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The ocular surface is protected from desiccation by the tear film. Alterations to the tear film can lead to the development of dry-eye disease (DED). The prevalence of DED is 5–30%, and increases with age. DED is characterized by increased tear osmolality due to lack of tear production or increased evaporation. Hyperosmolality damages ocular surface cells and leading to inflammation of the ocular surface. Osmoprotectants such as betaine can limit the ensuing damage. This chapter outlines evidence for betaine as an osmoprotectant on the ocular surface. Betaine tear concentration is 2.5 ± 1.9 µMm. Betaine is transported into human corneal limbal epithelial cells via the osmoregulated betaine/γ-aminobutyric acid (GABA) transporter, BGT-1. 10 mM betaine reduces cell shrinkage in hyperosmolar media, and limits cell death via the apoptotic pathway, reducing activation of caspase-8, -9 and -3/7. Betaine downregulates production of the key inflammatory mediator, Tumor Necrosis Factor-(TNF)-α by approximately 50%. This evidence points to a role for betaine in maintenance of the ocular surface in dry-eye disease and indicates the potential for betaine to be used in ocular therapies for dry-eye.

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