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J Diabetes Complications. 1994 Apr-Jun;8(2):105-10.

Effects of autonomic neuropathy on glucose, fatty acid, and ketone body metabolism following insulin withdrawal in patients with insulin-dependent diabetes.

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1
Diabetic Clinic, General Hospital, Birmingham, United Kingdom.

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.

PMID:
8061346
DOI:
10.1016/1056-8727(94)90059-0
[Indexed for MEDLINE]

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