The concentration of glycogen β-particles was measured in the inner retinal layers of normal and streptozotocin-diabetic rats with quantitative electron microscopic technics. Diabetes was uncontrolled and of short duration (thirty days). Blood glucose levels in the normal and diabetic animals were 76 ± 8 S.E. and 340 ± 25 S.E. mg./100 ml. Diabetes caused glycogen accumulation in the amacrine, bipolar, ganglionic, Müller and capillary mural cells. Quantitative estimates showed significant increases (p < 0.001) in the glycogen concentrations of cells in the nerve fiber layer (NFL), inner plexiform layer (IPL) and inner nuclear layer (INL) of the diabetic retinas.
The glycogen concentrations increased from 6.4 ± 0.41 β-particles per square micron in the normal to 10.5 ± 0.85 in the diabetic Müller endfeet (NFL); from 12.9 ± 1.5 to 38.6 ± 5.0 in the Müller processes (IPL); from 0.81 ± 0.13 to 3.37 ± 0.49 in the neural processes (IPL); from 2.7 ± 0.66 to 17.3 ± 2.4 in the amacrine cell bodies (INL). Diabetic glycogen accumulation occurred at a greater rate in the neurons than in the Müller cells. The amacrine neurons were the most severely affected and contained massive glycogen deposits in their cytoplasm.
The glycogen concentration in the neurons was less than that of the Müller cells. However, the Müller cells represent only ∼10 per cent of the total cytoplasm of the IPL, whereas the neurons occupy ∼90 per cent of this layer. From the above data, it is evident that the neurons contain about one third of the total glycogen of the normal IPL. In the diabetic IPL, the total glycogen is approximately evenly distributed between the neural and glial compartments.