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dc.contributor.authorUsui, Ryotaen
dc.contributor.authorSakuramachi, Yuien
dc.contributor.authorSeino, Yusukeen
dc.contributor.authorMurotani, Kentaen
dc.contributor.authorKuwata, Hitoshien
dc.contributor.authorTatsuoka, Hisatoen
dc.contributor.authorHamamoto, Yoshiyukien
dc.contributor.authorKurose, Takeshien
dc.contributor.authorSeino, Yutakaen
dc.contributor.authorYabe, Daisukeen
dc.contributor.alternative矢部, 大介ja
dc.date.accessioned2019-03-04T00:53:48Z-
dc.date.available2019-03-04T00:53:48Z-
dc.date.issued2018-07-
dc.identifier.issn2040-1116-
dc.identifier.urihttp://hdl.handle.net/2433/236655-
dc.description.abstractAims/Introduction: The glucose‐lowering effects of the glucagon‐like peptide‐1 receptor agonist, liraglutide, have been shown to rely on remaining β‐cell function. However, the possible associations of remaining β‐cell function with the glucose‐lowering effects of liraglutide in combination with basal insulin remain unknown and warrant investigation. Materials and Methods: This was a single‐center, retrospective, observational study carried out in a private hospital in Osaka, Japan. Type 2 diabetes patients who received a prescription change from insulin therapy, both multiple‐dose insulin and basal insulin‐supported oral therapy, to liraglutide and basal insulin combination and continued the therapy for 54 weeks without additional oral antidiabetic drugs or bolus insulin were retrospectively analyzed. Results: Among the 72 participants who received a prescription change from multiple‐dose insulin and basal insulin‐supported oral therapy to liraglutide and basal insulin combination, 57 continued the therapy for 54 weeks. Of those who continued the therapy without receiving additional oral antidiabetic drugs or bolus insulin, seven participants achieved glycated hemoglobin < 7.0% at 54 weeks, but 30 participants did not. The participants who achieved glycated hemoglobin < 7.0% at 54 weeks had a significantly higher C‐peptide immunoreactivity index, a β‐cell function‐related index frequently used in Japanese clinical settings. The receiver operating curve analysis showed that the C‐peptide immunoreactivity index cut‐off value for the achievement of glycated hemoglobin <7.0% at 54 weeks is 1.103. Conclusions: The current findings show that the glucose‐lowering effects of liraglutide rely on remaining β‐cell function, even when used with basal insulin; and suggest that liraglutide and basal insulin combination might require additional bolus insulin to fully compensate insulin insufficiency in individuals with reduced β‐cell function.en
dc.format.mimetypeapplication/pdf-
dc.language.isoeng-
dc.publisherWileyen
dc.rights© 2017 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.en
dc.subjectβ‐Cell functionen
dc.subjectBasal insulinen
dc.subjectLiraglutideen
dc.titleRetrospective analysis of liraglutide and basal insulin combination therapy in Japanese type 2 diabetes patients: The association between remaining β-cell function and the achievement of the glycated hemoglobin target 1 year after initiationen
dc.typejournal article-
dc.type.niitypeJournal Article-
dc.identifier.jtitleJournal of Diabetes Investigationen
dc.identifier.volume9-
dc.identifier.issue4-
dc.identifier.spage822-
dc.identifier.epage830-
dc.relation.doi10.1111/jdi.12773-
dc.textversionpublisher-
dc.addressCenter for Diabetes, Endocrinology and Metabolism, Kansai Electric Power Hospitalen
dc.addressCenter for Diabetes, Endocrinology and Metabolism, Kansai Electric Power Hospitalen
dc.addressDepartments of Endocrinology and Diabetes Metabolic Medicine, Nagoya University Graduate School of Medicineen
dc.addressDivision of Biostatistics, Clinical Research Center, Aichi Medical University Hospitalen
dc.addressCenter for Diabetes, Endocrinology and Metabolism, Kansai Electric Power Hospital, Osaka・Yutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Instituteen
dc.addressCenter for Diabetes, Endocrinology and Metabolism, Kansai Electric Power Hospital, Osaka・Yutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Instituteen
dc.addressCenter for Diabetes, Endocrinology and Metabolism, Kansai Electric Power Hospital・Yutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Institute・Center for Metabolism and Clinical Nutrition, Kansai Electric Power Hospitalen
dc.addressCenter for Diabetes, Endocrinology and Metabolism, Kansai Electric Power Hospital・Yutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Instituteen
dc.addressCenter for Diabetes, Endocrinology and Metabolism, Kansai Electric Power Hospital・Yutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Instituteen
dc.addressCenter for Diabetes, Endocrinology and Metabolism, Kansai Electric Power Hospital・Yutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Institute・Division of Molecular and Metabolic Medicine, Department of Physiology and Cell Biology, Kobe University Graduate School of Medicine・Department of Diabetes, Endocrinology and Nutrition, Kyoto University Graduate School of Medicineen
dc.identifier.pmid29106046-
dcterms.accessRightsopen access-
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