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QJM Advance Access originally published online on December 19, 2008
QJM 2009 102(3):169-174; doi:10.1093/qjmed/hcn163
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© The Author 2008. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

The influence of liberal alcohol consumption on glucose metabolism in patients with type 1 diabetes: a pilot study

D. Kerr1,2, S. Penfold1, S. Zouwail3, P. Thomas2,4 and J. Begley1,2,3

From the 1Diabetes & Endocrine Centre, 2Centre of Postgraduate Medical Research and Education, 3Department of Clinical Biochemistry, Royal Bournemouth Hospital and 4Dorset Research and Development Support Unit, Bournemouth University, Bournemouth, UK

Address correspondence to Dr S. Zouwail, Clinical Biochemistry, Royal Bournemouth Hospital, Castle Lane East, Bournemouth, Dorset, BH7 7DW, UK. email: soha.zouwail{at}poole.nhs.uk

Received 18 July 2008 and in revised form 19 November 2008


   Abstract

Background: Little is known about the consequences of excessive alcohol ingestion in patients with type 1 diabetes.

Aim: To examine the metabolic effects of acute ingestion of liberal amounts of alcohol in patients with type 1 diabetes.

Design: A pilot study using a randomized, placebo controlled, double blind design in Hospital Clinical Research Unit.

Methods: The study included 10 patients with type 1 diabetes (seven male, age 43.9 ± 9.0 years, duration of diabetes 17.3 ± 13.8 years, HbA1c 8.0 ± 1.5%) who had a standard 600-calorie lunch on two separate occasions, together with either white wine (men eight units, women six units), or an equivalent volume of alcohol-free wine. Bloods were collected before lunch and hourly for 4 h for glucose, intermediary metabolites, counter-regulatory hormones and inflammatory markers.

Results: There were no significant differences between alcohol and alcohol-free days in levels of glucose, triglycerides, free fatty acids, glycerol, cortisol and growth hormone. In contrast, lactate levels rose in response to the meal but with alcohol the overall response was augmented (P = 0.014). β-Hydroxybutyrate levels were suppressed post prandially on the alcohol-free day but were significantly elevated with alcohol (P < 0.001).

Conclusions: A rise in ketones following alcohol ingestion occurred despite subjects being in a strictly controlled environment with no interruption in insulin administration. Such individuals might be at risk of significant ketosis in less-controlled circumstances where insulin administration might be more erratic. Patient education material should contain information to highlight these potential problems.


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