title: Effects of autonomic neuropathy on glucose, fatty acid, and ketone body metabolism following insulin withdrawal in patients with insulin-dependent diabetes.
abstract: It has been postulated that sympathetic denervation due to autonomic neuropathy may protect against the development of diabetic ketoacidosis in patients with insulin-dependent diabetes. We tested this hypothesis by withdrawing exogenous insulin from five men with established insulin-dependent diabetes and severe symptomatic autonomic neuropathy. Six men also with insulin-dependent diabetes of more than 5-years duration but no clinical evidence of neuropathy served as controls. Normoglycemia was maintained during the night before the study using a variable intravenous insulin infusion that was terminated at 0800 h the following morning (time 0 min). During a 600-min observation period following termination of the insulin infusion the rise (mean +/- SEM) in blood glucose concentration between 0 min and 600 min was comparable between the autonomic neuropathy and control groups (8.2 +/- 1.3 versus 8.3 +/- 1.1 mmol/L; p > 0.1). The rise in plasma nonesterified fatty acids was significantly less for the autonomic neuropathy patients (0.96 +/- 0.06 versus 1.65 +/- 0.14 mmol/L; p < 0.01) with a similar trend for the rise in total ketone body concentration (2.74 +/- 0.85 versus 3.72 +/- 0.38 mmol/L). Capillary pH at 600 min, however, was not significantly different between the groups (23 +/- 2 versus 20 +/- 1 mmol/L). In conclusion, plasma fatty acids and ketone body concentrations rise less rapidly following withdrawal of insulin in patients with insulin-dependent diabetes and autonomic neuropathy suggesting that such patients may have a degree of protection against the development of diabetic ketoacidosis.
authors.affiliation: Diabetic Clinic, General Hospital, Birmingham, United Kingdom.
authors.forename: A J
authors.initials: AJ
authors.lastname: Krentz
authors.forename: B M
authors.initials: BM
authors.lastname: Singh
authors.forename: A D
authors.initials: AD
authors.lastname: Wright
authors.forename: M
authors.initials: M
authors.lastname: Nattrass
mesh_terms: D000328:Adult; D001342:Autonomic Nervous System Diseases / Q000378:metabolism*; D001481:Basal Metabolism; D001786:Blood Glucose / Q000378:metabolism; D003714:Denervation; D003922:Diabetes Mellitus, Type 1 / Q000188:drug therapy* / Q000378:metabolism; D016883:Diabetic Ketoacidosis / Q000517:prevention & control; D003929:Diabetic Neuropathies / Q000378:metabolism*; D005227:Fatty Acids / Q000097:blood; D006801:Humans; D007260:Infusion Pumps; D007328:Insulin / Q000008:administration & dosage*; D007657:Ketone Bodies / Q000097:blood; D008066:Lipolysis / Q000502:physiology; D008297:Male; D008875:Middle Aged
chemical_list: D001786:Blood Glucose; D005227:Fatty Acids; D007328:Insulin; D007657:Ketone Bodies