Translational Diabetes

As in Tübingen described (Stefan et. al 2008), metabolically benign and malign obesity can be dissected, the latter comprising whole-body insulin resistance, hepatic steatosis, and subclinical inflammation.
As adipose tissue is central to obesity, we will study its contribution to these types of obesity. To this end, we will analyze these subjects’ adipose tissue by transcriptomics, proteomics, metabolomics, and (epi-)genomics.
Another central finding was the identification of subjects who do not respond to lifestyle intervention with fat loss, a phenomenon predominantly, but not exclusively, attributable to PPARδ SNPs. We will analyze PPARδ-independent mechanisms in human skeletal muscle by the aforementioned “omics” methods.
Identified biomarkers/mechanisms will be further investigated in vitro, in mouse models, and in the human cohorts of the German Center for Diabetes Research (DZD).


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