title: 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.
abstract: 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.
authors.affiliation: Institute of Clinical Neuroscience, The Sahlgrenska Academy at Göteborg University, Sahlgrenska University Hospital, Mölndal, Sweden. maria.blomqvist@neuro.gu.se
authors.forename: Maria
authors.initials: M
authors.lastname: Blomqvist
authors.forename: Martin
authors.initials: M
authors.lastname: Carrier
authors.forename: Tara
authors.initials: T
authors.lastname: Andrews
authors.forename: Knut
authors.initials: K
authors.lastname: Pettersson
authors.forename: Jan-Eric
authors.initials: JE
authors.lastname: Månsson
authors.forename: Britt-Marie
authors.initials: BM
authors.lastname: Rynmark
authors.forename: Pam
authors.initials: P
authors.lastname: Fredman
authors.forename: Karsten
authors.initials: K
authors.lastname: Buschard
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D004195:Disease Models, Animal; D005227:Fatty Acids / Q000494:pharmacology*; D005947:Glucose / Q000494:pharmacology*; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D011236:Prediabetic State / Q000097:blood / Q000503:physiopathology; D051381:Rats; D011924:Rats, Zucker; D013433:Sulfoglycosphingolipids / Q000378:metabolism / Q000494:pharmacology*
chemical_list: D001786:Blood Glucose; D005227:Fatty Acids; D007328:Insulin; D013433:Sulfoglycosphingolipids; D005947:Glucose