Abstract

Diabetes mellitus is a bipartite disease characterized by an immediate need to regulate the metabolism of carbohydrate, protein and fat and accompanied by an ultimate peril of degenerative complications. Despite expert clinical efforts to control hyperglycaemia, it is a universal experience that complications continue to appear with increasing frequency as a product of the duration of the disease. Advanced systemic lesions sometimes occur in patients with only mild disturbances of carbohydrate tolerance, hence, the hypothesis has been advanced that diabetic angiopathy is a collateral phenomenon progressing simultaneously but somewhat independently of the more easily monitored metabolic defects. But all diabetics, regardless of the severity of their disease, share one common factor; they experience insulin deficit for periods throughout the day when their beta cells fail to release insulin appropriately. Ironically enough, relative hyperinsulinism is also commonplace amongst diabetic subjects either as a belated but exaggerated response to a stimulus or because of the imperfections of manual insulin therapy. Insulin is involved in most metabolic processes and the hormone must be available in the correct pattern with the appropriate duration, dosage and timing to support all of its necessary functions, some of which may be necessary to prevent vascular disease. Recent evidence strongly indicates that rigid control of blood sugar is accompanied by a reduction in microvascular complications (Crofford et al, 1975). Studies in animals by Mauer et al (1974), Sutherland et al (1975), Weil et al (1975), Orloff et al (1975) and Gray and Watkins (1976) have shown that stabilization of carbohydrate metabolism, either by insulin or transplantation of the whole gland or islets, prevents or substantially reduces the incidence of eye, kidney and nerve complications. It is also pertinent that kidneys transplanted from normal rats to diabetic rats develop typical nephropathic lesions whereas kidneys transplanted from diabetic to normal rats show either an arrest or reversal of pre-existing lesions (Lee et al, 1974). It seems, therefore, that a return to physiological normality by the appropriate delivery of insulin might well prevent, arrest, and possibly reverse the systemic complications of diabetes. The current status of total pancreas transplant and islet cell implant has

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