Microparticles produced from the membrane surface of adipocytes promote lipid biosynthesis and angiogenesis in adipose tissues. Thus, they are deeply associated with the onset of metabolic disorders. Despite our understanding of their roles in physiological or pathological responses, we know little about the mechanism by which microparticles are produced from adipocytes. Based on our previous studies using rat megakaryocytes or mast cells during exocytosis, we proposed that membrane curvature induced by amphiphilic reagents, such as chlorpromazine or salicylate, facilitate or inhibit the formation of microparticles. Since the plasma membranes in adipocytes share many common biophysiological features with those in megakaryocytes or mast cells during exocytosis, the same stimulatory or inhibitory mechanism of microparticle formation would exist in adipocytes. Therefore, we hypothesize here that amphiphilic reagents would also change the membrane curvature in adipocytes, and that such changes would facilitate or inhibit the microparticle formation from adipocytes. Our hypothesis is unique because it sheds light for the first time on the physiological mechanism by which microparticles are produced in adipocytes. It is also important because the idea could have novel therapeutic implications for metabolic disorders that are triggered by increases in the microparticle formation.
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