Abstract
The pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM) has been the subject of debate for many years, and it still remains poorly understood [55, 82]. Current dogma states that it is a heterogeneous disorder; indeed, several patients have now been identified with mutant insulins [63, 69] or one of a variety of syndromes characterized by abnormal insulin receptors, extreme insulin resistance, and acanthosis nigricans [16,17,29]. Also, in some series, up to 10% are islet cell antibody-positive [14]. However, these groups together represent only a small minority of those with NIDDM, and while new syndromes will probably be described in the future, it seems reasonable to assume that the bulk of patients share a common etiology.
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