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In vivo administration of the C16:0 fatty acid isoform of sulfatide increases pancreatic sulfatide and enhances glucose-stimulated insulin secretion in Zucker fatty (fa/fa) rats

Journal article
Authors Maria K. Blomqvist
M. Carrier
T. Andrews
K. Pettersson
Jan-Eric Månsson
Britt-Marie Rynmark
Pam Fredman
K. Buschard
Published in Diabetes Metab Res Rev
Volume 21
Issue 2
Pages 158-66
Publication year 2005
Published at Institute of Clinical Neurosciences, Section of Experimental Neuroscience
Pages 158-66
Language en
Keywords Animals, Blood Glucose/*metabolism, Disease Models, Animal, Fatty Acids/*pharmacology, Glucose/*pharmacology, Insulin/blood/*secretion, Islets of Langerhans/drug effects/*secretion, Male, Prediabetic State/blood/physiopathology, Rats, Rats, Zucker, Sulfoglycosphingolipids/metabolism/*pharmacology
Subject categories Neurochemistry


BACKGROUND: Sulfatide is present in the secretory granules of beta cells and has been shown, in vitro, to be involved in insulin processing and secretion. Of particular interest is one of the major sulfatide isoforms in the beta cells, the C16:0 fatty acid isoform, which has been shown to be involved in insulin crystal preservation in vitro. The aim of this study was to investigate the ability of C16:0 fatty acid isoform of sulfatide to affect insulin secretion and/or action and glycaemic control in the adipogenic 'prediabetic' Zucker rat. METHODS: The C16:0 sulfatide was administered to Zucker rats for 10 weeks, and fasting levels of plasma insulin and glucose were measured as well as levels after an intravenous (i.v.) glucose load. In addition, the sulfatide expression, examined by thin-layer chromatography-enzyme-linked immunosorbent assay and mass spectrometry, in the pancreas of C16:0 sulfatide-treated Zucker rats was compared to controls. RESULTS: The in vivo treatment of Zucker rats with C16:0 sulfatide resulted in significantly elevated glucose-stimulated insulin secretion (60-80% increase, p < 0.05), without significant changes in glucose tolerance. The treatment was associated with an ameliorated first-phase insulin response (3-4-fold, p = 0.009, 0.016) and a 60% increase of pancreatic sulfatide content (p = 0.001), possible by an uptake of C16:0 sulfatide. The fasting hyperinsulinaemia and blood glucose levels were unchanged. CONCLUSIONS: The treatment with C16:0 sulfatide elevates glucose-stimulated insulin secretion and enhances sulfatide content in the pancreas of Zucker rats.

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