The ocular surface in type 2 diabetes: pathophysiology and impact of anti-diabetic drugs

Type 2 diabetes is a chronic, systemic, metabolic disorder characterized by persistent hyperglycemia and associated with a broad spectrum of complications, including those affecting the ocular surface. This article reviews the structural, biochemical, and neuropathic changes observed in the ocular surface of patients with diabetes. Hyperglycemia and associated metabolic imbalances lead to tear film instability, inflammation, oxidative stress, and peripheral neuropathy, contributing to the pathogenesis of dry eye disease, impaired corneal wound healing and corneal neuropathy. In addition, systemic factors such as glycemic control, inflammatory cytokines, and microvascular impairment have direct impact on ocular surface homeostasis. This review also evaluates the effects of antidiabetic therapies on the ocular surface. Recent studies suggest that drugs such as metformin, sodium-glucose co-transporter 2 inhibitors, glucagon like peptide-1 receptor agonists, and insulin along with glucose control, may offer the ocular surface protective benefits. Evidence supports their roles in reducing ocular surface inflammation, promoting corneal nerve regeneration, and improving tear film homeostasis. A comprehensive understanding of these factors may facilitate improved screening, early diagnosis, and integrative management of ocular surface disorders in type 2 diabetes.