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.
