Table 3.
Reference | Group | Type | Platform | Altered metabolites | Conclusion |
---|---|---|---|---|---|
Munipally et al. (2011) | 35 control subjects, 22 NPDR patients and 24 PDR patients | Serum | HPLC | Greater expression of kynurenine, kynurenic acid and 3‐hydroxykynurenine in NPDR and PDR↑ | Results indicate a probable association of IDO and tryptophan metabolites with DR |
Barba et al. (2010) | 22 patients with T1DM with PDR and 22 non‐diabetic patients with a macular hole | Vitreous | 1H NMR | Lactate and glucose↑; galactitol and ascorbic acid↓ | Apart from the greater abundance of lactate and glucose, significant deficits of galactitol and ascorbic acid are the main metabolic fingerprints of vitreous fluid from PDR patients |
Li et al. (2011) | 2 perspectives studies | Serum | GC‐MS | Fatty acids, amino acids and glucose | Results showed the usefulness and validity of combining both Western and Chinese medicine to study the subtypes of DR and the mechanisms involved |
Freeman et al. (2011) | STZ‐diabetic and healthy control rats | SN, DRG, TG | GC‐MS, UHPLC‐MS | Increase in glucose and polyol pathway intermediates in diabetes; upregulation of mitochondrial oxidative phosphorylation and perturbation of lipid metabolism were found in the distal SN that were not present in the corresponding cell bodies of the DRG or the cranial TG↑ | Spatial metabolic dysfunction suggests a failure of energy homeostasis and/or oxidative stress, specifically in the distal axon/Schwann cell‐rich SN |
DR, diabetic retinopathy; DRG, lumbar 4/5 dorsal root ganglia; GC‐MS, gas chromatography‐mass spectrometry; HPLC, high‐performance liquid chromatography; IDO, indoleamine 2, 3‐dioxygenase; NPDR, non‐proliferative diabetic retinopathy; PDR, proliferative diabetic retinopathy; STZ, streptozotocin; SN, sciatic nerve; T1DM, type 1 diabetes mellitus; TG, the trigeminal ganglia; UHPLC‐MS, ultra‐high‐performance liquid chromatography‐mass spectrometry.