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Transplanted Bone Marrow-Derived Cells Contribute to Human Adipogenesis
Mikael Rydén1, Mehmet Uzunel2, Joanna L Hård3
1Department of Medicine (H7), Karolinska Institutet, 141 86 Stockholm, Sweden.
Cell Metabolism
|July 21, 2015
Summary
Bone marrow (BM) and peripheral blood stem cell (PBSC) progenitors supply about 10% of adult human fat cells. This contribution increases significantly in obese individuals, with progenitors contributing via differentiation and fusion.
Area of Science:
- Cell Biology
- Hematology
- Metabolic Health
Background:
- Human white adipocytes have a high turnover rate, necessitating a continuous supply of precursor cells for adipogenesis.
- The contribution of bone marrow (BM)-derived progenitor cells to mammalian adipogenesis is debated, with conflicting results from animal models.
Purpose of the Study:
- To quantify the contribution of BM/PBSC-derived progenitor cells to the adult human subcutaneous adipocyte population.
- To investigate factors influencing this contribution, such as gender, age, body fat mass, and transplantation parameters.
Main Methods:
- Analysis of 65 subjects who received allogeneic BM or PBSC transplantation.
- Quantification of donor cell contribution to the subcutaneous adipocyte population.
- Exome and whole-genome sequencing of single adipocytes.
Main Results:
- BM/PBSC-derived progenitor cells constitute approximately 10% of the subcutaneous adipocyte population throughout adulthood.
- Donor cell contribution is independent of gender, age, and transplantation parameters but is significantly influenced by body fat mass.
- Obese individuals showed up to a 2.5-fold increase in donor cell contribution to adipocytes.
- Evidence suggests BM/PBSC-derived progenitors contribute to adipose tissue through both differentiation and cell fusion.
Conclusions:
- Bone marrow serves as a reservoir for adipocyte progenitors in humans, particularly evident in the context of transplantation.
- Obesity enhances the contribution of BM/PBSC-derived progenitors to adipose tissue, highlighting a potential mechanism in metabolic disease.
