Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12040
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dc.contributor.authorLamont, Benjamin Jen
dc.contributor.authorAndrikopoulos, Sofianosen
dc.date.accessioned2015-05-16T01:41:06Z
dc.date.available2015-05-16T01:41:06Z
dc.date.issued2014-03-07en
dc.identifier.citationThe Journal of Endocrinology 2014; 221(1): T43-61en
dc.identifier.govdoc24424288en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/12040en
dc.description.abstractIncretin-based therapies appear to offer many advantages over other approaches for treating type 2 diabetes. Some preclinical studies have suggested that chronic activation of glucagon-like peptide 1 receptor (GLP1R) signalling in the pancreas may result in the proliferation of islet β-cells and an increase in β-cell mass. This provided hope that enhancing GLP1 action could potentially alter the natural progression of type 2 diabetes. However, to date, there has been no evidence from clinical trials suggesting that GLP1R agonists or dipeptidyl peptidase-4 (DPP4) inhibitors can increase β-cell mass. Nevertheless, while the proliferative capacity of these agents remains controversial, some studies have raised concerns that they could potentially contribute to the development of pancreatitis and hence increase the risk of pancreatic cancer. Currently, there are very limited clinical data to directly assess these potential benefits and risks of incretin-based therapies. However, a review of the preclinical studies indicates that incretin-based therapies probably have only a limited capacity to regenerate pancreatic β-cells, but may be useful for preserving any remaining β-cells in type 2 diabetes. In addition, the majority of preclinical evidence does not support the notion that GLP1R agonists or DPP4 inhibitors cause pancreatitis.en
dc.language.isoenen
dc.subject.otherDPP4en
dc.subject.otherGLP1en
dc.subject.otherisletsen
dc.subject.othermiceen
dc.subject.otherpancreatitisen
dc.subject.otherratsen
dc.subject.otherβ-cellsen
dc.subject.otherAnimalsen
dc.subject.otherDiabetes Mellitus, Type 2.drug therapyen
dc.subject.otherHumansen
dc.subject.otherHypoglycemic Agents.adverse effects.therapeutic useen
dc.subject.otherIncretins.adverse effects.therapeutic useen
dc.subject.otherPancreas.drug effects.growth & developmenten
dc.titleHope and fear for new classes of type 2 diabetes drugs: is there preclinical evidence that incretin-based therapies alter pancreatic morphology?en
dc.typeJournal Articleen
dc.identifier.journaltitleThe Journal of Endocrinologyen
dc.identifier.affiliationDepartment of Medicine (Austin Health), The University of Melbourne, Melbourne, Victoria, Australiaen
dc.identifier.doi10.1530/JOE-13-0577en
dc.description.pagesT43-61en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/24424288en
dc.type.austinJournal Articleen
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
item.cerifentitytypePublications-
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