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|dc.identifier.citation||Critical Care, 2014; 18(1):205-1-205-10||en|
|dc.description.abstract||Hyperglycaemia occurs frequently in the critically ill, even in those patients without a history of diabetes. The mechanisms underlying hyperglycaemia in this group are complex and incompletely defined. In health, the gastrointestinal tract is an important modulator of postprandial glycaemic excursions and both the rate of gastric emptying and the so-called incretin hormones, glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide, are pivotal determinants of postprandial glycaemia. Incretin-based therapies (that is, glucagon-like peptide- 1 agonists and dipeptidyl-peptidase-4 inhibitors) have recently been incorporated into standard algorithms for the management of hyperglycaemia in ambulant patients with type 2 diabetes and, inevitably, an increasing number of patients who were receiving these classes of drugs prior to their acute illness will present to ICUs. This paper summarises current knowledge of the incretin effect as well as the incretin-based therapies that are available for the management of type 2 diabetes, and provides suggestions for the potential relevance of these agents in the management of dysglycaemia in the critically ill, particularly to normalise elevated blood glucose levels.||en|
|dc.description.statementofresponsibility||Mark P Plummer, Marianne J Chapman, Michael Horowitz, and Adam M Deane||en|
|dc.rights||© 2014 BioMed Central Ltd.||en|
|dc.subject||Animals; Humans; Diabetes Mellitus, Type 2; Hyperglycemia; Blood Glucose; Glucagon-Like Peptide 1; Incretins; Dipeptidyl-Peptidase IV Inhibitors||en|
|dc.title||Incretins and the intensivist: what are they and what does an intensivist need to know about them?||en|
|dc.identifier.orcid||Chapman, M. [0000-0003-0710-3283]||en|
|dc.identifier.orcid||Horowitz, M. [0000-0002-0942-0306]||en|
|dc.identifier.orcid||Deane, A. [0000-0002-7620-5577]||en|
|Appears in Collections:||Medicine publications|
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