PerspectiveLet's shift lipid burden-From large to small adipocytes

Adipose tissue mass in mammals expands by increasing both volume and total number of the adipocytes. The simultaneous existence of large and small adipocytes and their unsynchronized growth, even within the same adipose tissue depot, argues against simple filling-up of nascent small adipocytes with lipids and lipid droplets. Consequently, it is tempting to speculate about signals provoking shift of lipid loading from mature large to small adipocytes. Very recently, microvesicles have been shown (i) to harbor the glycosylphosphatidylinositol-anchored (c)AMP-degrading phosphodiesterase Gce1 and the 5′-nuceotidase CD73, (ii) to be released (preferably) from large adipocytes, (iii) to interact (preferably) with small adipocytes and (iv) to transfer Gce1 and CD73 to plasma membranes and lipid droplets of the small adipocytes where they degrade (c)AMP. This sequence of events leads to upregulation of lipid storage in small adipocytes in response to the microvesicle-encoded “take-over” signal from large adipocytes. A model is proposed for the maturation of small adipocytes driven by large cells along a gradient of microvesicle-derived inter-adipocyte signals. Pharmacological modulation of the communication between adipocytes for their maturation may be useful for the therapy of metabolic diseases.