Presentation description

Obesity rates are rising globally, increasing concern as it is a major risk factor for developing cardiovascular disease, the leading cause of death worldwide. The rising prevalence of obesity has increased interest in adipose tissue (AT) and the underlying mechanisms of fat expansion and energy expenditure. AT is generally divided into two types; white adipose tissue (WAT) which stores excess energy as triglycerides and brown adipose tissue (BAT) which oxidizes fatty acids and releases energy in the form of heat. A third type called beige or bright adipocytes has recently been identified in humans and rodents and is associated with improved cardiometabolic outcomes. The developmental origins of WAT and BAT are well characterized; however, the origins of beige adipocyte formation and activation are largely unknown. Elucidating the mechanism of beige adipocyte development and recruitment are of immense interest and for potential therapies to increase beige fat formation. Bone morphogenic proteins (BMPs) are known to play a significant role in a variety of processes including the development and function of beige adipocytes. Previous work has identified BMP binding endothelial binding regulator (BMPER) is a modulator of BMPs. Our lab has shown that BMPER colocalized with the Pdgfra+ adipose progenitor cell (APCs) population which give rise to BAT and WAT in mice and humans. Our lab discovered that ablation of BMPER in the Pdgfra+ population results in a complete absence of beige fat cell recruitment in response to cold or beta-adrenergic stimulation in mice. This study identifies BMPER as a novel determinant of beige fat development, which could be targeted to enhance beige fat mass to protect from obesity-induced metabolic dysregulation.