Adipocytes and Metabolism Unit

Research Focus

Pathological changes in adipose tissue are a major underlying cause of systemic insulin resistance and the metabolic syndrome. However, due to an inability to identify and target dysfunctional adipocytes, the mechanisms underlying this functional impairment are unknown. Based on our previous work together with ongoing projects in the laboratory, we conclude that both white and brown adipose tissues are functionally and developmentally diverse and that differences between cell populations within these different depots can be detected at the cell surface. 

Thus, our primary objective is to identify individual cell populations and signaling pathways responsible for the initiation of local and subsequent systemic insulin resistance. 

To this end, we apply state of the art genetic and biochemical technologies and develop novel methods to functionally describe and target alterations at the adipocyte cell surface during the initial events triggering the transition from obesity to insulin resistance. Utilizing our expertise in endocrinology, method development, and cell surface proteins, we investigate the hypothesis that pathological changes in individual adipocyte subpopulations initiate adipose tissue dysfunction, resulting in the metabolic syndrome, and that these change can be visualized and targeted via the cell surface. 

We reach for a major shift in the understanding of how the metabolic syndrome is initiated to unravel novel therapeutic strategies to restore or maintain functional adipocytes. 

To achieve this, we are

1. establishing and applying new methodology to identify adipose selective surface epitopes and combine this knowledge with the characterization of murine brown and white adipocyte heterogeneity. 
2. visualizing and characterizing changes in surface epitopes and adipocyte lineages during the induction of insulin resistance, and
3. developing genetic and pharmacological intervention strategies preventing the transition from obesity towards insulin resistance and the metabolic syndrome.