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.

A novel population of adipocytes that play essential roles in adaptive thermogenesis via cell autonomous and non-autonomous effects and regulate systemic glucose metabolism in mice.

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

The production of beige adipocytes following cold exposure is blocked as mice get older and leads to changes in the expression of metabolic genes.

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

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.

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.

Intermittent fasting affects intestinal immunity through new interactions between macrophages and ILC3s, increasing ILC3 secretion of IL-22 and thus promoting white adipose tissue beigeing, and improving metabolism.

An update on the role of lncRNAs in adipogenesis and adipose tissue function, aimed at promoting the identification of new drug targets for obesity and metabolic diseases.

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.