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dc.contributor.authorOram, RA
dc.contributor.authorJones, AG
dc.contributor.authorBesser, REJ
dc.contributor.authorKnight, BA
dc.contributor.authorShields, BM
dc.contributor.authorBrown, RJ
dc.contributor.authorHattersley, AT
dc.contributor.authorMcDonald, TJ
dc.date.accessioned2018-09-06T10:57:28Z
dc.date.issued2013-10-12
dc.description.abstractAIMS/HYPOTHESIS: Classically, type 1 diabetes is thought to proceed to absolute insulin deficiency. Recently developed ultrasensitive assays capable of detecting C-peptide under 5 pmol/l now allow very low levels of C-peptide to be detected in patients with long-standing type 1 diabetes. It is not known whether this low-level endogenous insulin secretion responds to physiological stimuli. We aimed to assess how commonly low-level detectable C-peptide occurs in long-duration type 1 diabetes and whether it responds to a meal stimulus. METHODS: We performed a mixed-meal tolerance test in 74 volunteers with long-duration (>5 years) type 1 diabetes, i.e. with age at diagnosis 16 (9-23) years (median [interquartile range]) and diabetes duration of 30 (19-41) years. We assessed fasting and stimulated serum C-peptide levels using an electrochemiluminescence assay (detection limit 3.3 pmol/l), and also the urinary C-peptide:creatinine ratio (UCPCR). RESULTS: Post-stimulation serum C-peptide was detectable at very low levels (>3.3 pmol/l) in 54 of 74 (73%) patients. In all patients with detectable serum C-peptide, C-peptide either increased (n = 43, 80%) or stayed the same (n = 11) in response to a meal, with no indication of levels falling (p < 0.0001). With increasing disease duration, absolute C-peptide levels fell although the numbers with detectable C-peptide remained high (68%, i.e. 25 of 37 patients with >30 years duration). Similar results were obtained for UCPCR. CONCLUSIONS/INTERPRETATION: Most patients with long-duration type 1 diabetes continue to secrete very low levels of endogenous insulin, which increase after meals. This is consistent with the presence of a small number of still functional beta cells and implies that beta cells are either escaping immune attack or undergoing regeneration.en_GB
dc.description.sponsorshipThis paper presents independent research that was funded by Diabetes UK and supported by the NIHR Exeter Clinical Research Facility. The views expressed are those of the authors and not necessarily those of Diabetes UK, the NHS, the NIHR or the Department of Health. ATH is supported by a Wellcome Trust Senior Investigator award. RAO is a Clinical Training Fellow funded by Diabetes UK. TJM is an NIHR CSO Clinical Scientist Fellow. AGJ is an NIHR Doctoral Research Fellow. REJB was a DUK Clinical Training Fellow when she contributed to this work.en_GB
dc.identifier.citationVol. 57 (1), pp. 87–191en_GB
dc.identifier.doi10.1007/s00125-013-3067-x
dc.identifier.urihttp://hdl.handle.net/10871/33936
dc.language.isoenen_GB
dc.publisherSpringer Verlagen_GB
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pubmed/24121625en_GB
dc.rights© The Author(s) 2013. Open Access. This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.en_GB
dc.subjectAdulten_GB
dc.subjectC-Peptideen_GB
dc.subjectDiabetes Mellitus, Type 1en_GB
dc.subjectFemaleen_GB
dc.subjectHumansen_GB
dc.subjectInsulinen_GB
dc.subjectInsulin-Secreting Cellsen_GB
dc.subjectMaleen_GB
dc.subjectYoung Adulten_GB
dc.titleThe majority of patients with long-duration type 1 diabetes are insulin microsecretors and have functioning beta cellsen_GB
dc.typeArticleen_GB
dc.date.available2018-09-06T10:57:28Z
dc.descriptionPublisheden_GB
dc.descriptionThis is the final version of the article. Available from Springer Verlag via the DOI in this record.en_GB
dc.identifier.journalDiabetologiaen_GB


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