{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:55:27Z","timestamp":1787014527049,"version":"build-2736575974"},"reference-count":25,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2012,6,20]],"date-time":"2012-06-20T00:00:00Z","timestamp":1340150400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Sleep Research"],"published-print":{"date-parts":[[2013,2]]},"abstract":"<jats:title>Summary<\/jats:title>\n                  <jats:p>\n                    We investigate the effects of exenatide on excessive daytime sleepiness (EDS), driving performance and depression score in patients with type 2 diabetes with EDS. Eight obese patients with diabetes but without obstructive sleep apnoea (OSA) participated in a placebo\u2010controlled single\u2010blind study during which multiple wakefulness and sleep latency test, Epworth score, driving performance, depression score, fasting glucose and glycated haemoglobin (HbA1c) levels were assessed at baseline, end of placebo and treatment phase at baseline and after 22\u2003weeks of treatment. Mean (\u00b1standard error of the mean) age, body mass index (kg\u2003m\n                    <jats:sup>2<\/jats:sup>\n                    ) and HbA1c [mmol\u2003mol\n                    <jats:sup>\u22121<\/jats:sup>\n                    (%)] of patients at baseline were 50\u2003\u00b1\u20034.9\u2003years, 37.6\u2003\u00b1\u20031.1 and 65\u2003\u00b1\u200319 (8.06\u2003\u00b1\u20030.41), respectively. When compared to placebo, exenatide treatment was associated with a decrease in both subjective and objective sleepiness, based on the Epworth score reduction and the sleep latency increase assessed by multiple objective sleepiness and sustained attention (OSLER) tests, respectively. Mean sleep latency time (adjusted for change in HbA1c and weight) were 32.1\u2003\u00b1\u20031.7, 29.1\u2003\u00b1\u20031.7 and 37.7\u2003\u00b1\u20031.7, respectively (\n                    <jats:italic>P\u2003<\/jats:italic>\n                    =\n                    <jats:italic>\u2003<\/jats:italic>\n                    0.002). Modelling for covariates suggested that improvement in mean sleep latency time is predicted by changes in weight (\n                    <jats:italic>P\u2003<\/jats:italic>\n                    =\n                    <jats:italic>\u2003<\/jats:italic>\n                    0.003), but not by changes in HbA1c (\n                    <jats:italic>P\u2003<\/jats:italic>\n                    =\n                    <jats:italic>\u2003<\/jats:italic>\n                    0.054). Epworth sleepiness score was reduced significantly (values for placebo versus exenatide: 11.3\u2003\u00b1\u20031.2 versus 5.7\u2003\u00b1\u20031.3;\n                    <jats:italic>P\u2003<\/jats:italic>\n                    =\n                    <jats:italic>\u2003<\/jats:italic>\n                    0.003). No significant change was noted in the depression score and driving performance. Exenatide is associated with a significant reduction in objective sleepiness in obese patients with type 2 diabetes without OSA, independent of HbA1c levels. These findings could form a basis for further studies to investigate the pathophysiological mechanisms of sleepiness in obese patients with type 2 diabetes.\n                  <\/jats:p>","DOI":"10.1111\/j.1365-2869.2012.01030.x","type":"journal-article","created":{"date-parts":[[2012,6,20]],"date-time":"2012-06-20T08:09:33Z","timestamp":1340179773000},"page":"70-75","source":"Crossref","is-referenced-by-count":21,"title":["Exenatide improves excessive daytime sleepiness and wakefulness in obese patients with type 2 diabetes without obstructive sleep apnoea"],"prefix":"10.1111","volume":"22","author":[{"given":"ISKANDAR","family":"IDRIS","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"HAITHAM","family":"ABDULLA","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"SEAN","family":"TILBROOK","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"ROY","family":"DEAN","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"NABEEL","family":"ALI","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2012,6,20]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2004.04.063"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.2337\/dc10-1119"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2005-0035"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.2105\/AJPH.87.10.1649"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.clinthera.2007.01.015"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1989.03430110069030"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1164\/ajrccm.154.1.8680676"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1186\/1475-2840-5-22"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-5491.2007.02248.x"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2869.2004.00417.x"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1038\/377339a0"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1012456108"},{"key":"e_1_2_7_14_1","unstructured":"National Institute for Health and Clinical Excellence (NICE).Type 2 diabetes: newer agents for blood glucose control in type 2 diabetes (Clinical Guideline 87).2009. 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