title: [Severe vascular dysfunction shown in transplanted islets].
abstract: Despite recent advances in clinical islet transplantation, a surprisingly large number of islets (approximately 1 million) are still required to obtain insulin independence in type 1 diabetes. The reasons for this are obscure and likely multifactorial. One explanation may be disturbances in engraftment of the transplanted islets, i.e. the adaptation of the islet transplant to its new surroundings with regard to e.g. revascularization and blood perfusion. Endogenous islets have a dense glomerular-like angioarchitecture. Transplantation of isolated islets causes a disruption of their vascular connections, making the islets dependent on the formation of new blood vessels for optimal function. Evidence from experimental islet transplantation indicates an insufficient revascularization of transplanted islets with subsequent chronically decreased blood perfusion and oxygen tension, which has metabolic consequences within the tissue.
authors.affiliation: Medicincentrum, Akademiska sjukhuset, Uppsala. Per-Ola.Carlsson@medcellbiol.uu.se
authors.forename: Per-Ola
authors.initials: PO
authors.lastname: Carlsson
authors.forename: Arne
authors.initials: A
authors.lastname: Andersson
authors.forename: Magnus
authors.initials: M
authors.lastname: Johansson
authors.forename: Göran
authors.initials: G
authors.lastname: Mattsson
authors.forename: Richard
authors.initials: R
authors.lastname: Olsson
authors.forename: Leif
authors.initials: L
authors.lastname: Jansson
mesh_terms: D000818:Animals; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology / Q000601:surgery; D007515:Islets of Langerhans / Q000098:blood supply* / Q000166:cytology / Q000378:metabolism; D016381:Islets of Langerhans Transplantation / Q000009:adverse effects / Q000502:physiology; D051379:Mice; D008833:Microcirculation / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D009389:Neovascularization, Pathologic / Q000209:etiology*; D018919:Neovascularization, Physiologic / Q000502:physiology*