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dc.contributor.authorBrown, James E. P.
dc.contributor.authorThomas, Steven
dc.contributor.authorDigby, Janet E.
dc.contributor.authorDunmore, Simon J.
dc.date.accessioned2006-11-30T16:40:19Z
dc.date.available2006-11-30T16:40:19Z
dc.date.issued2002
dc.date.submitted2006-11-30
dc.identifier.citationFEBS Letters, 513(2-3): 189-192
dc.identifier.issn0014-5793
dc.identifier.pmid11904148
dc.identifier.doi10.1016/S0014-5793(02)02296-2
dc.identifier.urihttp://hdl.handle.net/2436/6313
dc.description.abstractElevated islet uncoupling protein-2 (UCP-2) impairs beta-cell function and UCP-2 may be increased in clinical obesity and diabetes. We investigated the effects of glucose and leptin on UCP-2 expression in isolated human islets. Human islets were incubated for 24 h with glucose (5.5-22 mmol/l)+/-leptin (0-10 nmol/l). Some islet batches were incubated at high (22 mmol/l), and subsequently lower (5.5 mmol/l), glucose to assess reversibility of effects. Leptin effects on insulin release were also measured. Glucose dose-dependently increased UCP-2 expression in all islet batches, maximally by three-fold. This was not fully reversed by subsequently reduced glucose levels. Leptin decreased UCP-2 expression by up to 75%, and maximally inhibited insulin release by 47%, at 22 mmol/l glucose. This is the first report of UCP-2 expression in human islets and provides novel evidence of its role in the loss of beta-cell function in diabetes.
dc.format.extent160852 bytes
dc.format.mimetypeapplication/pdf
dc.language.isoen
dc.publisherElsevier BV
dc.relation.urlhttp://www.ingentaconnect.com/content/els/00145793/2002/00000513/00000002/art02296
dc.subjectGene Expression
dc.subjectGlucose toxicity
dc.subjectType 2 diabetes
dc.subjectβ-Cell
dc.titleGlucose induces and leptin decreases expression of uncoupling protein-2 mRNA in human islets.
dc.typeJournal article
dc.format.digYES
refterms.dateFOA2018-08-21T15:37:18Z
html.description.abstractElevated islet uncoupling protein-2 (UCP-2) impairs beta-cell function and UCP-2 may be increased in clinical obesity and diabetes. We investigated the effects of glucose and leptin on UCP-2 expression in isolated human islets. Human islets were incubated for 24 h with glucose (5.5-22 mmol/l)+/-leptin (0-10 nmol/l). Some islet batches were incubated at high (22 mmol/l), and subsequently lower (5.5 mmol/l), glucose to assess reversibility of effects. Leptin effects on insulin release were also measured. Glucose dose-dependently increased UCP-2 expression in all islet batches, maximally by three-fold. This was not fully reversed by subsequently reduced glucose levels. Leptin decreased UCP-2 expression by up to 75%, and maximally inhibited insulin release by 47%, at 22 mmol/l glucose. This is the first report of UCP-2 expression in human islets and provides novel evidence of its role in the loss of beta-cell function in diabetes.


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