Abstract
Biochemical mechanisms of cataract in diabetes mellitus
Highlights
In the 1990s, the incidence of type 1 diabetes in children varies between 3.4 and 6.3% depending on the country, with an increased incidence in children under 5 years [1]
Diabetes mellitus is associated with many systemic complications, ocular impairment being quite common among adult patients
Cataract is a multifactorial disorder, diabetes mellitus playing an central role in its pathogenesis
Summary
In the 1990s, the incidence of type 1 diabetes in children varies between 3.4 and 6.3% depending on the country, with an increased incidence in children under 5 years [1]. The intracellular accumulation of sorbitol generates a hyperosmotic effect, with the formation of hydropic fibers of the lens that degenerate and lead to cataract formation. DHAP is reduced by NADH to diacylglycerol (DAG) which is an activator of PKC Once this protein kinase is activated, all three isoforms are activated: PKC-β, increases VEGF (vascular endothelial growth factor), PAI-1 (plasminogen activator inhibitor-1) NADPH (nicotinamide adenine dinnucleotide phosphate) and decreases eNOS (endothelial nitric oxide synthase) expressions, which will trigger the angiogenesis process. Increased glucose levels in aqueous humor can lead to glycation of lens proteins, a process that generates increased levels of AGEs [16,18]. AGEs formed by lipids, nucleic acids and proteins, bind to specific cell surface receptors and lead to ROS generation. Increased serum levels of malondialdehyde, thiobarbituric acid reactive substances, decreased SOD levels, suggest the existence of OS in diabetic patients and lens degeneration [20,21]
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