The potential role of glucagon-like peptide-1 or its analogues in enhancing glycaemic control in critically ill adult patients

Combes, J.; Borot, Sophie; Mougel, F.; Penfornis, A.

doi:10.1111/j.1463-1326.2010.01311.x

Cited by 12 publications

(5 citation statements)

References 111 publications

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“…Hence, a number of strategies have been designed to minimize catabolic illness and, ideally, enhance outcome. 55 Such therapies include the administration of endocrine (growth hormone, 56,57 insulin, 58 glucagon-like peptide-1, 59 steroids) or other agents (ß-blocker), 60 glycemic control, 61 various types of anesthesia (epidural anesthesia, intravenous opioids), 28,62 as well as nutritional support, in particular the provision of specific nutrients such as polyols (xylitol, sorbitol), fructose, [63][64][65] and amino acids (glutamine, arginine, branched chain amino acids, 66-68 aketoanalogues). 69 Due to lack of effectiveness (branched chain amino acids, glutamine, 70 a-ketoanalogues, intravenous opioids), unavailability in North America (polyols, fructose), cost and side effects (growth hormone, steroids, xylitol), 71,72 only two treatment modalities are presently used in clinical practice -glycemic control and nutritional support.…”

Section: Anticatabolic Strategiesmentioning

confidence: 99%

Perioperative catabolism

Schricker

Lattermann

2015

Can J Anesth/J Can Anesth

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Section: Anticatabolic Strategiesmentioning

confidence: 99%

Perioperative catabolism

Schricker

Lattermann

2015

Can J Anesth/J Can Anesth

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“…In addition, the complex pathogenesis of stress hyperglycaemia would suggest that an agent that has both insulintropic and glucagonostatic effects, such as GLP‐1, is likely to be effective. For these reasons, the use of incretin‐based therapies in the critically ill is appealing .…”

Section: Potential Novel Therapeutic Options and Priorities For Futurmentioning

confidence: 99%

Dysglycaemia in the critically ill – significance and management

Deane

Horowitz

2013

Diabetes Obesity Metabolism

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Hyperglycaemia frequently occurs in the critically ill, in patients with diabetes, as well as those who were previously glucose-tolerant. The terminology 'stress hyperglycaemia' reflects the pathogenesis of the latter group, which may comprise up to 40% of critically ill patients. For comparable glucose concentrations during acute illness outcomes in stress hyperglycaemia appear to be worse than those in patients with type 2 diabetes. While several studies have evaluated the optimum glycaemic range in the critically ill, their interpretation in relation to clinical recommendations is somewhat limited, at least in part because patients with stress hyperglycaemia and known diabetes were grouped together, and the optimum glycaemic range was regarded as static, rather than dynamic, phenomenon. In addition to hyperglycaemia, there is increasing evidence that hypoglycaemia and glycaemic variability influence outcomes in the critically ill adversely. These three categories of disordered glucose metabolism can be referred to as dysglycaemia. While stress hyperglycaemia is most frequently managed by administration of short-acting insulin, guided by simple algorithms, this does not treat all dysglycaemic categories; rather the use of insulin increases the risk of hypoglycaemia and may exacerbate variability. The pathogenesis of stress hyperglycaemia is complex, but hyperglucagonaemia, relative insulin deficiency and insulin resistance appear to be important. Accordingly, novel agents that have a pathophysiological rationale and treat hyperglycaemia, but do not cause hypoglycaemia and limit glycaemic variability, are appealing. The potential use of glucagon-like peptide-1 (or its agonists) and dipeptyl-peptidase-4 inhibitors is reviewed.

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“…This effect is induced largely by the intestinal hormones, glucagon-like peptide (GLP)-1 and glucose-dependent insulinotropic peptide (GIP) [ 7 , 8 ]. Understanding the incretin effect in critical illness is relevant, given the recent interest in using incretin analogues in the management of hyperglycaemia in the intensive care unit (ICU) [ 9 ]. Thus, incretin analogues may be associated with a lower risk of hypoglycaemia [ 10 , 11 ] than current insulin treatment regimens [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

The incretin effect in critically ill patients: a case–control study

et al. 2015

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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.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-015-1118-z) contains supplementary material, which is available to authorized users.

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The potential role of glucagon-like peptide-1 or its analogues in enhancing glycaemic control in critically ill adult patients

Cited by 12 publications

References 111 publications

Perioperative catabolism

Perioperative catabolism

Dysglycaemia in the critically ill – significance and management

The incretin effect in critically ill patients: a case–control study

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