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Questions about the relation between metabolic control and the microvascular complications of diabetes mellitus have filled many pages with controversy. Until very recently, definitive answers were not possible because complete and sustained metabolic normalization could not be achieved with conventional forms of therapy, because estimates of control based on sporadic measurements of sugar in blood or urine did not provide the requisite precision, and because the disputed anatomic lesions appeared to evolve very slowly. However, the application of new approaches to all these questions is beginning to foster a consensus that the lesions of diabetes may be consequent to the . . .
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Norbert Freinkel (1981) studied this question.
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