Diabetes produces dramatic changes in retinal microvasculature, trigge
ring endothelial cell proliferation and microaneurysms. Capillaries be
come weakened, releasing blood into vitreal and retinal spaces. Photor
eceptors become occluded and separated from the choriocapillaris, resu
lting in visual acuity decline, detachment and cell death. Several mod
els have been developed that have proved useful for the study of this
disease, resulting in a better understanding of the processes involved
. Streptozotocin treatment affects the pancreatic beta cells, rapidly
reducing them until insulin is no longer synthesized in sufficient amo
unts. The galactosemic model shifts metabolism away from glucose, incr
easing aldose reductase and retinal polyol metabolism. Finally, two we
eks of cycled oxygen from high to low tension every 24 hours, followed
by return to room air, triggers microangiogenesis in developing retin
as. Use of these models, separately or in combination, as well as elec
troretinographic analysis, has begun to reveal the events taking place
as diabetic retinopathy progresses. Endothelial cells become separate
d from pericytes as basement membranes thicken, and vascular endotheli
al growth factor increases, triggering their proliferation. Finally, e
arly changes occurring within photoreceptors can now be studied.