White adipose tissue (WAT) plays a significant role in metabolic regulation and energy homeostasis, which can be disrupted in the setting of obesity. Obesity can lead to health complications including insulin resistance, type 2 diabetes and fatty liver disease, which are caused in part by the deposition of lipid in peripheral tissues following saturation of WAT depots. Recent studies have shown that activating adipogenesis, or enhancing healthy WAT expansion, can reduce obesity induced complications and results in a metabolically healthy phenotype. Thus, by redirecting fat from non-adipose tissues back into adipose tissue, complications associated with obesity may be alleviated. Indeed, a protein recently shown to promote metabolically healthy obesity is tripartite motif containing 28 (Trim28), which was suspected to act in an epigenetic manner during development and not directly in adipose tissue per se. However, to our knowledge there have not been any studies that definitively demonstrate the role of Trim28 specifically in WAT. Here, we demonstrate that adipose specific Trim28 KO mice have increased adiposity on a normal chow and high-fat diet. Consistent with previous findings, this increased adiposity was not associated with decrements in glucose tolerance, and was demonstrated to increase the expression of genes consistent with lipid storage and browning in both visceral and subcutaneous WAT depots. We also demonstrate that triglyceride species are altered in visceral fat depots and reduced in the plasma and liver of KO mice compared with controls. Furthermore, we show that the magnitude of this effect was exacerbated in female mice, suggesting that Trim28 could play a role in gender specific differences in relation to complications associated with obesity. These data suggest that Trim28 expression may be a potential mechanism important for promoting adipose tissue expansion and improving lipid storage in the setting of obesity.