in bone metabolism 2018transfer abstract 16 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Adiponectin, the most prevalent adipo-cytokine in plasma plays critical metabolic and anti-inflammatory roles is fast emerging as an important molecular target for the treatment of metabolic disorders. Adiponectin action is critical in multiple organs including cardio-vascular system, muscle, liver, adipose tissue, brain and bone. Adiponectin signaling in bone has been a topic of active investigation lately. Human association studies and multiple mice models of gene deletion/modification failed to define a clear cause and effect of adiponectin signaling in bone. The most plausible reason could be the multimeric forms of adiponectin that display differential binding to receptors (adipoR1 and adipoR2) with cell-specific receptor variants in bone. Discovery of small molecule agonist of adipoR1 suggested a salutary role of this receptor in bone metabolism. The downstream signaling of adipoR1 in osteoblasts involves stimulation of oxidative phosphorylation leading to increased differentiation via the likely suppression of wnt inhibitor, sclerostin. On the other hand, the inflammation modulatory effect of adiponectin signaling suppresses the RANKL (receptor activator of nuclear factor κ-B ligand) – to – OPG (osteprotegerin) ratio in osteoblasts leading to the suppression of osteoclastogenic response. This review will discuss the adiponectin signaling and its role in skeletal homeostasis and critically assess whether adipoR1 could be a therapeutic target for the treatment of metabolic bone diseases. Adiponectin, the most prevalent adipo-cytokine in plasma plays critical metabolic and anti-inflammatory roles is fast emerging as an important molecular target for the treatment of metabolic disorders. Adiponectin action is critical in multiple organs including cardio-vascular system, muscle, liver, adipose tissue, brain and bone. Adiponectin signaling in bone has been a topic of active investigation lately. Human association studies and multiple mice models of gene deletion/modification failed to define a clear cause and effect of adiponectin signaling in bone. The most plausible reason could be the multimeric forms of adiponectin that display differential binding to receptors (adipoR1 and adipoR2) with cell-specific receptor variants in bone. Discovery of small molecule agonist of adipoR1 suggested a salutary role of this receptor in bone metabolism. The downstream signaling of adipoR1 in osteoblasts involves stimulation of oxidative phosphorylation leading to increased differentiation via the likely suppression of wnt inhibitor, sclerostin. On the other hand, the inflammation modulatory effect of adiponectin signaling suppresses the RANKL (receptor activator of nuclear factor κ-B ligand) – to – OPG (osteprotegerin) ratio in osteoblasts leading to the suppression of osteoclastogenic response. This review will discuss the adiponectin signaling and its role in skeletal homeostasis and critically assess whether adipoR1 could be a therapeutic target for the treatment of metabolic bone diseases. Catabolic Elsevier Mitochondrial biogenesis Elsevier Inflammatory cytokines Elsevier Therapeutics Elsevier Osteoanabolic Elsevier Sanyal, Sabyasachi oth Chattopadhyay, Naibedya oth Enthalten in Elsevier McLaughlin, Richard J. ELSEVIER The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types 2022 the official journal of the International Cytokine Society Oxford [u.a.] (DE-627)ELV008219540 volume:112 year:2018 pages:116-131 extent:16 https://doi.org/10.1016/j.cyto.2018.06.012 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.83 Rheumatologie Orthopädie VZ AR 112 2018 116-131 16 |
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10.1016/j.cyto.2018.06.012 doi GBV00000000000453.pica (DE-627)ELV045182361 (ELSEVIER)S1043-4666(18)30260-6 DE-627 ger DE-627 rakwb eng 610 VZ 44.83 bkl Pal China, Shyamsundar verfasserin aut Adiponectin signaling and its role in bone metabolism 2018transfer abstract 16 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Adiponectin, the most prevalent adipo-cytokine in plasma plays critical metabolic and anti-inflammatory roles is fast emerging as an important molecular target for the treatment of metabolic disorders. Adiponectin action is critical in multiple organs including cardio-vascular system, muscle, liver, adipose tissue, brain and bone. Adiponectin signaling in bone has been a topic of active investigation lately. Human association studies and multiple mice models of gene deletion/modification failed to define a clear cause and effect of adiponectin signaling in bone. The most plausible reason could be the multimeric forms of adiponectin that display differential binding to receptors (adipoR1 and adipoR2) with cell-specific receptor variants in bone. Discovery of small molecule agonist of adipoR1 suggested a salutary role of this receptor in bone metabolism. The downstream signaling of adipoR1 in osteoblasts involves stimulation of oxidative phosphorylation leading to increased differentiation via the likely suppression of wnt inhibitor, sclerostin. On the other hand, the inflammation modulatory effect of adiponectin signaling suppresses the RANKL (receptor activator of nuclear factor κ-B ligand) – to – OPG (osteprotegerin) ratio in osteoblasts leading to the suppression of osteoclastogenic response. This review will discuss the adiponectin signaling and its role in skeletal homeostasis and critically assess whether adipoR1 could be a therapeutic target for the treatment of metabolic bone diseases. Adiponectin, the most prevalent adipo-cytokine in plasma plays critical metabolic and anti-inflammatory roles is fast emerging as an important molecular target for the treatment of metabolic disorders. Adiponectin action is critical in multiple organs including cardio-vascular system, muscle, liver, adipose tissue, brain and bone. Adiponectin signaling in bone has been a topic of active investigation lately. Human association studies and multiple mice models of gene deletion/modification failed to define a clear cause and effect of adiponectin signaling in bone. The most plausible reason could be the multimeric forms of adiponectin that display differential binding to receptors (adipoR1 and adipoR2) with cell-specific receptor variants in bone. Discovery of small molecule