Speaker
Description
Obesity is a major global public health issue characterized by an excessive accumulation of lipids that impairs health. White adipose tissue is responsible for this storage through its main cells, adipocytes. The expansion of this tissue relies on two mechanisms: an increase in adipocyte size (hypertrophy) and an increase in adipocyte number (hyperplasia). Although the combined effects of these mechanisms remain insufficiently understood, they play a crucial role in the development of obesity-associated metabolic diseases.
Adipocyte diameter ranges from about 20$\mu$m to 200$\mu$m, leading to large variations in cell volume. Moreover, adipocyte size distribution is typically bimodal, with two characteristic populations around 30$\mu$m and 130$\mu$m, with inter-individual variability. In this work, we introduce a system of ordinary differential equations describing adipocyte size dynamics based on lipid fluxes. The model reproduces experimental size distributions while accounting for cell variability.
The number of adipocytes is difficult to measure in vivo, and current estimation methods in organisms such as rats or humans remain approximate. Here, we propose a method to estimate adipocyte number during weight loss. Assuming that adipocyte number remains constant during this process, the total number of cells can be inferred from variations in adipocyte size.
