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Diabetic retinopathy and carbohydrate metabolism

Those of you who have had dealings with diabetics will be only too aware of the disabling nature of diabetic retinopathy. This condition is a long-term complication of diabetes that often does not become manifest for 10-20 years after the onset of the disease. Initially the sufferer may experience visual disturbance, but as the condition progresses the result is total blindness. Diabetic retinopathy is now the most common cause of non-congenital blindness in this country. The pathology is well described by many workers in the field (Caird & Pirie, 1969; Kohner & Oakley, 1975). Essentially diabetic retinopathy is a disease of the microvascular system in the retina. Blood is supplied by the optic artery and enters the retina near the optic disc. From here arteries radiate out and branch to form a capillary network lying within the retina. Initially microaneurysms, areas of focal thickening and capillary non-perfusion are seen. Eventually these progress to exudates, haemorrhages and the proliferative stages of new vessel fofmation. Although sufferers from this condition have been helped considerably in the last few years with the techniques of photocoagulation, these do not necessarily offer a permanent cure or provide a method of prevention. In order to have any hope of permanent prevention much more needs to be understood about the initial pathological lesion occurring in the retinal vascular system. Epidemiological studies have not provided us with any strong lead, although it is well established that the risk of retinopathy increases with the duration and the age at onset of the diabetes (Sorsby, 1966). Increasingly, though, investigators and clinicians in this field are becoming convinced of the importance of well-controlled, low blood glucose concentrations, in the prevention of the onset of long-term diabetic complications (Cahill et al. 1976). Retinopathy is only one of a number of long-term complications of diabetes. Others include cataract, nephropathy and neuropathy. It is of interest that the tissues affected (retina, lens, kidney and nervous tissue) all share the characteristic of being insensitive to the effects of insulin. Tissues such as muscle and adipose tissue are sensitive to the effects of insulin. In these tissues insulin allows glucose carried in the blood to be taken up. These insulin-sensitive tissues never exhibit any of the long-term degenerative changes of diabetes, whereas the tissues affected by the long-term complications of diabetes are all insensitive to insulin. This means that they bear the full brunt of any raised blood glucose levels. As the blood glucose rises the level of glucose in these tissues also rises. The ‘juvenile-onset’ type of diabetes is of course characterized by a lack of endogenous insulin where as the ‘maturity-onset’ diabetics often exhibit hyper-