In this study the investigators hypothesize that pathological alterations in adipose tissue biology already occur during the development and progression of obesity in children and adolescents. The investigators aim to identify and characterize mechanisms and molecular targets that affect the development of adipose tissue and ensuing obesity in childhood and adolescence.
The investigators aim to identify how adipose tissue dysfunction in childhood contributes to the development of obesity and related comorbidities and to characterize factors that play a role in the development of adipose dysfunction in children. The investigators will employ a translational approach which is based on the characterization of adipose tissue biology in samples of children to determine alterations leading to adipose tissue dysfunction. These include assessment of the composition (including BAT), remodeling, function, metabolism and inflammation of adipose tissue as well as the adipokine profile. For the assessment of clinical relevance, these experimental data will then be correlated with the clinical phenotype. Finally, we aim to identify factors responsible for early adipose tissue dysfunction and characterize them for their clinical and functional relevance.
Study Type
OBSERVATIONAL
Enrollment
1,000
Center for Pediatric Research Leipzig (CPL)
Leipzig, Saxony, Germany
RECRUITINGAdipose tissue dysfunction
Adipose tissue dysfunction is assessed by evaluation of adipocyte size and number (hypertrophy vs. hyperplasia), adipocyte proliferation and differentiation, (lipid) cellular metabolism, inflammation, gene expression, fibrosis, and others; the association of AT dysfunction with clincial phenotype will be assessed
Time frame: 10 years
Presence of brown adipose tissue (BAT)
Adipose tissue samples will be evaluated for the presence of BAT on histological and molecular level and association with clinical phenotype will be investigated
Time frame: 10 years
Inflammation of adipose tissue
Inflammation will be assessed by evaluating macrophage infiltration on histological and molecular expression level. Also, association with clinical phenotype will be assessed.
Time frame: 10 years
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