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Articles in PresS, published online ahead of print December 11, 2001
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00447.2001
Submitted on October 4, 2001
Accepted on December 4, 2001
1 Division of Endocrinology, Diabetes and Metabolism, Washington University School of Medicine, St. Louis, MO, USA
* To whom correspondence should be addressed. E-mail: pcryer{at}imgate.wustl.edu.
We tested the hypothesis that increased endogenous cortisol secretion reduces autonomic neuroendocrine and neurogenic symptom responses to subsequent hypoglycemia. Twelve healthy young adults were studied on two separate occasions, once following infusions of a pharmacological dose of 
1-24 ACTH (100 µg/h) from 0930 to 1200h and 1330 to 1600h (which raised plasma cortisol levels to ~45 µg/dL) on Day 1 and once following saline infusions on Day 1. Hyperinsulinemic (2.0 mU.kg-1.min.) stepped hypoglycemic clamps (90, 75, 65, 55 and 45 mg/dL glucose steps) were performed on the morning of Day 2 on both occasions. These markedly elevated antecedent endogenous cortisol levels reduced the adrenomedullary (P = 0.004, final plasma epinephrine levels of 489 ± 64 v. 816 ± 13 pg/mL), sympathetic neural (P = 0.0022, final plasma norepinephrine levels of 244 ± 15 v. 342 ± 22 pg/mL), parasympathetic neural ( P = 0.0434, final plasma pancreatic polypeptide levels of 312 ± 37 v. 424 ± 56 pg/mL) and neurogenic (autonomic) symptom (P = 0.0097, final symptom score of 7.1 ± 1.5 v. 10.6 ± 1.6) responses to subsequent hypoglycemia. Growth hormone, but not glucagon or cortisol, responses were also reduced. The findings that increased endogenous cortisol secretion reduces autonomic neuroendocrine and neurogenic symptom responses to subsequent hypoglycemia are potentially relevant to cortisol mediation of hypoglycemia-associated autonomic failure, and thus a vicious cycle of recurrent iatrogenic hypoglycemia, in people with diabetes mellitus.
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