Catecholamines released from the sympathochromaffin system produce metabolic changes similar to those of diabetes mellitus. However, increased sympathochromaffin activity does not appear to be a feature of insulin-dependent diabetes mellitus (IDDM), although physiologic catecholamine increments may contribute to short-term metabolic derangements under some conditions. Increased glycemic sensitivity to epinephrine is a feature of IDDM but is the result of the inability to secrete insulin rather than of increased cellular sensitivity to catecholamines. Absolute insulin deficiency results in increased metabolic (glycemic, lipolytic, and ketogenic) sensitivity to catecholamines. More generalized hypersensitivity occurs in diabetic autonomic neuropathy. However, the clinical relevance of these alterations in sensitivity remains to be established. On the other hand, decreased sympathochromaffin activity is common and causes considerable morbidity and some mortality in people with diabetes. In addition to increased sensitivity to catecholamines, decreased sympathochromaffin activity results in the clinical syndromes of postural hypotension, hypoglycemia unawareness, defective glucose counterregulation, or a combination of these. The latter two syndromes cause an increased frequency of severe iatrogenic hypoglycemia, at least during intensive therapy of IDDM. Thus, decreased rather than increased sympathochromaffin activity often complicates IDDM. Clearly, ways to prevent, correct, or compensate for this component of diabetic autonomic neuropathy must be learned before diabetes can be managed effectively and safely in all patients who suffer from the disease until diabetes mellitus is eradicated.

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