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

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.

Crosstalk between IL10-producing immune cells and adipocytes within adipose tissue is an important determinant of thermogenesis and systemic energy balance.

Cartilage cells transition through a proliferative intermediate to give rise to bone and marrow fat cells in long bones.

TRIM23 plays a critical role in the switching from early to late adipogenic enhanceosomes by stabilizing the PPARγ protein.

The ALK7 receptor functions cell-autonomously and homeostatically in adult adipocytes to regulate catecholamine sensitivity in response to the diet.

A group of cells that can become adipocytes controls the formation of blood vessels in the bone marrow, and also regulates the differentiation of resident mesenchymal progenitor cells.

Maternal obesity and excess of the adipocyte hormone leptin delays the emergence of synaptic inhibition in the developing brain mice.

PTRF (Cavin-1) mediates metabolism-regulated ribosomal transcription in mature adipocytes, independent of its role in caveolae formation.

An interaction between the brown fat protein CIDEA and the phospholipid phosphatidic acid is vital for the expansion of intracellular lipid droplets for energy storage.