Diabetic retinopathy (DR) is the leading cause of blindness, and chronic hyperglycemia is the primary factor for developing diabetic retinopathy. DR pathophysiology involves abnormal vascular permeability with vascularization in the proliferative stage. A deficiency of DHA plays a crucial role in developing diabetic retinopathy. Lack of DHA is linked with abnormal electroretinogram (ERG) and retinal dysfunction. Many studies reported the beneficial effects of DHA on visual functions. We have evaluated the percentage of DHA and ARA in the retina to investigate the relationship between and measured retinal function in diabetic mice and diabetic patients. The present studies demonstrated that the reduction of DHA in diabetic mice and patients correlated with the levels of fatty acid elongation, metabolism, and inflammation markers. Interestingly, the retina DHA levels were 50% more deficient in diabetic patients than control patients. A similar trend was observed in preclinical, and retina DHA levels were modulated for diabetic mice compared to control mice. In this study, we have used the db/db mice extensively in recent years to study diabetic retina pathogenesis and to investigate potential therapeutic interventions. We found that DHA levels in the retina are less than 55% in db/db mice compared to control mice. ERG and OCT were used after six months to determine the effect of DHA reduction on retinal function. ERG showed a significant decrease in a-wave and b-wave function in the retina of db/db mice compared to control mice. This data indicates that in addition to DHA reduction, an abnormal ERG, a significant decrease in retinal thickness, and alteration in retina microvascular changes in db/db mice. These results warranted a study of further DHA links to DR pathogenesis. This novel strategy would open the possibilities for developing preventive approaches to DR. Increasing the retinal DHA will help treat and prevent diabetic retinopathy.
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Dhavamani et al. (2024) studied this question.
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