In patients with type 2 diabetes, the overexpression of N-glycosidically linked human type 1 cytokeratin may disrupt the lens capsule and affect permeability, contributing to cataract progression, according to findings published in Clinical Ophthalmology.
After aging, diabetes is one of the most significant risk factors for cataracts. There are several ways that Type 2 diabetes mellitus facilitates the formation of cataracts. While the link between the overproduction of sorbitol and increased osmotic pressure has been studied at length, according to investigators, there is increasing evidence that lens capsule alterations also are responsible for cataract development.
To better understand cataract development, researchers analyzed the glycosylation profile of human lens epithelial cells (HLECs) from anterior lens capsules of patients with type 2 diabetes mellitus and non-diabetic patients undergoing routine cataract surgery.
They found that metabolic and age-related cataracts show different demographics and progression patterns. Patients with type 2 diabetes exhibit a relatively faster progression and are diagnosed at an earlier age compared with patients without diabetes with age-related cataracts.
Specifically, hematoxylin-eosin staining revealed HLECs alterations in samples from people with diabetes. From lectins with different sugar specificities, concanavalin A showed significant differences, labeling homogeneously in the cytoplasm and cell membranes in non-diabetic capsules. In diabetic capsules, in addition to membrane and cytoplasm labeling, there were perinuclear vesicles with high concanavalin A labeling, according to the study. Two-dimensional gel electrophoresis showed that diabetes patients have a ~65-kDa spot with an isoelectric point of 5.5 with a higher density compared with capsules in non-diabetic patients. Liquid chromatography-tandem mass spectrometry analysis showed 62% homology with type-1 cytokeratin. Immunohistochemistry using anti-pan cytokeratin antibody revealed co-localization with concanavalin A, and a lectin blot revealed with concanavalin A showed a band of ~65 kDa. This molecular weight corresponds to human type 1 cytokeratin.
Investigators noted that a significant limitation of the study is the small number of samples.
Disclosure: One study author declared affiliations with the biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of authors’ disclosures.
Ramos-Martínez I, Vivanco-Rojas O, Juárez-Domínguez B, et al. Abnormal n-glycosylation of human lens epithelial cells in type-2 diabetes may contribute to cataract progression. Clin Ophthalmol. 2021;15(3):1365-1373. doi:10.2147/OPTH.S300242
This article originally appeared on Ophthalmology Advisor