Adipositas - Ursachen, Folgeerkrankungen, Therapie 2021; 15(03): 162
DOI: 10.1055/s-0041-1735700
Abstracts
Wiesbaden: Adipositas-Kongress 2021

52 Effects of aging on stem cell function and ectopic fat accumulation in the musculoskeletal system

Marina Leer
1   German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Adipocyte Development and Nutrition, Nuthetal, Deutschland
,
George Soultoukis
1   German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Adipocyte Development and Nutrition, Nuthetal, Deutschland
,
Francisco J. Garcia-Carrizo
1   German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Adipocyte Development and Nutrition, Nuthetal, Deutschland
,
Tim J. Schulz
1   German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Adipocyte Development and Nutrition, Nuthetal, Deutschland
2   German Center for Diabetes Research (DZD), München-Neuherberg, Deutschland
› Institutsangaben
 

Background

The musculoskeletal system enables body movement and its deterioration is a crucial aspect of age-related functional decline. In bone tissue, beyond supporting hematopoiesis, MSCs differentiate into osteochondrogenic progenitor cells to form osteocytes and chondrocytes, or into adipogenic progenitor cells to ultimately become adipocytes. In the muscle, MSCs undergo adipogenic lineage commitment for healthy adipocyte turnover, but also secrete signals to support satellite cells which replenish the myofibrocyte pool. Thus, MSCs regulate cellular regeneration of osseous, cartilage, haematopoietic, and adipose tissue in bones, as well as adipose tissue and myofibres in the muscle. During aging, an accumulation of fat cells in the bone marrow cause a pathogenic expansion of ectopic bone marrow adipose tissue, which contributes to the development of osteoporosis and weakening of bones. Muscle-resident MSCs are prone to cause fatty infiltration and myofibre pathogenesis. These shifts in cell populations cause loss of osteocyte progenitors leading to osteoporosis in the bone, whereas in the muscle they impair regeneration thereby promoting the onset of sarcopenia.



Publikationsverlauf

Artikel online veröffentlicht:
24. September 2021

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