Our cellular metabolism division is examining a newly discovered regulatory mechanism involving hormone-sensitive lipase (HSL), a protein historically known only for breaking down fat. New evidence shows HSL also functions within the nucleus of fat cells, helping regulate adipocyte development and stability. When HSL function is impaired, fat tissue can shrink abnormally, leading to metabolic complications similar to those seen in obesity.

This dual role of HSL challenges decades of assumptions about fat metabolism and opens new therapeutic avenues. Researchers are now investigating how nuclear lipid signaling influences metabolic disease progression. These findings could support next-generation metabolic therapies targeting cellular fat regulation rather than simply reducing fat mass.