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type=\u0022text\/css\u0022 rel=\u0022stylesheet\u0022 href=\u0022\/\/d282kpwvnogo5m.cloudfront.net\/sites\/default\/files\/cdn\/css\/http\/css_Xg7z6oCTVgud_Q0huYz9x9iiD5H_2YPSJ5z2ZViSWdY.css\u0022 media=\u0022all\u0022 \/\u003E\n\u003Clink rel=\u0027stylesheet\u0027 type=\u0027text\/css\u0027 href=\u0027\/sites\/all\/modules\/contrib\/panels\/plugins\/layouts\/onecol\/onecol.css\u0027 \/\u003E\u003C\/head\u003E\u003Cbody\u003E\u003Cdiv class=\u0022panels-ajax-tab-panel panels-ajax-tab-panel-sageoa-tab-art\u0022\u003E\u003Cdiv class=\u0022panel-display panel-1col clearfix\u0022 \u003E\n  \u003Cdiv class=\u0022panel-panel panel-col\u0022\u003E\n    \u003Cdiv\u003E\u003Cdiv class=\u0022panel-pane pane-highwire-markup\u0022 \u003E\n  \n      \n  \n  \u003Cdiv class=\u0022pane-content\u0022\u003E\n    \u003Cdiv class=\u0022highwire-markup\u0022\u003E\u003Cdiv xmlns=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022 id=\u0022content-block-markup\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cdiv class=\u0022article fulltext-view \u0022\u003E\u003Cspan class=\u0022highwire-journal-article-marker-start\u0022\u003E\u003C\/span\u003E\u003Cdiv class=\u0022section abstract\u0022 id=\u0022abstract-1\u0022\u003E\u003Ch2\u003ESummary\u003C\/h2\u003E\n            \u003Cp id=\u0022p-1\u0022\u003EEvidence supports an interaction between obstructive sleep apnea (OSA) and type 2 diabetes mellitus (T2DM). OSA is highly prevalent in persons with T2DM, with some estimates of the prevalence of moderate to severe OSA (defined as an apnea-hypopnia index =5) as high as 61% [Einhorn D et al. \u003Cem\u003EEndocr Pract\u003C\/em\u003E 2007], but the direction of causality is not yet clear. This article provides an overview of the relationship between OSA and T2DM.\u003C\/p\u003E\n         \u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003EDiabetes Mellitus\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EObesity\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EPulmonary Clinical Trials\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003ESleep Disorders\u003C\/li\u003E\u003C\/ul\u003E\u003Cul class=\u0022kwd-group clinical-trial\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003EDiabetes Mellitus\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EPulmonary \u0026amp; Critical Care\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EObesity\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EPulmonary Clinical Trials\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EFeatured Meeting - Specialty page\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003ESleep Disorders\u003C\/li\u003E\u003C\/ul\u003E\u003Cp id=\u0022p-2\u0022\u003EEvidence supports an interaction between obstructive sleep apnea (OSA) and type 2 diabetes mellitus (T2DM). OSA is highly prevalent in persons with T2DM, with some estimates of the prevalence of moderate to severe OSA (defined as an apnea-hypopnia index [AHI] \u22655) as high as 61% [Einhorn D et al. \u003Cem\u003EEndocr Pract\u003C\/em\u003E 2007], but the direction of causality is not yet clear.\u003C\/p\u003E\u003Cp id=\u0022p-3\u0022\u003EPatrick L\u00e9vy, MD, PhD, University Joseph Fourier, Grenoble, France, gave an overview of the relationship between OSA and T2DM. In a consecutive series of 60 patients with T2DM, 77% had an AHI\u22655, and adjusted HbA1C levels increased with increasing severity of OSA [Aronsohn RS et al. \u003Cem\u003EAm J Respir Crit Care Med\u003C\/em\u003E 2010].\u003C\/p\u003E\u003Cp id=\u0022p-4\u0022\u003EData also suggest that OSA is independently associated with altered glucose metabolism to promote the development of T2DM. Adjusted odds ratios for the incidence of diabetes in moderate to severe OSA compared with no OSA range from 1.43 to 13.45 [Pamidi S, Tasali E. \u003Cem\u003EFront Neurol\u003C\/em\u003E 2012].\u003C\/p\u003E\u003Cp id=\u0022p-5\u0022\u003EYoung lean men with OSA had reduced insulin sensitivity and higher total insulin secretion than controls despite similar glucose levels after an oral glucose tolerance test [Pamidi S et al. \u003Cem\u003EDiabetes Care\u003C\/em\u003E 2012]. Increasing severity of AHI was independently associated with impaired glucose metabolism in a multicentric cohort of 1599 subjects without T2DM [Priou P et al. \u003Cem\u003EDiabetes Care\u003C\/em\u003E 2012].