Abstract
To identify the role of lipocalin-2 (LCN2) in diabetic cataract (DC) and diabetic retinopathy (DR), diabetes models were established in wild-type (WT) and LCN2 gene knockout (LCN2-/-) mice by streptozotocin (STZ), this study aimed to investigate the metabolic alterations and underlying pathways in the lens and retina. Untargeted metabolomic analysis was performed on the lenses and retinas of WT and LCN2-/- diabetic mice, and relevant pathways were predicted through bioinformatics analysis. LCN2 was notably elevated in the anterior capsules of DC and the vitreous humor of DR. Metabolic profiling of the lenses and retinas of diabetic mice indicated that the differential metabolites were mostly amino acids, fatty acids, carbohydrates, and their derivatives. In the lenses of STZ-induced WT mice, the differential abundance score (DA-score) revealed an increase in metabolites associated with the citrate (or TCA) cycle and glucagon signaling pathway, whereas a decrease was observed in metabolites related to cholesterol metabolism. After the knockout of LCN2, the DA-score indicated that the majority of metabolites involved in cholesterol metabolism, cysteine and methionine metabolism, and tryptophan metabolism were diminished. In the STZ-induced retina, there was an increase in metabolites associated with the mTOR signaling pathway, and this increase was inhibited by the knockout of LCN2. Numerous metabolites exhibited substantial alterations in the lenses and retinas of diabetic mice. Untargeted metabolomics has provided insights into the function of LCN2 in DC and DR. These changes in metabolites, along with their related pathways, could be the mechanisms by which LCN2 modulated DC and DR.
Published Version
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