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Increased bone mass in mice lacking the adipokine apelin
Lalita Wattanachanya1, Wei-Dar Lu, Ramendra K Kundu
1Veterans Affairs Medical Center (111 N), 4150 Clement Street, San Francisco, California 94121, USA.
Endocrinology
|April 16, 2013
Summary
Mice lacking the adipokine apelin showed increased bone mass due to enhanced bone formation. This suggests apelin acts as an antianabolic factor in bone, influencing skeletal homeostasis.
Area of Science:
- Bone biology
- Endocrinology
- Skeletal homeostasis
Background:
- Adipose tissue influences skeletal homeostasis through adipokines.
- Apelin, an adipokine, may affect bone mass, but its in vivo role is unclear.
Purpose of the Study:
- To investigate the physiological role of apelin in regulating skeletal homeostasis in vivo.
- To examine the direct effects of apelin on bone cells in vitro.
Main Methods:
- Comparison of skeletal phenotypes between apelin knockout (APKO) and wild-type mice.
- In vitro studies on primary mouse osteoblasts (OBs) and bone cells.
- Dynamic histomorphometry to assess bone formation and remodeling.
Main Results:
- APKO mice exhibited increased cancellous bone volume and cortical bone perimeter.
- Increased bone formation and mineral apposition rates were observed in APKO mice.
- Apelin increased osteoblast proliferation and suppressed apoptosis in vitro, but did not affect mineralized nodule formation or osteoclast activity.
Conclusions:
- Apelin functions as a physiologically significant antianabolic factor in bone.
- The absence of apelin leads to increased bone mass, suggesting complex effects on bone remodeling.
- Apelin's role in bone may involve modulation of insulin sensitivity.
