Significance
One promising strategy for the treatment or prevention of obesity-mediated health complications is augmenting brown adipose tissues (BAT), which is a specialized fat that actively dissipate energy in the form of heat and maintain energy balance. In this study, we determined how pre-exposing human brown adipose progenitors (BAP) to angiogenic factors in 2D and how bioprinted microenvironments in 3D affected brown adipogenic differentiation and metabolic activity. We demonstrated that white and brown adipogenesis, and thermogenesis were regulated by tuning the bioprintable matrix stiffness and construct structure. This study not only unveils the interaction between BAP and 3D physiological microenvironments, but also presents a novel tissue engineered strategy to manage obesity and other related metabolic disorders.
Statement of significance
One promising strategy for the treatment or prevention of obesity-mediated health complications is augmenting brown adipose tissues (BAT), which is a specialized fat that actively dissipate energy in the form of heat and maintain energy balance. In this study, we determined how pre-exposing human brown adipose progenitors (BAP) to angiogenic factors in 2D and how bioprinted microenvironments in 3D affected brown adipogenic differentiation and metabolic activity. We demonstrated that white and brown adipogenesis, and thermogenesis were regulated by tuning the bioprintable matrix stiffness and construct structure. This study not only unveils the interaction between BAP and 3D physiological microenvironments, but also presents a novel tissue engineered strategy to manage obesity and other related metabolic disorders.