Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/18966
Title: The effect of insulin administration on c-peptide in critically ill patients with type 2 diabetes.
Austin Authors: Crisman, Marco;Lucchetta, Luca;Luethi, Nora;Cioccari, Luca;Lam, Que T ;Eastwood, Glenn M ;Bellomo, Rinaldo ;Mårtensson, Johan
Affiliation: Department of Pathology, Austin Health, Heidelberg, Victoria, Australia
Section of Anaesthesia and Intensive Care Medicine, Department of Physiology and Pharmacology, Karolinska Institutet, 171 77, Stockholm, Sweden.
Department of Anesthesia and Intensive Care, Azienda Ospedaliero-Universitaria "Ospedali Riuniti", Trieste, Italy
Department of Epidemiology and Preventive Medicine, Australian and New Zealand Intensive Care Research Centre, Monash University, Melbourne, Victoria, Australia
Department of Intensive Care, Austin Health, Heidelberg, Victoria, Australia
Issue Date: Dec-2017
metadata.dc.date: 2017-05-12
Publication information: Annals of intensive care 2017; 7(1): 50
Abstract: In critically ill patients with permissive hyperglycemia, it is uncertain whether exogenous insulin administration suppresses or enhances c-peptide secretion (a marker of pancreatic beta-cell response). We aimed to explore this effect in patients with type 2 diabetes. We prospectively enrolled a cohort of 45 critically ill patients with type 2 diabetes managed according to a liberal glucose protocol (target blood glucose 10-14 mmol/l). We recorded the administration of insulin and oral hypoglycemic agents and measured plasma c-peptide as surrogate marker of endogenous insulin secretion on the first two consecutive days in ICU. Overall, 20 (44.4%) patients required insulin to achieve target blood glucose. Insulin-treated patients had higher glycated hemoglobin A1c, more premorbid insulin-requiring type 2 diabetes, and greater blood glucose levels but lower c-peptide levels on admission. Premorbid insulin-requiring diabetes was independently associated with lower admission c-peptide, whereas greater plasma creatinine was independently associated with higher levels. Increases in c-peptide were positively correlated with an increase in blood glucose both in patients who did (r = 0.54, P = 0.01) and did not (r = 0.56, P = 0.004) receive insulin. However, insulin administration was independently associated with a greater increase in c-peptide (P = 0.04). This association was not modified by the use of oral insulin secretagogues. C-peptide, a marker of beta-cell response, responds to and is influenced by glycemia and renal function in critically ill patients with type 2 diabetes. In addition, in our cohort, exogenous insulin administration was associated with a greater increase in c-peptide in response to hyperglycemia. Trial Registration Australian New Zealand Clinical Trials Registry (ACTRN12615000216516).
URI: http://ahro.austin.org.au/austinjspui/handle/1/18966
DOI: 10.1186/s13613-017-0274-5
ORCID: 0000-0001-8739-7896
The University of Melbourne, Victoria, Australia
0000-0002-1650-8939
0000-0001-8739-7896
PubMed URL: 28497374
ISSN: 2110-5820
Type: Journal Article
Subjects: Blood glucose
C-peptide
Critical care, beta-cell
Diabetes mellitus
Insulin
Appears in Collections:Journal articles

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