title: Unaltered pancreatic islet blood perfusion in islet amyloid polypeptide-deficient mice.
abstract: OBJECTIVE
  Several biological activities have been ascribed to islet amyloid polypeptide (IAPP). However, their physiological relevance remains unclear. Previous studies in rats with exogenous administration of IAPP suggest that the peptide may increase splanchnic vascular resistance and redistribute the blood flow within the pancreas to the islets. In this study, the use of IAPP-deficient mice allowed us to evaluate possible effects of the lack of IAPP on splanchnic blood perfusion and we could thereby circumvent the potentially pharmacological actions of exogenously administered IAPP.
  
  
  METHODS
  Regional splanchnic blood flow was measured after exogenous administration of IAPP and in IAPP-deficient mice.
  
  
  METHODS
  Blood flow values were determined using a non-radioactive microsphere technique in anesthetized animals.
  
  
  RESULTS
  No differences in whole pancreatic blood flow or islet blood flow could be detected in IAPP-deficient mice when compared with control mice; neither did IAPP deficiency affect the glucose-induced increase in islet blood flow. Duodenal, ileal and colonic blood flows were similar in IAPP-deficient and control mice. Exogenous administration of IAPP selectively increased islet blood flow in wild-type control mice.
  
  
  CONCLUSIONS
  The present findings in the IAPP-deficient mice suggest that the vascular effects seen in the islets after exogenous administration of IAPP to normal mice reflect pharmacological, rather than physiological effects of the peptide. We conclude that the lack of endogenous IAPP within the splanchnic vascular system does not alter the blood perfusion of pancreatic islets or other splanchnic organs.
authors.affiliation: Department of Medical Cell Biology, Biomedical Center, Box 571, Uppsala University, SE-751 23 Uppsala, Sweden. Per-Ola.Carlsson@medcellbiol.uu.se
authors.forename: Per-Ola
authors.initials: PO
authors.lastname: Carlsson
authors.forename: Ella
authors.initials: E
authors.lastname: Karlsson
authors.forename: Hindrik
authors.initials: H
authors.lastname: Mulder
authors.forename: Samuel
authors.initials: S
authors.lastname: Gebre-Medhin
mesh_terms: D000682:Amyloid / Q000172:deficiency* / Q000235:genetics* / Q000494:pharmacology; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D007275:Injections, Intravenous; D007328:Insulin / Q000097:blood; D007422:Intestines / Q000098:blood supply; D007515:Islets of Langerhans / Q000098:blood supply*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D012039:Regional Blood Flow / Q000502:physiology; D013152:Splanchnic Circulation / Q000502:physiology*
chemical_list: D000682:Amyloid; D001786:Blood Glucose; D007328:Insulin