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Updated: May 31, 2026
A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders
Published on: June 8, 2014
Omentin-1 exerts bone-sparing effect in ovariectomized mice
1Institute of Endocrinology and Metabolism, Second Xiangya Hospital of Central South University, 139# Middle Renmin Road, Changsha, Hunan 410011, People's Republic of China.
Unlabelled:
Omentin-1 inhibited osteoblast differentiation in vitro. In co-culture systems of osteoblasts and osteoclast precursors, omentin-1 reduced osteoclast formation by stimulating osteoprotegerin (OPG) and inhibiting receptor activator for nuclear factor κB ligand (RANKL) production in osteoblasts. In vivo, adenovirus-mediated overexpression of omentin-1 suppressed bone turnover and restored bone mineral density (BMD) and bone strength in ovariectomized mice.
Introduction:
Omentin-1 (also intelectin-1) is a recently identified visceral adipose tissue-derived cytokine that is highly abundant in plasma. This study was undertaken to investigate the effects of omentin-1 on bone metabolism.
Methods:
Osteoblast differentiation was assessed by measuring alkaline phosphatase activity, osteocalcin production and matrix mineralization. OPG and RANKL protein expression and secretion in osteoblasts were detected by Western blot and ELISA, respectively. The effect of recombinant omentin-1 on osteoclast formation was examined in co-culture systems of osteoblasts and osteoclast precursors. The effects of intravenous administration of adenoviral-delivered omentin-1 on bone mass, bone strength, and bone turnover were also examined in ovariectomized mice.
Results:
In vitro, omentin-1 inhibited osteoblast differentiation, while it had no direct effect on osteoclast differentiation; it also reduced osteoclast formation in the co-culture systems through stimulating OPG and inhibiting RANKL production in osteoblasts. In vivo, adenovirus-mediated overexpression of omentin-1 partially restored BMD and bone strength in ovariectomized mice, accompanied by decreased levels of plasma osteocalcin and tartrate-resistant acid phosphatase-5b and lower serum RANKL/OPG ratios.
Conclusion:
The present study suggests that omentin-1 ameliorates bone loss induced by estrogen deficiency via downregulating the RANKL/OPG ratio.
Insights
Omentin-1, a cytokine, was found to inhibit osteoblast differentiation and reduce osteoclast formation by modulating OPG and RANKL. This suggests omentin-1 may protect against bone loss from estrogen deficiency.
Area of Science:
- Endocrinology
- Bone Biology
- Metabolic Research
Background:
- Omentin-1 (intelectin-1) is a visceral adipose tissue-derived cytokine abundant in plasma.
- Its role in bone metabolism was previously uncharacterized.
Purpose of the Study:
- To investigate the effects of omentin-1 on bone metabolism.
- To determine omentin-1's potential in ameliorating bone loss.
Main Methods:
- In vitro assessment of osteoblast differentiation and osteoclast formation.
- Co-culture systems of osteoblasts and osteoclast precursors.
- In vivo studies using adenovirus-mediated omentin-1 delivery in ovariectomized mice.
Main Results:
- Omentin-1 inhibited osteoblast differentiation in vitro.
- Omentin-1 reduced osteoclast formation by increasing osteoprotegerin (OPG) and decreasing receptor activator for nuclear factor κB ligand (RANKL) production in osteoblasts.
- Adenovirus-mediated omentin-1 overexpression in vivo restored bone mineral density and bone strength in ovariectomized mice.
Conclusions:
- Omentin-1 ameliorates bone loss associated with estrogen deficiency.
- This effect is mediated by downregulating the RANKL/OPG ratio.
