Beyond Hyperglycemia, Evidence for Retinal Neurodegeneration in Metabolic Syndrome

We evaluated the retinal effects of systemic metabolic changes clustered under the umbrella of metabolic syndrome (MetS) in comparison with age-matched healthy subjects.

Spectral-domain optical coherence tomography (OCT) retinal segmentation analysis of 29 patients with MetS and 36 control subjects was performed. Patients with diabetes mellitus (DM), uncontrolled hypertension, retinopathy, high myopia or hyperopia, and posterior segment surgery, were excluded from analysis. The control group (CG) was selected from age- and sex-matched healthy lean subjects. Mean thickness values of individual retinal layers in nine macular early treatment of diabetic retinopathy study (ETDRS) subfields were determined.

The MetS group had a significantly thinner ganglion cell layer in two (MetS, 52.4 ± 5.1 μm; CG, 54.8 ± 3.8 μm; P = 0.030), thinner inner plexiform layer in three (MetS, 39.8 ± 4.4 μm; CG, 43.0 ± 3.5 μm; P = 0.003), thinner photoreceptor layer in seven (MetS, 79.4 ± 2.9 μm; CG, 81.1 ± 2.9 μm; P = 0.009) of nine ETDRS subfields. No difference was found in nerve fiber, inner nuclear, outer plexiform, and outer nuclear layers.

The patients with MetS had thinner inner retinal layers and photoreceptor layer in OCT segmentation analysis, which suggests that inherent factors of MetS, such as insulin resistance and adipose tissue-derived inflammation, might have a neurodegenerative effect independent of the hyperglycemic levels associated with DM. Therefore, beyond glycemic control measures, weight reduction also might be advised to overweight patients with type 2 DM and MetS to prevent the occurrence of retinal neurodegeneration.