Why the study?
A comprehensive understanding of the regulatory mechanisms mediating white adipose tissue browning is lacking, which holds potential therapeutic value in combating obesity.
This study provides a comprehensive gene regulatory network underlying white adipose tissue browning, offering insights into the genetic architecture of brite adipogenesis which may inform future obesity therapies.
Strain variation maps core WAT browning networks; leaves open human translation for obesity therapies.
Recruitment of brite/beige cells, known as browning of white adipose tissue (WAT), is an efficient way to turn an energy-storing organ into an energy-dissipating one and may therefore be of therapeutic value in combating obesity. However, a comprehensive understanding of the regulatory mechanisms mediating WAT browning is still lacking. Here, we exploit the large natural variation in WAT browning propensity between inbred mouse strains to gain an inclusive view of the core regulatory network coordinating this cellular process. Combining comparative transcriptomics, perturbation-based validations, and gene network analyses, we present a comprehensive gene regulatory network of inguinal WAT browning, revealing up to four distinct regulatory modules with key roles for uncovered transcriptional factors, while also providing deep insights into the genetic architecture of brite adipogenesis. The presented findings therefore greatly increase our understanding of the molecular drivers mediating the intriguing cellular heterogeneity and plasticity of adipose tissue.
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Li et al. (2019) studied this question.
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