Normal adipose tissue development is critical for maintaining a healthy metabolic state. An excess accumulation of adipose tissue mass in childhood or adolescence results in obesity. This is often associated with pathological metabolic and cardiovascular alterations. In this project, we aim to identify and characterize regulators of adipose tissue development and obesity. For this, we apply a translational approach combining in vitro and in vivo studies with the analyses of adipose tissue samples of lean and obese children (Leipzig Adipose Childhood Cohort).
Alterations in Adipose Tissue Biology and Function with Development of Obesity (Leipzig Adipose Tissue Biopsy Childhood Cohort)
We aim to address which alterations occur in adipose tissue biology and function during normal development and during progression of obesity in children. Adipose tissue samples are frequently obtained from children undergoing surgery in the Division of Paediatric Surgery as well as the Division of Paediatric Orthopaedics (Leipzig Adipose Tissue Childhood Cohort, NCT02208141). Analyzing these samples, we assess alterations in gene expression, adipose tissue composition, metabolic function and the capacity of adipose progenitor cells to differentiate and proliferate. We found that first alterations in adipose tissue biology occur in early childhood (Landgraf K, 2015). We apply the Seahorse technology to assess mitochondrial function of adipocytes under different conditions. Furthermore, we characterize adipose tissue inflammation and the presence of brown adipose tissue (Rockstroh D, 2016).
We further identify regulators of normal and disturbed adipose tissue function and subsequently perform functional characterization by looking at their role for adipocyte differentiation in vitro (cell lines and primary predadipocytes) and in vivo by using the zebrafish (Danio rerio) as a model for obesity and associated diseases (Landgraf K, 2017).
We are particularly interested in molecular mechanisms mediating adipocyte dysfunction in obesity and the development of metabolic and cardiovascular comorbidities. In this regard, the role of microRNAs (Rockstroh 2016) and adipocytokines (Schwartze 2016) in regard to adipocyte development and function.
