Altered retinal metabolism in diabetes. I. Microanalysis of lipid, glucose, sorbitol, and myo-inositol in the choroid and in the individual layers of the rabbit retina.

Total lipid, sucrose, glucose, sorbitol and myo-inositol contents in individual layers from normal and alloxan-diabetic rabbit retinas were measured using gravimetric and enzymatic microtechniques. Pure samples of nine retinal layers were microdissected from freeze-dried retinal cryosections. The lipid content was measured by loss of weight after ethanol and hexane extraction. Retinal lipid varied 3-fold across the retina and was not influenced by diabetes. Sucrose, glucose, sorbitol, and myo-inositol were measured with fluorimetric microassays. Sucrose infused intravenously prior to sampling the tissue did not traverse the outer blood retinal barrier of the normal or the diabetic retina. In both normals and diabetics, glucose followed a diffusional curve, with outer and inner retinal concentrations, respectively, equal to choroidal blood and vitreal glucose concentrations. Sorbitol was elevated in all retinal layers of diabetic animals. The peak sorbitol concentrations, of 2 mmol/kg defatted dry weight in diabetics, were not high enough to be osmotically significant. Retinal myo-inositol, of the order found in brain tissue (10-30 mmol/kg defatted dry tissue), was decreased by 22-40% in all retinal layers of the diabetics. The results indicate that diabetes affects the metabolism of retinal structures independently of the small blood vessel disease that is the hallmark of diabetes of long duration. It is conceivable that primary intraretinal metabolic alterations cause, aggravate, or perpetuate the well known degenerative processes that occur in retinal blood vessels in diabetes.