UCP1 protein: The molecular hub of adipose organ plasticity

Abstract

In all mammals, adipocytes are cells with abundant cytoplasmic lipids forming the parenchyma of the adipose organ. White adipocytes store highly energetic molecules to release them, in the form of free fatty acids to survive between meals. Brown adipocytes trough their unique mitochondrial UCP1 protein burn glucose and lipids to perform thermogenesis in order to survive in cold environments. A third type of adipocytes appears in the subcutaneous depot of the adipose organ of female mice during pregnancy and lactation: the pink adipocytes. The pink adipocytes are mammary gland alveolar epithelial cells with the essential role of producing and secreting milk for pup feeding. Our data suggest that they derive from the transdifferentiation of white adipocytes. Different metabolic and environmental challenges highlight the extraordinary plasticity of the mammalian adipose organ. Cold exposure leads to an increase of the “brown” component of the adipose organ (browning) to warrant thermal homeostasis. Under positive energy balance, the “white” component enlarges (whitening) to allow storage of the excess of nutrients. Finally, during pregnancy the “pink” component develops (pinking) in the subcutaneous depots to satisfy pup nutritional needs. The plasticity of the adipose organ appears to occur not only through proliferation and differentiation of stem cells but, distinctively, via a direct transformation of mature adipocytes that under proper stimuli, by reprogramming their genome, change phenotype and function.Obese white adipocytes die for pyroptosis causing a macrophage fat infiltration with metabolic consequences. Browning of obese fat could offer an appropriate strategy to combat the epidemic metabolic syndrome.