Adipocyte (dys)function in human disease
Adipogenesis, Cell-cell communication, Gene regulation
Research aim
Understanding the molecular mechanisms behind adipocyte (dys)function in obesity, insulin resistance, lipodystrophy and cancer.
About us
The relationship between obesity and various human diseases including type 2 diabetes and cancer is well established and represents a major medical problem worldwide. Emerging evidence indicates that adipocyte dysfunction plays a key role, rather than simply the increase in the number of adipocytes or the increased amount of lipids per adipocyte associated with obesity. An important element of adipocyte dysfunction lies in its gene regulatory program, which determines for example the cellular metabolism of adipocytes and their endocrine or paracrine output. One of the key players in adipocyte gene regulation is the transcription factor PPARγ, which is also the target of anti-diabetic drugs named thiazolidinediones. Specific research topics are:
Healthy adipocyte function. Proper adipocyte function, including the differentiation of pre-adipocytes into mature adipocytes is a highly regulated and complex process. We investigate gene regulation in (pre)adipocytes, and how specific gene products contribute to adipocyte differentiation, maintenance and function; our approaches include the identification and characterization of rare human mutations in the PPARγ gene and other key genes.
PPARγ in cancer. While the transcription factor PPARγ is an established regulator of adipocyte function, its role in cancer is far less understood. Based on our expertise in adipocytes, we aim to elucidate the role of PPARγ in various cancer types, also making use or organoids.