Diabetologie und Stoffwechsel 2019; 14(S 01): S52-S53
DOI: 10.1055/s-0039-1688259
Poster
Sehen und Fühlen
Georg Thieme Verlag KG Stuttgart · New York

Glucosamine is neuroprotective in the diabetic retina

R Eshwaran
1   Experimental Pharmacology Mannheim, Medical Faculty Mannheim, European Center for Angioscience, Universität Heidelberg, Mannheim, Germany
,
M Kolibabka
2   5th Medical Clinic, Medical Faculty Mannheim, Universität Heidelberg, Mannheim, Germany
,
K Kohl
2   5th Medical Clinic, Medical Faculty Mannheim, Universität Heidelberg, Mannheim, Germany
,
HP Hammes
2   5th Medical Clinic, Medical Faculty Mannheim, Universität Heidelberg, Mannheim, Germany
,
T Wieland
1   Experimental Pharmacology Mannheim, Medical Faculty Mannheim, European Center for Angioscience, Universität Heidelberg, Mannheim, Germany
,
Y Feng
1   Experimental Pharmacology Mannheim, Medical Faculty Mannheim, European Center for Angioscience, Universität Heidelberg, Mannheim, Germany
› Author Affiliations
Further Information

Publication History

Publication Date:
07 May 2019 (online)

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Background and Aim:

Diabetic retinopathy is the most common microvascular complication of diabetes which presents with concomitant neuronal damage. Glucosamine is a hexose amino sugar that exhibits anti-inflammatory and anti-oxidative properties and might be involved in the modulation of endothelial cell activity. In this study, we therefore investigated the potential of glucosamine treatment in diabetic retinopathy.

Materials and methods:

Diabetes was induced by i.p. injection with streptozotocin in 8-week-old C57Bl6 mice. The mice were treated with glucosamine from the following week and analyzed 6 months after diabetes induction. Optical Coherence Tomography (OCT) and electroretinography (ERG) were used to evaluate retinal neuronal function. Retinal vascular alteration was assessed using retinal digest preparations.

Results:

Glucosamine did not alter blood glucose and HbA1c levels between the groups, but significantly increased body weight exclusively in non-diabetic animals. Retinal thickness was uniform throughout the groups. Glucosamine treatment was able to rescue the loss of b-wave seen through electroretinography in diabetic animals compared with non-diabetic controls. Only diabetic retinas showed a significant decrease in pericyte number and an increase in the formation of acellular capillaries. Pericyte loss and formation of acellular capillaries were not altered by glucosamine treatment.

Conclusion:

Our results suggest that glucosamine treatment might be neuro- but not vasoprotective in the diabetic retina.