Genetic inactivation of the transcription factor, Zfp423, in visceral white adipocyte precursors leads to the formation of thermogenic adipocytes in visceral fat depots and improves insulin sensitivity in obese mice.

A brown-to-white adipogenic transdifferentiation process in the periureter region of mouse renal adipose tissue gives rise to a population of cold-inducible adipocytes with a transcriptome distinct from subcutaneous beige adipocytes.

The activation of beige adipocyte thermogenesis by cold temperatures and β3-adrenergic receptor agonists induce beige adipocyte formation, function and perdurance.

Fibro-inflammatory progenitors represent a subpopulation of perivascular cells in visceral adipose tissues of mice that promote inflammation and fibrosis.

Clock protein NR1D1 regulates white adipose tissue expansion and development of obesity-related pathology.

A hybrid mouse/human model using mesenchymal progenitor cells reveals dynamics of human adipose tissue development and mechanisms that may enhance human adipose thermogenic capacity.

The regulation of sympathetic innervation density by beige adipocytes in subcutaneous fat is important during a critical developmental window, but dispensable during adulthood.

Single-cell expression profiling and genetic lineage analysis show that aging impairs adipocyte differentiation from precursor cells and blocks the thermogenic activation of adipocytes during cold exposure.

Combined fate mapping and genetic deletion studies reveal that PDGFRα+ cells and PDGFRα gene itself are required for adipose tissue development but not for adult tissue homeostasis.

Diet-induced obesity in mice led to a duration of diet-dependent bone marrow adipocyte whitening, which drove monocyte expansion and skewing towards a tissue-invasive phenotype, likely contributing to ensuing tissue infiltration that accompanies obesity and diabetes.