title: Monocarboxylate transporter expression remains unchanged during the development of diabetic retinal neuropathy in the rat.
abstract: OBJECTIVE
  To determine the effect of diabetes on monocarboxylate transporter (MCT) expression in the rat retina.
  
  
  METHODS
  Diabetes was induced in Wistar rats by a single intraperitoneal injection of streptozotocin (62.5 mg/kg). Rats were killed after 10 weeks, and the retinal levels of PKCalpha, bFGF, glial fibrillary acidic protein (GFAP), caspase-3, and MCT1, -2, and -4 were assessed with immunoblot analysis and RT-PCR. Hippocampal samples were used as a comparison. In other animals, the retinas were processed histologically and sections stained for the breakdown of DNA (TUNEL procedure) and for the distribution of MCT1, -2, and -4.
  
  
  RESULTS
  Diabetic rats exhibited cataract formation, elevated blood glucose levels, and polydipsia. Retinal levels and distribution of MCT1, 2, and -4 were similar in the diabetic and age-matched control groups; however, the early retinopathy markers bFGF and PKCalpha were significantly elevated in the diabetic retinas but not in the hippocampal samples. ERG recordings showed decreased oscillatory potentials in the diabetic group, and TUNEL staining was most evident in the photoreceptor layer. Activated caspase-3 levels were elevated in the diabetic retina.
  
  
  CONCLUSIONS
  The expression of retinal MCT1, -2, and -4 is unaffected after 10 weeks of diabetes in rats. It appears unlikely that diabetic retinal neuropathy is a result of a hyperglycemic induction of altered MCT expression.
authors.affiliation: Nuffield Laboratory of Ophthalmology, Oxford University, Oxford, United Kingdom. cjlayton@bigpond.com
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Layton
authors.forename: Glyn
authors.initials: G
authors.lastname: Chidlow
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Casson
authors.forename: John P M
authors.initials: JP
authors.lastname: Wood
authors.forename: Mark
authors.initials: M
authors.lastname: Graham
authors.forename: Neville N
authors.initials: NN
authors.lastname: Osborne
mesh_terms: D000818:Animals; D015153:Blotting, Western; D053148:Caspase 3; D020169:Caspases / Q000235:genetics / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D003930:Diabetic Retinopathy / Q000378:metabolism*; D004596:Electroretinography; D016222:Fibroblast Growth Factor 2 / Q000235:genetics / Q000378:metabolism; D015870:Gene Expression; D005904:Glial Fibrillary Acidic Protein / Q000235:genetics / Q000378:metabolism; D007124:Immunoenzyme Techniques; D020287:In Situ Nick-End Labeling; D008297:Male; D027501:Monocarboxylic Acid Transporters / Q000235:genetics* / Q000378:metabolism; D009124:Muscle Proteins / Q000235:genetics* / Q000378:metabolism; D011493:Protein Kinase C / Q000235:genetics / Q000378:metabolism; D051571:Protein Kinase C-alpha; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012160:Retina / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D027981:Symporters / Q000235:genetics* / Q000378:metabolism; D000099233:Monocarboxylate Transport Protein 1
chemical_list: D053148:Caspase 3; D020169:Caspases; D016222:Fibroblast Growth Factor 2; D005904:Glial Fibrillary Acidic Protein; D027501:Monocarboxylic Acid Transporters; D009124:Muscle Proteins; D011493:Protein Kinase C; D051571:Protein Kinase C-alpha; D012333:RNA, Messenger; D027981:Symporters; D000099233:Monocarboxylate Transport Protein 1; C516342:Slc16a3 protein, rat; C091633:Slc16a7 protein, rat; C505410:Casp3 protein, rat