Decreased Epinephrine Responses to Hypoglycemia during Sleep

• Published in: The New England journal of medicine Vol. 338; no. 23; pp. 1657 - 1662
• Main Authors: Jones, Timothy W, Porter, Paul, Sherwin, Robert S, Davis, Elizabeth A, O'Leary, Peter, Frazer, Fiona, Byrne, Geoffrey, Stick, Stephen, Tamborlane, William V
• Format: Journal Article
• Language: English
• Published: Boston, MA Massachusetts Medical Society 04-06-1998
• Subjects: Adolescent; Biological and medical sciences; Blood Glucose - analysis; Catecholaminergic system; Circadian Rhythm; Diabetes; Diabetes Mellitus, Type 1 - blood; Epinephrine - blood; Female; Glucose; Glucose Clamp Technique; Human Growth Hormone - blood; Humans; Hydrocortisone - blood; Hyperglycemia; Hypoglycemia; Hypoglycemia - blood; Hypoglycemia - chemically induced; Insulin; Insulin - administration & dosage; Insulin - blood; Male; Medical sciences; Neuropharmacology; Neurotransmitters. Neurotransmission. Receptors; Norepinephrine - blood; Pharmacology. Drug treatments; Reference Values; Sleep - physiology; Endocrinopathy; Human; Epinephrine; Evaluation; Agonist; Correlation; Diabetes mellitus; Hypoglycemia; Hypothesis; Sleep; α-Adrenergic receptor; Neuromediator; Adolescent; Risk factor; Response latency; Comparative study
• ISSN: 0028-4793; 1533-4406
• DOI: 10.1056/NEJM199806043382303

Intensive therapy aimed at achieving plasma glucose concentrations and glycosylated hemoglobin values as close to normal as safely possible has been recommended for most patients with type I diabetes mellitus, because such treatment lowers the risks of the complications of diabetes.
1
However, intensive therapy also increases the risk of severe hypoglycemia,
2
and hypoglycemia is the main obstacle to the success of intensive therapy in such patients.
Patients with type I diabetes are susceptible to hypoglycemia for many reasons, including the nonphysiologic nature of insulin treatment, inconsistencies in food intake and exercise, and most important, defective counterregulatory responses to hypoglycemia.
3
– . . .