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Abstract
Besides the thymus-dependent immune system, growing evidence suggests that the functional state of the beta cell plays a role in the pathogenesis of Type 1 (insulin-dependent) diabetes. Increased incidence of diabetes has been described after increased insulin production and vice versa, and actual hyperinsulinemia has been observed in relation to the diabetogenesis. Prophylactic insulin treatment and intensive insulin therapy at diagnosis are discussed.
The studies referred to are mostly animal model investigations of BB rats and NOD mice and-to a lesser degree- of streptozotocin- and encephalomyocarditis-virus-induced diabetes. Also human evidence exists, but naturally of a more sporadic character.
Three possible mechanisms behind the beta cell sensitivity as a function of their activity are suggested: increased antigen expression (including both gangliosides and proteins) in beta cells with high activity which could activate the destruction caused by the immune system, and increased susceptibility to the toxicity of interleukins and to diabetogenic agents.
With respect to developing preventive treatment the described research area may turn out to be very important. Further studies both in animal models and in humans are awaited.