ESPE Yearbook of Paediatric Endocrinology

kathrin.landgraf@medizin.uni-leipzig.de JCEM 2022; 107(2): e836–e851https://pubmed.ncbi.nlm.nih.gov/34448000

Brief Summary: This study investigated the association of the novel adipose-derived stem cell (ASC) markers Mesenchymal Stem cell Antigen 1 (MSCA1) and CD36 with adipose tissue function in samples collected from children undergoing elective surgery in the Leipzig AT Childhood Cohort.

Previous work demonstrate that different subpopulation of adipocyte progenitor cells exist which differ in terms of proliferation and differentiation [1,2]. These cells are of particular interest in obesity research as they play a crucial role in adipose tissue development and the pathogenesis of obesity. However, the ASC population is not well defined in humans, and more research is needed to better define the different ASC subsets and the function of ASC marker genes. The surface markers CD36 and MSCA1 have been recently connected to adipogenic differentiation and adipocyte metabolism [3,4], suggesting that these genes might play a role during obesity-related AT accumulation.

Here, the authors found that CD36 expression was decreased in children with overweight and obesity and was positively associated with the differentiation capacity of ASCs in vitro. Expression of MSCA1 was positively correlated with traits of AT dysfunction (adipocyte hypertrophy and C-reactive protein) and was further associated with increased mitochondrial respiration in vitro.

Expansion of adipose tissue is either regulated by hypertrophy (e.g. increase in adipocyte volume) or hyperplasia (e.g. increase in cell number), the latter dependent on adipogenic differentiation from progenitor cells within the adipose tissue. It is thus crucial to identify biomarkers that define adipocyte progenitor subpopulations associated with early obesity. In previous studies, the role of CD36 and MSCA1 has been evaluated in adult patients with morbid obesity [3,5], but their role in early obesity progression has not been addressed so far. Thus, the strength of this study is that it was performed in healthy children, allowing a better insight into early processes involved in obesity development. Future studies may address the molecular mechanisms that link these progenitor makers with early obesity progression.

References: 1. Maumus, M. et al. Native human adipose stromal cells: localization, morphology and phenotype. Int. J. Obes. (Lond). 35, 1141–53 (2011). 2. Li, H. et al. Adipogenic potential of adipose stem cell subpopulations. Plast. Reconstr. Surg. 128, 663–672 (2011). 3. Gao, H. et al. CD36 Is a Marker of Human Adipocyte Progenitors with Pronounced Adipogenic and Triglyceride Accumulation Potential. Stem Cells 35, 1799–1814 (2017). 4. Hernández-Mosqueira, C., Velez-delValle, C. & Kuri-Harcuch, W. Tissue alkaline phosphatase is involved in lipid metabolism and gene expression and secretion of adipokines in adipocytes. Biochim. Biophys. Acta 1850, 2485–96 (2015). 5. Estève, D. et al. Human white and brite adipogenesis is supported by MSCA1 and is impaired by immune cells. Stem Cells 33, 1277–91 (2015).