Our research is devoted to adipose tissue development and the regulation of adipose tissue plasticity in response to physiological challenges and metabolic stress. I will introduce two of our recent projects.

The first project focuses on age-related visceral adiposity. The average fat mass in adults increases dramatically with early aging, and older people often suffer from visceral obesity and related adverse metabolic disorders. Unfortunately, how aging leads to fat accumulation is poorly understood. It is known that adipocyte turnover is very low in young mice, similar to that in young humans. We find that mice mimic age-related fat expansion in humans. In vivo lineage tracing shows that massive adipogenesis, especially in the visceral fat, is triggered during aging. We then identify a novel Committed Preadipocyte population uniquely enriched in Aged mice (CP-A), existing both in mice and humans, with a global activation of proliferation and adipogenesis pathways. These findings define a new fundamental mechanism involved in fat tissue aging and offer prospects for preventing and treating age-related metabolic disorders.

The second project focuses on brown adipocyte heterogeneity. Brown adipose tissue (BAT) is a thermogenic organ that plays an important role in human energy homeostasis. It is now well-accepted that recruiting and activating BAT can correct dyslipidemia and prevent obesity-related metabolic disorders. BAT is thought to have a homogeneous population of BAs. We recently identified a new BA subpopulation with low uncoupling protein 1 (UCP1) expression (BA-L), which coexists with the classical BA with high UCP1 expression (BA-H). BA-L accounts for more than half of BAs in the interscapular BAT of mice housed at room temperature. Compared to BA-Hs, BA-Ls have significantly larger lipid droplets, distinct mitochondrial morphology, lower mitochondrial content, and lower basal mitochondrial respiration. Upon cold exposure, BA-Ls switch into BA-Hs cells. Unfortunately, this cold induced cellular switch declines during early aging. I will give our recent updates on the function of the newly identified BA-Ls, and how BA heterogeneity is regulated in healthy adults and during aging.