Reactive metabolites impair neuroretinal function

M Kolibabka; A Schlotterer; N Dietrich; T Fleming; P Nawroth; HP Hammes

doi:10.1055/s-0036-1580823

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Diabetologie und Stoffwechsel 2016; 11 - P76
DOI: 10.1055/s-0036-1580823

Reactive metabolites impair neuroretinal function

M Kolibabka ¹, A Schlotterer ¹, N Dietrich ¹, T Fleming ², P Nawroth ², HP Hammes ¹

¹5th Medical Department, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany
²Department of Medicine I and Clinical Chemistry, University of Heidelberg, Heidelberg, Germany

Congress Abstract

Reactive metabolites are involved in the development of neurovascular dysfunction observed in diabetic retinopathy. Accumulation of reactive metabolites such as methylglyoxal (MG) is found under chronic hyperglycemia. However, the direct effect of MG on the neurovascular unit has not been identified. The aim of this study was to determine the effects of MG on neuroretinal functions as assessed by electroretinography.

8-weeks-old normoglycemic Wistar rats were treated with MG (50mmol/L) for 4 weeks. Retinal levels of MG were measured at 7 days in a subgroup of MG supplemented and unsupplemented animals by derivatisation with 1,2-diamino-4,5-dimethoxybenzene and HPLC of the resulting quinoxaline adduct. At the end of the supplementation period, photopic multifocal electroretinography (mfERG) was used to analyze neuroretinal function and spectral-domain optical coherence tomography (SD-OCT) to quantify loss of retinal neurons.

After 7 days oral supplementation of MG lead to a significant increase of retinal MG compared to unsupplemented animals (8.82 ± 0.79 pmol/mg vs. 5.82 ± 0.84 pmol/mg; p < 0.01). After 4 weeks of treatment, the MG group showed a 34% loss of the b-wave amplitude (1.12 ± 0.12µV/field vs. 0.73 ± 0.14µV/field, Control vs. MG; p < 0.01). Neither a-wave amplitude (0.47 ± 0.17µV/field vs. 0.52 ± 0.16µV/field; n.s.) nor retinal thickness were significantly affected (190.2 ± 3.7 µm vs. 191.0 ± 7.7 µm; n.s.).

Methylglyoxal alone is able to disrupt the function of the retinal neurovascular unit. As the b-wave amplitude reflects the function of several different cell types in the inner retina, the major contributor on a cellular level needs to be identified.