In just the past few decades, the prevalence of obesity has nearly tripledworldwide, with the main driver of this growing epidemic being an imbalance in energy metabolism. Here, energy in dominates energy out resulting in the pathological expansion and remodeling of one’s white adipose tissue (WAT). This is often accompanied by metabolic diseases such as type 2 diabetes, cardiovascular disease, and ectopic fat accumulation. Contrary to energy storing WAT, mammals also contain thermogenic fat cells- brown and beige adipocytes. Thermogenic fat possesses the unique ability to utilize substrates such as glucose and fatty acids to produce heat. Therefore, the generation of thermogenic fat has great clinical utility in targeting metabolically unhealthy WAT. However, thermogenic fat presence as well as function declines with both age and obesity. Thus, understanding the molecular pathways and mechanisms that regulate both white and thermogenic fat development and function is critical for the generation of therapies to thwart obesity and metabolic syndrome. Here, we identify platelet derived growth factor-b (PDGFRb) signaling as a regulator of both WAT and beige fat development. PDGFRb is a membrane bound receptor tyrosine kinase involved in numerous signal transduction pathways. We have found that deleting PDGFRb in white adipocyte progenitor cells (APCs) impairs adult WAT homeostasis, resulting in lipodystrophy, fibrotic tissue accumulation and immune cell infiltration. Mechanistically, PDGFRb is essential in specification of the adult white APC lineage, with embryonic deletion of PDGFRb in adult white APCs resulting in a lineage switch. PDGFRb deficient APCs instead develop into macrophages, not white adipocytes, impairing adult WAT function. In contrast to white fat development, we have additionally uncovered the role of PDGFRb in cold induced beige fat development. Here, we find that PDGFRb expression increases in beige APCs throughout the aging process to negatively regulate beige fat formation via downstream Stat1 phosphorylation. Deleting PDGFRb in aged beige APCs restores beige fat generation in response to cold temperature challenge. Interestingly however, loss of PDGFRb in aged beige APCs does not restore their ability to undergo beige adipogenesis. Instead, we find that with aging, the immune cell composition within the adipose tissue niche is disrupted, hindering beige fat formation. Targeting the PDGFRb- Stat1 pathway, either genetically or pharmacologically, restores the presence and activation of these immune cells to promote beiging and improve whole body metabolism. Overall, these studies highlight the PDGFRb signaling pathway as a promising potential target in combatting the current obesity epidemic.