\u003C\/p\u003E\u003Cp id=\u0022p-6\u0022\u003ESleep fragmentation and intermittent hypoxia can lead to insulin resistance and pancreatic \u03b2-cell dysfunction through sympathetic activation, alterations in the HPA axis (ie, increase in levels of cortisol), oxidative stress, activation of inflammatory pathways that promote the release of interleukin-6 and tumor necrosis factor-\u03b1, and adverse changes in adipokine profiles including a reduction in adiponectin.\u003C\/p\u003E\u003Cp id=\u0022p-7\u0022\u003EIntermittent hypoxia causes reduced muscle glucose utilization in the soleus muscle in lean mice [Iiyori N et al. \u003Cem\u003EAm J Respir Crit Care Med\u003C\/em\u003E 2007] and increased \u03b2-cell proliferation and cell death presumably due to oxidative stress [Xu J et al. \u003Cem\u003EFree Radic Biol Med\u003C\/em\u003E 2009]. An increase in free fatty acid uptake by the liver induced by intermittent hypoxia may upregulate transcriptional pathways of lipid biosynthesis through HIF-1, leading to liver insulin resistance and nonalcoholic steatohepatitis conceivably through accelerated adipose tissue lipolysis [Mirrakhimov AE, Polotsky VY. \u003Cem\u003EFront Neurol\u003C\/em\u003E 2012].\u003C\/p\u003E\u003Cp id=\u0022p-8\u0022\u003EIn morbidly obese people, chronic intermittent hypoxia is an independent predictor for nonalcoholic fatty liver disease (NAFLD), hepatic fibrosis, and fibroinflammation [Aron-Wisnewsky J et al. \u003Cem\u003EJ Hepatol\u003C\/em\u003E 2012]. Chronic intermittent hypoxia was found to have differential metabolic effects in lean and obese mice, inducing NAFLD, oxidative stress, and inflammation in only the obese mice [Drager LF et al. \u003Cem\u003EObesity\u003C\/em\u003E 2011].\u003C\/p\u003E\u003Cp id=\u0022p-9\u0022\u003EIn uncontrolled studies, it has been initially evidenced that long-term continuous positive airway pressure (CPAP) reduced HbA1C levels in diabetic individuals with sleep-disordered breathing [Babu AR et al. \u003Cem\u003EArch Intern Med\u003C\/em\u003E 2005]. Also, a rapid improvement in insulin sensitivity in patients with OSA obtained after initiation of CPAP may reflect a reduction in sympathetic activity [Harsch IA et al. \u003Cem\u003EAm J Respir Crit Care Med\u003C\/em\u003E 2004]. The effect was smaller in obese patients, which suggests that in obese patients, insulin sensitivity is determined more by obesity than OSA.\u003C\/p\u003E\u003Cp id=\u0022p-10\u0022\u003EAnthropometric variables (weight, body mass index, subcutaneous fat, visceral fat) improved significantly in a group of OSA patients who underwent 3 months of CPAP compared with sham CPAP [Sharma SK et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2011]. This may explain the overall improvement in the metabolic profile in this study where the study group was highly selected (ie, untreated moderately obese subjects presenting with dysmetabolism). So far, this paper provided the most impressive results but most randomized controlled trials did not confirm this metabolic improvement during OSA treatment [Weinstock TG et al. \u003Cem\u003ESleep\u003C\/em\u003E 2012; Sivam S et al. \u003Cem\u003EEur Respir J\u003C\/em\u003E 2012; Hoyos CM et al. \u003Cem\u003EThorax\u003C\/em\u003E 2012]. Pepin et al. recently published a summary explaining the conflicting results [\u003Cem\u003EThorax\u003C\/em\u003E 2012]. The duration of CPAP, patient age, comorbidities, and the severity of OSA and intermittent hypoxia all appear to be critical factors in the relative success of CPAP in treating OSA.\u003C\/p\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2013 MD Conference Express\u00ae\u003C\/li\u003E\u003C\/ul\u003E\u003Cspan class=\u0022highwire-journal-article-marker-end\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Cspan id=\u0022related-urls\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Ca href=\u0022http:\/\/mdc.sagepub.com\/content\/13\/4\/14.abstract\u0022 class=\u0022hw-link hw-link-article-abstract\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView Summary\u003C\/a\u003E\u003C\/div\u003E  \u003C\/div\u003E\n\n  \n  \u003C\/div\u003E\n\u003C\/div\u003E\n  \u003C\/div\u003E\n\u003C\/div\u003E\n\u003C\/div\u003E\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_openurl.js?nznx9e\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}