Cryer P E
Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110.
Diabetes. 1989 Apr;38(4):405-9. doi: 10.2337/diab.38.4.405.
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.
交感嗜铬系统释放的儿茶酚胺会引发与糖尿病类似的代谢变化。然而，交感嗜铬活性增加似乎并非胰岛素依赖型糖尿病（IDDM）的特征，尽管在某些情况下生理性儿茶酚胺增加可能会导致短期代谢紊乱。IDDM的一个特征是对肾上腺素的血糖敏感性增加，但这是由于无法分泌胰岛素所致，而非细胞对儿茶酚胺的敏感性增加。绝对胰岛素缺乏会导致对儿茶酚胺的代谢（血糖、脂解和生酮）敏感性增加。在糖尿病性自主神经病变中会出现更广泛的超敏反应。然而，这些敏感性改变的临床相关性仍有待确定。另一方面，交感嗜铬活性降低很常见，并且会在糖尿病患者中导致相当高的发病率和一定的死亡率。除了对儿茶酚胺的敏感性增加外，交感嗜铬活性降低还会导致体位性低血压、低血糖无意识、葡萄糖反调节缺陷或这些情况的组合等临床综合征。后两种综合征会导致严重医源性低血糖的发生率增加，至少在IDDM强化治疗期间如此。因此，交感嗜铬活性降低而非增加常常使IDDM复杂化。显然，在所有糖尿病患者能够有效且安全地管理糖尿病直至根除糖尿病之前，必须找到预防、纠正或补偿糖尿病性自主神经病变这一组成部分的方法。
