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Meibomian gland lipid secretion, commonly known as meibum, refers to the holocrine lipid-rich secretions produced by meibomian glands, which are large sebaceous glands embedded in the tarsal plates of the eyelids (30-40 in the upper lid and 20-30 in the lower). These lipids form the outermost tear film lipid layer (TFLL), creating a hydrophobic barrier that prevents excessive evaporation of the aqueous tear layer, stabilizes the tear film, lubricates the ocular surface, and protects the cornea and conjunctiva from desiccation and environmental hazards. Secretion occurs through blinking-induced pressure from the orbicularis and Riolan muscles, delivering meibum via ductules to eyelid margins where it mixes with tears. The composition includes non-polar lipids like wax esters (32%), cholesterol esters (27%), triglycerides, free fatty acids, and polar lipids such as phospholipids, synthesized locally in maturing meibocytes via pathways involving PPARγ and enzymes like ELOVL1-7. In disease, particularly meibomian gland dysfunction (MGD), altered lipid profiles—such as reduced unsaturated fatty acids, decreased cholesterol esters, increased saturated lipids, and elevated free linoleic acid—lead to viscous, toothpaste-like meibum, tear film instability, inflammation, and dry eye symptoms. While not a molecular therapeutic target like a receptor or enzyme, MGD treatments target gland function indirectly through therapies like minocycline, which reduces branched-chain fatty acids, or lid hygiene to improve expressibility. No direct drugs interact with this secretion as a target, but lipidomic changes serve as biomarkers for MGD diagnosis and monitoring.
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