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Updated: Jun 19, 2026
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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
Growth hormone regulates the balance between bone formation and bone marrow adiposity
Philip J Menagh1, Russell T Turner, Donald B Jump
1Department of Nutrition and Exercise Sciences, Oregon State University, Corvallis, OR 97331, USA.
Summary
Growth hormone (GH) influences bone and fat cells. Studies show GH enhances osteoblast and adipocyte precursors, promoting bone growth while reducing marrow fat accumulation.
Area of Science:
- Endocrinology
- Bone Biology
- Metabolic Regulation
Background:
- Aging is associated with decreased cancellous bone and increased bone marrow fat.
- Osteoblasts and adipocytes originate from a shared precursor cell.
- Growth hormone (GH) regulates both osteoblast and adipocyte differentiation and function.
Purpose of the Study:
- To investigate the relationship between GH and bone marrow adiposity.
- To examine the effects of GH signaling deficiency on bone and fat mass.
- To determine the role of GH in regulating the common precursor pool.
Main Methods:
- Hypophysectomized (HYPOX) rat model.
- GH signaling-deficient mouse models.
- Assessment of bone growth, mineralizing perimeter, bone marrow adiposity, and lipid content.
- Hormone replacement therapies (GH, estradiol, IGF-1, thyroxine, cortisone, PTH).
Main Results:
- HYPOX rats showed reduced body weight, bone growth, and IGF-1 levels, but increased bone marrow adiposity and lipid content.
- GH replacement in HYPOX rats normalized bone marrow adiposity, precursor pool size, and mineralizing perimeter.
- GH and IGF-1 deficient mice exhibited increased bone marrow adiposity.
- Estradiol, IGF-1, thyroxine, and cortisone were ineffective in reversing HYPOX effects on adiposity.
Conclusions:
- GH signaling deficiency leads to increased bone marrow adiposity, independent of reciprocal changes in bone mass.
- GH expands both osteoblast and adipocyte precursor pools.
- GH promotes osteoblast differentiation while simultaneously suppressing bone marrow lipid accumulation.
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