Publication Date

1994

Document Type

Dissertation/Thesis

First Advisor

Gasser, Kenneth W.

Degree Name

M.S. (Master of Science)

Department

Department of Biological Sciences

LCSH

Pancreas--Secretions

Abstract

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.

Comments

Includes bibliographical references (pages [74]-82)

Extent

82 pages

Language

eng

Publisher

Northern Illinois University

Rights Statement

In Copyright

Rights Statement 2

NIU theses are protected by copyright. They may be viewed from Huskie Commons for any purpose, but reproduction or distribution in any format is prohibited without the written permission of the authors.

Media Type

Text

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