Andrea Frontini

TL;DR: It is demonstrated that Prdm16 is a cell-autonomous determinant of a brown fat-like gene program and thermogenesis in subcutaneous adipose tissues and reduced the brown fat phenotype in white adipose tissue stimulated by β-adrenergic agonists.

TL;DR: It is shown that adipocyte-specific deletion of the coregulatory protein PRDM16 caused minimal effects on classical brown fat but markedly inhibited beige adipocyte function in subcutaneous fat following cold exposure or β3-agonist treatment, indicating that PRDM 16 and beige fat cells are required for the "browning" of white fat and the healthful effects of sub cutaneous adipose tissue.

TL;DR: It is demonstrated that human adults indeed possess BAT and thus imply possibilities of future therapeutic strategies for the treatment of obesity, including maintenance of brown adipocytes and stimulation of the growth of preexisting brown precursors.

TL;DR: Murine white and brown adipocytes are found together in dissectible visceral and subcutaneous fat depots supplied by specific vessels and nerves, forming a multi-depot organ with plastic properties.

TL;DR: Quantitative analysis showed that cold acclimation induced an increase in brown adipocytes and an almost equal reduction in white adipocytes; however, there were no significant differences in total adipocyte count or any signs of apoptosis or mitosis, in line with the hypothesis of the direct transformation of white into Brown adipocytes.