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(Investigative Ophthalmology and Visual Science. 2005;46:2878-2885.)
© 2005 by The Association for Research in Vision and Ophthalmology, Inc.
DOI:  10.1167/iovs.04-1458
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Monocarboxylate Transporter Expression Remains Unchanged during the Development of Diabetic Retinal Neuropathy in the Rat

Christopher J. Layton,1 Glyn Chidlow,1 Robert J. Casson,1 John P. M. Wood,1 Mark Graham,2 and Neville N. Osborne1

1From the Nuffield Laboratory of Ophthalmology, Oxford University, Oxford, United Kingdom; and 2AstraZeneca R&D, Loughborough, United Kingdom.

PURPOSE. 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 PKC{alpha}, 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 PKC{alpha} 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.




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