Gasser, Kenneth W.
M.S. (Master of Science)
Department of Biological Sciences
Pancreatic exocytosis involves a coordinated coupling between membrane fusion and the activation of ion channels for fluid secretion. This coupling may exist in part due to the mechanisms that regulate electrolyte transport in intracellular secretory granules. The granule K+ transport was shown to be a function of KATP channels based on inhibition of the transport by cytosolic concentrations of ATP (95%), sulphonylureas tolbutamide and glibenclamide (64%), lysophospholipids (51%) and sensitivity to pH and KCl concentrations. The secretory granule Cl" channel was shown to respond to membrane alterations by phospholipase A2 and its reaction products, lysophospholipids and unesterified fatty acids. These products increased the Cl" transport by up to 450% and are known to alter the fluidity and thickness of most membranes. The Cl" channel responded optimally to unsaturated fatty acids with chain lengths of 18 to 20 carbons. The overall ability of fatty acids to stimulate Cl" transport followed the order: linoleic (18:2) ~ oleic (18:1) > linolenic (18:3) ~ arachidonic (20:4) > stearic (18:0) > palmitoleic (16:1) > lignoceric (24:0) > palmitic (16:0) > capric (10:0). These results suggest a mechanism to coordinate secretory granule ion channels, and prevent net electrolyte transport prior to fusion with the apical membrane.
Holda, Jaclyn Renee, "Regulation of pancreatic secretory granule ion transport" (1994). Graduate Research Theses & Dissertations. 4689.
Northern Illinois University
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