title: The influence of alloxan-induced diabetes on Müller cell contraction-promoting activities in vitreous.
abstract: OBJECTIVE
  Previous studies from this laboratory revealed that vitreous insulin-like growth factor biological activity increases in diabetes and that this change can precede the onset of proliferative diabetic retinopathy. The goal of this study was to characterize this phenomenon in an animal model of alloxan-induced diabetes.
  
  
  METHODS
  Swine made diabetic with intravenous alloxan were euthanized at times varying from 0 to 90 days. Vitreous samples from normal and diabetic swine were evaluated for changes in Müller cell contraction-promoting activity, the presence of insulin-like growth factor binding protein (IGFBP), and carbonic anhydrase-I and -II. Ocular tissues from these animals were also evaluated for changes in contraction-promoting growth factors and IGFBP message levels.
  
  
  RESULTS
  Alloxan-induced diabetes is associated with significant increases in vitreous Müller cell contraction-promoting activity that are present in as few as 30 days and are sustained for at least 90 days. Biochemical studies revealed that the increases cannot be attributed to loss of growth factor-attenuating IGFBPs, changes in local expression of contraction-promoting growth factors, or vitreous hemorrhage.
  
  
  CONCLUSIONS
  The previously reported increases in Müller cell contraction-promoting activity detected in human diabetic vitreous are present in diabetic swine within 30 days of chemical induction. The increase does not appear to be attributable to loss of growth factor control, increases in local growth factor expression, or vitreous hemorrhage, suggesting that other mechanisms are involved. It is the authors' speculation that diabetes induces blood-vitreous barrier changes that allow a different subset of plasma proteins to enter vitreous fluids.
authors.affiliation: Department of Ophthalmology University of Alabama School of Medicine, Birmingham, Alabama 35294, USA.
authors.forename: Jeffery L
authors.initials: JL
authors.lastname: King
authors.forename: John O
authors.initials: JO
authors.lastname: Mason
authors.forename: Samuel C
authors.initials: SC
authors.lastname: Cartner
authors.forename: Clyde
authors.initials: C
authors.lastname: Guidry
mesh_terms: D000496:Alloxan / Q000633:toxicity; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D015153:Blotting, Western; D024401:Carbonic Anhydrase I / Q000378:metabolism; D024402:Carbonic Anhydrase II / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D003930:Diabetic Retinopathy / Q000378:metabolism*; D019084:Fluorescent Antibody Technique, Indirect; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006943:Hyperglycemia / Q000378:metabolism; D018969:Insulin-Like Growth Factor Binding Proteins / Q000378:metabolism; D008297:Male; D009457:Neuroglia / Q000378:metabolism*; D060888:Real-Time Polymerase Chain Reaction; D012160:Retina / Q000473:pathology*; D013552:Swine; D014822:Vitreous Body / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; D005904:Glial Fibrillary Acidic Protein; D018969:Insulin-Like Growth Factor Binding Proteins; D000496:Alloxan; D024401:Carbonic Anhydrase I; D024402:Carbonic Anhydrase II