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|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||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:||https://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
|Journal:||Annals of intensive care||PubMed URL:||28497374||ISSN:||2110-5820||Type:||Journal Article||Subjects:||Blood glucose
Critical care, beta-cell
|Appears in Collections:||Journal articles|
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