Abstract
Diabetes mellitus, whether type 1 (insulindependent diabetes mellitus; IDDM) or type 2 (noninsulin-dependent diabetes mellitus; NIDDM) results from an inadequate mass of functional pancreatic -cells. In the first case, the -cell mass is reduced by the autoimmune destruction of the -cells, while, in the latter, there is incomplete compensation to meet the demand often imposed by insulin resistance. This latter point is not always appreciated. However, only 20% of those people with severe insulin resistance due to obesity, Cushing’s disease, or acromegaly become diabetic, with the other 80% being able to compensate to
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