Intracapsular metformin bioactivity and its role in posterior capsule opacification
Abstract
Background/aims: Posterior capsule opacification (PCO) is the most frequent long-term complication after cataract surgery, caused by proliferation of residual lens epithelial cells (LECs). Metformin, a common antidiabetic drug with antifibrotic properties, may act as a pharmacological modulator of this process. The purpose was to assess whether systemically administered metformin reaches the human lens capsule and inhibits LEC proliferation at physiologically relevant concentrations.
Methods: Metformin concentrations were quantified in serum and lens capsule tissue of patients with type 2 diabetes mellitus undergoing cataract surgery using high performance liquid chromatography-tandem mass spectrometry. Patients were stratified into low-dose (≤1000 mg/day) and high-dose (>1000 mg/day) groups. Additionally, anterior lens capsules from non-diabetic donors were cultured with or without metformin (0.75 pg/µL), and LEC proliferation was monitored for 14 days by live-cell imaging.
Results: Metformin was detectable in both serum and capsule specimens, with a significant correlation between compartments (r=0.553, p=0.011). Capsule concentrations were similar across dose groups, while serum levels were higher in the low-dose group. In vitro, metformin significantly reduced LEC proliferation compared with controls (p<0.001).
Conclusion: Systemically administered metformin reaches the human lens capsule in vivo and suppresses LEC proliferation in vitro at clinically relevant…
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