agonist of adipoR1 suggested a salutary role of this receptor in bone metabolism. The downstream signaling of adipoR1 in osteoblasts involves stimulation of oxidative phosphorylation leading to increased differentiation via the likely suppression of wnt inhibitor, sclerostin. On the other hand, the inflammation modulatory effect of adiponectin signaling suppresses the RANKL (receptor activator of nuclear factor κ-B ligand) – to – OPG (osteprotegerin) ratio in osteoblasts leading to the suppression of osteoclastogenic response. This review will discuss the adiponectin signaling and its role in skeletal homeostasis and critically assess whether adipoR1 could be a therapeutic target for the treatment of metabolic bone diseases. Catabolic Elsevier Mitochondrial biogenesis Elsevier Inflammatory cytokines Elsevier Therapeutics Elsevier Osteoanabolic Elsevier Sanyal, Sabyasachi oth Chattopadhyay, Naibedya oth Enthalten in Elsevier McLaughlin, Richard J. ELSEVIER The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types 2022 the official journal of the International Cytokine Society Oxford [u.a.] (DE-627)ELV008219540 volume:112 year:2018 pages:116-131 extent:16 https://doi.org/10.1016/j.cyto.2018.06.012 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.83 Rheumatologie Orthopädie VZ AR 112 2018 116-131 16 |
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Enthalten in The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types Oxford [u.a.] volume:112 year:2018 pages:116-131 extent:16 |
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The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types |
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Adiponectin, the most prevalent adipo-cytokine in plasma plays critical metabolic and anti-inflammatory roles is fast emerging as an important molecular target for the treatment of metabolic disorders. Adiponectin action is critical in multiple organs including cardio-vascular system, muscle, liver, adipose tissue, brain and bone. Adiponectin signaling in bone has been a topic of active investigation lately. Human association studies and multiple mice models of gene deletion/modification failed to define a clear cause and effect of adiponectin signaling in bone. The most plausible reason could be the multimeric forms of adiponectin that display differential binding to receptors (adipoR1 and adipoR2) with cell-specific receptor variants in bone. Discovery of small molecule agonist of adipoR1 suggested a salutary role of this receptor in bone metabolism. The downstream signaling of adipoR1 in osteoblasts involves stimulation of oxidative phosphorylation leading to increased differentiation via the likely suppression of wnt inhibitor, sclerostin. On the other hand, the inflammation modulatory effect of adiponectin signaling suppresses the RANKL (receptor activator of nuclear factor κ-B ligand) – to – OPG (osteprotegerin) ratio in osteoblasts leading to the suppression of osteoclastogenic response. This review will discuss the adiponectin signaling and its role in skeletal homeostasis and critically assess whether adipoR1 could be a therapeutic target for the treatment of metabolic bone diseases. |
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Adiponectin, the most prevalent adipo-cytokine in plasma plays critical metabolic and anti-inflammatory roles is fast emerging as an important molecular target for the treatment of metabolic disorders. Adiponectin action is critical in multiple organs including cardio-vascular system, muscle, liver, adipose tissue, brain and bone. Adiponectin signaling in bone has been a topic of active investigation lately. Human association studies and multiple mice models of gene deletion/modification failed to define a clear cause and effect of adiponectin signaling in bone. The most plausible reason could be the multimeric forms of adiponectin that display differential binding to receptors (adipoR1 and adipoR2) with cell-specific receptor variants in bone. Discovery of small molecule agonist of adipoR1 suggested a salutary role of this receptor in bone metabolism. The downstream signaling of adipoR1 in osteoblasts involves stimulation of oxidative phosphorylation leading to increased differentiation via the likely suppression of wnt inhibitor, sclerostin. On the other hand, the inflammation modulatory effect of adiponectin signaling suppresses the RANKL (receptor activator of nuclear factor κ-B ligand) – to – OPG (osteprotegerin) ratio in osteoblasts leading to the suppression of osteoclastogenic response. This review will discuss the adiponectin signaling and its role in skeletal homeostasis and critically assess whether adipoR1 could be a therapeutic target for the treatment of metabolic bone diseases. |
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Adiponectin, the most prevalent adipo-cytokine in plasma plays critical metabolic and anti-inflammatory roles is fast emerging as an important molecular target for the treatment of metabolic disorders. Adiponectin action is critical in multiple organs including cardio-vascular system, muscle, liver, adipose tissue, brain and bone. Adiponectin signaling in bone has been a topic of active investigation lately. Human association studies and multiple mice models of gene deletion/modification failed to define a clear cause and effect of adiponectin signaling in bone. The most plausible reason could be the multimeric forms of adiponectin that display differential binding to receptors (adipoR1 and adipoR2) with cell-specific receptor variants in bone. Discovery of small molecule agonist of adipoR1 suggested a salutary role of this receptor in bone metabolism. The downstream signaling of adipoR1 in osteoblasts involves stimulation of oxidative phosphorylation leading to increased differentiation via the likely suppression of wnt inhibitor, sclerostin. On the other hand, the inflammation modulatory effect of adiponectin signaling suppresses the RANKL (receptor activator of nuclear factor κ-B ligand) – to – OPG (osteprotegerin) ratio in osteoblasts leading to the suppression of osteoclastogenic response. This review will discuss the adiponectin signaling and its role in skeletal homeostasis and critically assess whether adipoR1 could be a therapeutic target for the treatment of metabolic bone diseases. |
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