title: Impaired wound healing in an acute diabetic pig model and the effects of local hyperglycemia.
abstract: Diabetic wounds result in significant morbidity, prolonged hospitalization, and enormous health-care expenses. Pigs have been shown to have wound healing resembling that in humans. The aim of this study was to develop a large-animal model for diabetic wound healing. Diabetes was induced by streptozotocin injection in Yorkshire pigs. Full-thickness wounds were created and dressed with a sealed chamber. Nondiabetic pigs with or without high glucose wound fluid concentration served as controls. Glucose concentration in serum and wound fluid was measured and collected. Wound contraction was monitored, and biopsies were obtained for measurement of reepithelialization. Wound fluid was analyzed for insulin-like growth factor-1 (IGF-1), platelet-derived growth factor, and transforming growth factor. Glucose concentration in wound fluid initially followed serum levels and then decreased to undetectable on day 9. Reepithelialization was significantly delayed in diabetic pigs. In nondiabetic pigs, wounds treated in a local hyperglycemic environment, and thus excluding the effects of systemic hyperglycemia, showed no difference in wound closure compared with controls. This suggests that delayed wound healing in diabetes is not induced by local high-glucose concentration itself. Analysis of growth factor expression showed a marked reduction in IGF-1 in the diabetic wounds. Diabetic pigs have impaired healing that is accompanied by a reduction of IGF-1 in the healing wound and is not due to the local hyperglycemia condition itself.
authors.affiliation: Laboratory of Tissue Repair and Gene Transfer, Division of Plastic Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
authors.forename: Patrik
authors.initials: P
authors.lastname: Velander
authors.forename: Christoph
authors.initials: C
authors.lastname: Theopold
authors.forename: Tobias
authors.initials: T
authors.lastname: Hirsch
authors.forename: Oliver
authors.initials: O
authors.lastname: Bleiziffer
authors.forename: Baraa
authors.initials: B
authors.lastname: Zuhaili
authors.forename: Magdalena
authors.initials: M
authors.lastname: Fossum
authors.forename: Daniela
authors.initials: D
authors.lastname: Hoeller
authors.forename: Raphael
authors.initials: R
authors.lastname: Gheerardyn
authors.forename: Michael
authors.initials: M
authors.lastname: Chen
authors.forename: Scott
authors.initials: S
authors.lastname: Visovatti
authors.forename: Henry
authors.initials: H
authors.lastname: Svensson
authors.forename: Feng
authors.initials: F
authors.lastname: Yao
authors.forename: Elof
authors.initials: E
authors.lastname: Eriksson
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000503:physiopathology*; D005122:Exudates and Transudates / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000032:analysis; D006029:Glycosuria; D006943:Hyperglycemia; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D010982:Platelet-Derived Growth Factor / Q000378:metabolism; D034421:Sus scrofa; D016212:Transforming Growth Factor beta / Q000378:metabolism; D014945:Wound Healing / Q000502:physiology*
chemical_list: D001786:Blood Glucose; D010982:Platelet-Derived Growth Factor; D016212:Transforming Growth Factor beta; D007334:Insulin-Like Growth Factor I; D005947:Glucose