Insulin plays a fundamental role in whole-body glucose homeostasis. Central to this is the hormone's ability to rapidly stimulate the rate of glucose transport into adipocytes and muscle cells . Upon binding its receptor, insulin stimulates an intracellular signalling cascade that culminates in redistribution of glucose transporter proteins, specifically the GLUT4 isoform, from intracellular stores to the plasma membrane, a process termed ‘translocation’ [1,2]. This is an example of regulated membrane trafficking , a process that also underpins other aspects of physiology in a number of specialized cell types, for example neurotransmission in brain/neurons and release of hormone-containing vesicles from specialized secretory cells such as those found in pancreatic islets. These processes invoke a number of intriguing biological questions as follows. How is the machinery involved in these membrane trafficking events mobilized in response to a stimulus? How do the signalling pathways that detect the external stimulus interface with the trafficking machinery? Recent studies of insulin-stimulated GLUT4 translocation offer insight into such questions. In the present paper, we have reviewed these studies and draw parallels with other regulated trafficking systems.
Studies of the regulated assembly of SNARE complexes in adipocytes
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Dimitrios Kioumourtzoglou, Jessica B.A. Sadler, Hannah L. Black, Rebecca Berends, Cassie Wellburn, Nia J. Bryant, Gwyn W. Gould; Studies of the regulated assembly of SNARE complexes in adipocytes. Biochem Soc Trans 1 October 2014; 42 (5): 1396–1400. doi: https://doi.org/10.1042/BST20140114
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