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Pathologic expansion of white adipose tissue (WAT) in obesity is characterized by adipocyte hypertrophy, inflammation, and fibrosis; however, factors triggering this maladaptive remodeling are largely unknown. Here, we test the hypothesis that the potential to recruit new adipocytes from Pdgfrβ +  preadipocytes determines visceral WAT health in obesity. We manipulate levels of  Pparg , the master regulator of adipogenesis, in Pdgfrβ +  precursors of adult mice. Increasing the adipogenic capacity of Pdgfrβ +  precursors through  Pparg  overexpression results in healthy visceral WAT expansion in obesity and adiponectin-dependent improvements in glucose homeostasis. Loss of mural cell  Pparg  triggers pathologic visceral WAT expansion upon high-fat diet feeding. Moreover, the ability of the TZD class of anti-diabetic drugs to promote healthy visceral WAT remodeling is dependent on mural cell  Pparg . These data highlight the protective effects of de novo visceral adipocyte differentiation in these settings, and suggest Pdgfrβ +  adipocyte precursors as targets for therapeutic intervention in diabetes.

De novo adipocyte differentiation from Pdgfrβ+ preadipocytes protects against pathologic visceral adipose expansion in obesity