The white adipose tissue is the most predominant type of fat in the human body. It rapidly expands upon excess food intake and, in turn, becomes dysfunctional. This triggers a low-grade chronic inflammation, known as metaflammation, which has been causally linked to obesity-related metabolic complications (e.g., type 2diabetes, atherosclerosis). How the white adipose tissue expands determines the metabolic and inflammatory outcome for the good or the worse. This is determined on the level of the precursor cells that eventually form the lipid-laden mature fat cells in the adipose tissue. The function and maturation of these precursor cells are critically determined by a small subcellular structure called the primary cilium. The primary cilium functions as a cellular antenna that detects environmental cues and converts them into a cellular response. In this project, we aim to understand the role of primary cilia in controlling precursor cell function in the adipose tissue in response to excess energy intake. This will allow us to reveal how this little cellular antenna controls adipose tissue function and, in turn, metaflammation.
To provide a comprehensive analysis on how primary cilia control metaflammation, we will use genetic- and diet-induced obesity mouse models to study the impact on adipose tissue function. Furthermore, we will investigate the interaction between immune cells and other cells in the adipose tissue using state-of-art cell biology techniques.