Abstract

Dr. Priyanshi Awasthi, Prof. S. K. Singh, Dr. Diksha Sareen* and Prof. O. P. S. Maurya

ABSTRACT

Meibomian glands are modified sebaceous glands that line the upper and lower eyelids in a single row. They are embedded in the tarsal plate in a single line with 20 to 40 with a median of 30 in the upper lid. In the lower lid they are about 20-30 with a median of 26 glands. Their secretory products contain a complex mixture of lipids and proteins and are termed as meibum which is liquid at room temperature. The secreted lipid is stored in the duct system that terminates in the orifices with a muscular cuff that open onto the lids. It is released on the ocular surface in small amounts with each blink forming a reservoir with about 30 times more lipid than needed for each blink. According to the Tear film and Ocular Surface Society, (International workshop on MGD, 2011)[1] Meibomian gland dysfunction (MGD) is defined as a chronic, diffuse abnormality of the meibomian glands, commonly characterized by terminal duct obstruction and/or qualitative/ quantitative changes in the glandular secretion. It may result in alteration of the tear film, symptoms of eye irritation, clinically apparent inflammation, and ocular surface disease. Recently, a study from Ding et al (2015)[2] demonstrated that insulin stimulated the proliferation of immortalized human meibomian gland epithelial cells (HMGECs), whereas high glucose was found to be toxic for HMGECs . This suggests that insulin resistance/deficiency and hyperglycemia are deleterious for HMGECs which supports our hypothesis that diabetes may be associated with MGD.