Recently, it was discovered that certain depots of WAT, when subjected to certain stimuli, could take on a BAT phenotype: the browning of WAT.
Notably, patients with Cushing's syndrome, which is characterized by elevated circulating cortisol levels, have fat accumulation in certain depots, such as the central abdomen, the supraclavicular region the face, and the dorsocervical region, the pathognomonic "buffalo's hump".
WAT from certain depots, in response to appropriate stimuli, can undergo a process known as browning where it takes on characteristics of BAT, notably the induction of UCP1 (uncoupling protein 1) expression and the presence of multilocular lipid droplets and multiple mitochondria.
It has been shown that certain WAT depots are less prone to browning [ 29].
Postnatal maternal separation reduced the weight of certain adipose depots, but only in rats fed an HFS diet.
Savage and colleagues [ 27] reported a dominant negative mutation of PPARγ arising from a proline-467-leucine mutation, which resulted in severe peripheral and hepatic insulin resistance, partial lipodystrophy (the loss/reduction of certain fat depots) and hepatic steatosis.
Because fat mass is significantly reduced in Vgf C 57 and Vgf R -/- mice (e.g. Figure 2), certain fat depots were extremely difficult to identify and quantify on the C57Bl6 background, including visceral mesenteric fat, subcutaneous abdominal fat, and retroperitoneal fat.
Considerable numbers of brown adipocytes occur transiently within some white fat depots during early postnatal development (38) and can reappear in white fat depots under certain conditions in adulthood (39).
Certain mouse WAT depots have a greater propensity to form inducible brown fat [ 29], such as the inguinal WAT and perirenal WAT.
