Schade D S, Eaton R P
J Clin Endocrinol Metab. 1980 Jan;50(1):131-6. doi: 10.1210/jcem-50-1-131.
Stress-induced diabetic ketoacidosis is characterized by an elevation in stress hormone concentration. Whether metabolic decompensation induces or results from the secretion of stress hormones has not been examined. Our study examined the temporal relationship between the onset of stress (pyrogen-induced shaking chills and fever); the elevation in stress hormone concentation; and the rise in plasma glucose, ketone bodies, and nonesterified fatty acid concentration. Insulin deficiency, which may itself induce stress hormone secretion, was prevented by the continuous infusion of insulin (0.01 U/kg.h). Pyrogen administration induced malaise and fever in all diabetic volunteers and the rapid endogenous secretion of all stress hormones. The rise in plasma GH, catecholamines, and cortisol preceded the rise in plasma nonesterified fatty acid and ketone body concentrations by at least 30 min. The rise in plasma glucagon concentration preceded the rise in plasma glucose concentration by at lease 1 h. Thus, these studies support a primary role for stress hormones in initiating metabolic decompensation in stressed diabetic man.
应激诱导的糖尿病酮症酸中毒的特征是应激激素浓度升高。代谢失代偿是诱导应激激素分泌还是由其分泌所致尚未得到研究。我们的研究考察了应激发作（热原诱导的寒战和发热）、应激激素浓度升高以及血浆葡萄糖、酮体和非酯化脂肪酸浓度升高之间的时间关系。通过持续输注胰岛素（0.01 U/kg·h）预防了可能本身诱导应激激素分泌的胰岛素缺乏。热原给药在所有糖尿病志愿者中诱发不适和发热以及所有应激激素的快速内源性分泌。血浆生长激素、儿茶酚胺和皮质醇的升高比血浆非酯化脂肪酸和酮体浓度的升高至少提前30分钟。血浆胰高血糖素浓度的升高比血浆葡萄糖浓度的升高至少提前1小时。因此，这些研究支持应激激素在引发应激状态下糖尿病患者代谢失代偿中起主要作用。
