Paul Beaumont

GROWTH HORMONE, SORBITOL, AND DIABETIC CAPILLARY DISEASE

Abstract It is suggested that excessive secretion of growth hormone (G.H.) may be the cause of diabetic capillary disease. G.H. hypersecretion inhibits glucose metabolism and results in an accumulation of sorbitol. This in turn causes an osmotic imbalance resulting in damage to tissues.

CLASSIFICATION OF DIABETIC RETINOPATHY, WITH THERAPEUTIC IMPLICATIONS

Abstract A classification of diabetic retinopathy based on clinical observation and investigation is presented. There are four groups: diffuse capillary retinopathy, diabetic lipid retinopathy, diabetic obstructive retinopathy, and minimal diabetic retinopathy. Each group has distinct aetiological features, and the classification can be used to direct therapy.

Glycogen Accumulation in Retinal Neurons and Glial Cells of Streptozotocin-diabetic Rats: Quantitative Electron Microscopy

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.