title: Corneal function during normal and high serum glucose levels in diabetes.
abstract: OBJECTIVE
  To assess corneal structure and the effects of acute hyperglycemia on corneal function in subjects with type 1 diabetes.
  
  
  METHODS
  Twenty-one diabetic and 21 nondiabetic volunteers of similar age were recruited. Baseline measurements of intraocular pressure (IOP), corneal thickness (CT), corneal autofluorescence (CAF), corneal sensitivity (CST), central and temporal endothelial cell density (DenC and DenT), and coefficient of variation in cell area (CVC and CVT) were taken. Corneal edema was induced, and the percent recovery per hour (PRPH) from hypoxic edema and endothelial permeability to fluorescein were determined. These procedures were done twice in the diabetic subjects under controlled euglycemic (EG) and hyperglycemic (HG) conditions, and once in control subjects while they were fasting.
  
  
  RESULTS
  Substantial differences in baseline measurements were found for IOP, CT, CAF, CST, DenC, and CVT. The mean +/- SE corneal swelling in the HG diabetic subjects (51.6 +/- 2.3 microm) was less when compared to the swelling in the EG diabetic subjects (56.2 +/- 1.87 microm, P = 0.05) and the control subjects (58.9 +/- 1.56 microm, P = 0.011). During euglycemia, the mean +/- SE PRPH was less in diabetic subjects than in control subjects (65.0 +/- 3.20 versus 73.8 +/- 1.81%/hour, P = 0.02) but did not differ in diabetic subjects under EG and HG conditions (65.0 +/- 3.20 versus 67.7 +/- 3.1%/hour, P = 0.56). No significant differences were noted between groups in endothelial permeability.
  
  
  CONCLUSIONS
  In addition to differences in baseline corneal structure, diabetic subjects showed less corneal swelling and reduced corneal recovery from hypoxia than did control subjects. During acute hyperglycemia, corneal swelling was less than during euglycemia in diabetic subjects, which suggests that hyperglycemia affected corneal hydration control.
authors.affiliation: Morton D. Sarver Laboratory for Cornea and Contact Lens Research, School of Optometry, University of California at Berkeley, 94720-2020, USA.
authors.forename: N A
authors.initials: NA
authors.lastname: McNamara
authors.forename: R J
authors.initials: RJ
authors.lastname: Brand
authors.forename: K A
authors.initials: KA
authors.lastname: Polse
authors.forename: W M
authors.initials: WM
authors.lastname: Bourne
mesh_terms: D000208:Acute Disease; D000328:Adult; D001786:Blood Glucose / Q000502:physiology; D002452:Cell Count; D048429:Cell Size; D003315:Cornea / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000503:physiopathology*; D003930:Diabetic Retinopathy / Q000097:blood / Q000503:physiopathology*; D004728:Endothelium, Corneal / Q000378:metabolism / Q000473:pathology; D005260:Female; D015590:Fluorophotometry; D006801:Humans; D006943:Hyperglycemia / Q000097:blood / Q000503:physiopathology; D007429:Intraocular Pressure; D008297:Male; D008875:Middle Aged; D010539:Permeability; D012677:Sensation / Q000502:physiology
chemical_list: D001786:Blood Glucose