title: Retinal function in relation to improved glycaemic control in type 1 diabetes.
abstract: OBJECTIVE
  To study long-term changes in retinal function in response to sustained glycaemia reduction in participants with type 1 diabetes.
  
  
  METHODS
  Prospective study using objective measures of retinal function in 17 participants with type 1 diabetes mellitus and minimal to moderate retinopathy who switched from conventional subcutaneous injection to continuous subcutaneous infusion of insulin (CSII).
  
  
  RESULTS
  Glycated haemoglobin HbA(1c) gradually decreased from 9.1% at baseline before CSII to 7.4% after 1 year on CSII. Glycaemia was markedly reduced within 1 week after initiation of CSII and remained stable thereafter. Dark adaptation and retinal electroretinographic function at 1, 4 and 16 weeks after initiation of CSII were comparable with baseline values, whereas a significant improvement in rod photoreceptor dark adaptation and dark-adapted b-wave amplitudes were seen after 52 weeks (time to rod-cone break -25% [p < 0.0001], time to a standardised rod intercept -13% [p < 0.0001], dark-adapted rod b-wave full-field amplitude +15% [p = 0.0125], standard combined rod-cone b-wave amplitude +8% [p = 0.049]). No detectable change was observed in cone adaptation, electroretinographic cone function or retinopathy.
  
  
  CONCLUSIONS
  After initiation of CSII, the retinal visual pathway of the rods improved with a delay of more than 4 months, over a time scale comparable with the duration of the diabetic retinopathy early worsening response to sustained glycaemia reduction. This indicates that glycaemia has a long-term effect on the disposition of functional capacity in the retinal visual pathway of rod photoreceptors, the cells that appear to be driving the development of diabetic retinopathy.
authors.affiliation: Department of Ophthalmology, Glostrup Hospital, Nordre Ringvej 57, 2600 Glostrup, Denmark. STKRHO02@glo.regionh.dk
authors.forename: S K
authors.initials: SK
authors.lastname: Holfort
authors.forename: K
authors.initials: K
authors.lastname: Nørgaard
authors.forename: G R
authors.initials: GR
authors.lastname: Jackson
authors.forename: E
authors.initials: E
authors.lastname: Hommel
authors.forename: S
authors.initials: S
authors.lastname: Madsbad
authors.forename: I C
authors.initials: IC
authors.lastname: Munch
authors.forename: K
authors.initials: K
authors.lastname: Klemp
authors.forename: B
authors.initials: B
authors.lastname: Sander
authors.forename: M
authors.initials: M
authors.lastname: Larsen
mesh_terms: D000328:Adult; D003922:Diabetes Mellitus, Type 1 / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology*; D003930:Diabetic Retinopathy / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology*; D004594:Electrophysiology; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007328:Insulin / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012160:Retina / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*
chemical_list: D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D007328:Insulin