Selective adipocyte loss of Angiopoietin-2 prompts female-specific obesity and metabolic syndrome.

ABSTRACT: Thermogenic fat differentiation and function can be promoted through multiple pathways, resulting in a common cell phenotype characterized by the expression of Uncoupling Protein-1 and the ability to dissipate energy, but local and systemic stimuli are necessary to promote adequate thermogenic fat vascularization, which is a precondition for the transport of substrate and the dissipation of heat. Angiopoietin-2 is an important driver of vascularization, and its transcription is in part promoted by estrogen signaling. In this study we demonstrate that adipose tissue-specific knock out of Angiopoietin-2 causes a female-specific reduced thermogenic fat differentiation and function, resulting in obesity and impaired glucose tolerance with end-organ features consistent with metabolic syndrome.

SUBMITTER: Ni B 

PROVIDER: S-EPMC9486017 | biostudies-literature | 2022 Nov

REPOSITORIES: biostudies-literature