ArticleCritical care (London, England)2015
The incretin effect in critically ill patients: a case-control study.
Article in Critical care (London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01347801 (Mechanisms of Insulin Resistance in Critical Illness), which is not on this map. Cited by 10 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Mechanisms of Insulin Resistance in Critical Illness: Role of Systemic Inflammation and GLP-1
Who cites it
10 citing papers in PubMed.
- The attenuated incretin effect is associated with glucose intolerance in patients with hepatitis B-related acute-on-chronic liver failure.Frontiers in physiology · 2026Article
- The C-reactive protein-triglyceride-glucose index (CTI) as a predictor of mortality and hospital stay in critically ill patients: a retrospective cohort study.Lipids in health and disease · 2025Article
- Triglyceride-glucose index and prognosis in non-diabetic critically ill patients: data from the eICU database.Frontiers in medicine · 2025Article
- Triptolide Administration Alters Immune Responses to Mitigate Insulin Resistance in Obese States.Biomolecules · 2024Article
- Glycaemic control for patients with severe acute brain injury: Protocol for a systematic review.Acta anaesthesiologica Scandinavica · 2023Article
- Essential Minerals and Metabolic Adaptation of Immune Cells.Nutrients · 2022Review
- The Links of Ghrelin to Incretins, Insulin, Glucagon, and Leptin After Bariatric Surgery.Frontiers in genetics · 2021Article
- Updates in Glycemic Management in the Hospital.Current diabetes reports · 2019Review
- The effect of insulin administration on c-peptide in critically ill patients with type 2 diabetes.Annals of intensive care · 2017Article
- Inflammation Meets Metabolic Disease: Gut Feeling Mediated by GLP-1.Frontiers in immunology · 2016Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionPatients admitted to the intensive care unit often develop hyperglycaemia, but the underlying mechanisms have not been fully described. The incretin effect is reduced in patients with type 2 diabetes. Type 2 diabetes and critical illness have phenotypical similarities, such as hyperglycaemia, insulin resistance and systemic inflammation. Previous studies have shown beneficial effects of exogenous glucagon-like peptide (GLP)-1 on glycaemia in critically ill patients, a phenomenon also seen in patients with type 2 diabetes. In this study, we hypothesised that the incretin effect, which is mediated by the incretin hormones GLP-1 and glucose-dependent insulinotropic peptide (GIP), is impaired in critically ill patients.
methodsThe incretin effect (i.e., the relative difference between the insulin response to oral and intravenous glucose administration) was investigated in a cross-sectional case-control study. Eight critically ill patients without diabetes admitted to a mixed intensive care unit and eight healthy control subjects without diabetes, matched at group level by age, sex and body mass index, were included in the study. All subjects underwent an oral glucose tolerance test (OGTT) followed by an intravenous glucose infusion (IVGI) on the next day to mimic the blood glucose profile from the OGTT. Blood glucose, serum insulin, serum C-peptide and plasma levels of GLP-1, GIP, glucagon and proinflammatory cytokines were measured intermittently. The incretin effect was calculated as the increase in insulin secretion during oral versus intravenous glucose administration in six patients. The groups were compared using either Student's t test or a mixed model of repeated measurements.
resultsBlood glucose levels were matched between the OGTT and the IVGI in both groups. Compared with control subjects, proinflammatory cytokines, tumour necrosis factor α and interleukin 6, were higher in patients than in control subjects. The endogenous response of GIP and glucagon, but not GLP-1, to the OGTT was greater in patients. The insulin response to the OGTT did not differ between groups, whereas the insulin response to the IVGI was higher in patients. Consequently, the calculated incretin effect was lower in patients (23 vs. 57%, p=0.003).
conclusionsIn critically ill patients, the incretin effect was reduced. This resembles previous findings in patients with type 2 diabetes.
trial registrationClinicalTrials.gov identifier: NCT01347801 . Registered on 2 May 2011.
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