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doi: 10.1111/1753-0407.12211

Journal of Diabetes 7 (2015) 8–9

C O M M E N TA R Y

Advances in sleep research It is well established that there are relationships of sleepdisordered breathing (especially obstructive sleep apnea), sleep architecture, sleep duration, and other sleep disorders with various metrics of insulin resistance and dysglycemia. However, our understanding of these relationships is still evolving, and is sometimes confusing and occasionally contradictory. Comparison of studies is hampered by the lack of uniform definitions of what is being measured, limitations of self-reporting, short duration of studies, and accounting for severity of co-morbidities. Four articles in this issue of the Journal of Diabetes provide significant contributions to our understanding of the relationship between sleep and diabetes. Zhang et al. studied the prevalence of obstructive sleep apnea (OSA) in a population of type 2 diabetics (T2DM) hospitalized primarily for poor glycemic control and examined the relationships between demographics and co-morbidities.1 The hospital is an opportunistic setting for diagnosing OSA and, indeed, screening for OSA may become part of guidelines for in-hospital management of T2DM (AACE/ACE).2 Our Scripps research team helped validate the convenient portable Apnea-Link device used by this study to measure OSA, and found it to be comparable to polysomnography (Erman et al.).3 The researchers were careful in accounting for as many variables as possible, including potential ascertainment bias in who consented to the study versus who did not. The overall OSA prevalence of 66.7% is consistent with prior studies, although the prevalence at different severities of OSA is difficult to compare across studies. Also consistent was the observation that, controlling for co-morbidities, OSA did not appear to have an independent association with coronary artery disease, hypertension, or diabetic microvascular complications. A new additional observation was that “lowest oxygen saturation was independently associated with the presence of PDR (proliferative diabetic retinopathy) and cerebral infarction”. This needs to be confirmed and better understood, but it does suggest that measurement of oxygen saturation is an important part of OSA assessment that currently is not universal. The Discussion section does an excellent job of summarizing the epidemiologic research in this area to date and the suggested mechanisms underlying the associations. In summary, this study demonstrates that Beijing hospital adult populations with T2DM are similar to those in other countries with regard 8

to OSA and that the hospital setting can be very productive for screening individuals for OSA. Zheng et al. explore a subset of the REACTION study, which is commented on elsewhere in this journal.4 The study has the advantages of large size, over 18 000 subjects, direct glucose measurements, and a broad cross section of subjects with T2DM. It appears to be the largest such study conducted to date. Limitations include those of self-reporting sleep duration and quality, and especially the presence of sleep-disordered breathing. It is important to note that when self-reported snoring was factored in, the association between long sleep duration and worsened dysglycemia was no longer significant. Overall, this study is also an affirmation of prior observations that sleep duration has a U-shaped relationship to dysglycemia, with both shorter and longer duration sleepers having worse dysglycemia. Another interesting observation was that “the interaction between long sleep duration and TG seemed to be highly significant (P < 0.001), and the association of long sleep duration with HbA1 levels is attenuated if TG levels are adjusted, with P-value rising from 0.009 to 0.020.” This may relate to changes in insulin resistance, measures of which, such as HOMA-IR, were not performed. Zhu et al. offer novel and important insights into both the impact of sleep architecture and the relationship between sleep and dysglycemia in a pediatric and adolescent population.5 These populations have been grossly under-represented in sleep studies. Only three prior studies have examined sleep architecture in the pediatric population, each having methodological limitations that are overcome in this study. “This,” the authors state, “[appears to be] the first community-based study investigating the association between sleep architecture and glucose and/or insulin homeostasis in both normal and overweight children and adolescents.” The subjects were well characterized demographically and anthopometrically, and studied with the goldstandard polysomnography. This study demonstrated that “higher TST [total sleep time], SE [sleep efficiency], and Stage N3 [slow wave sleep] (% TST) were significantly correlated with lower 2-h glucose levels, higher insulin sensitivity and/or better β-cell function, whereas Stage N1 (% TST) and Stage N2 (% TST) had significant negative correlations with glucose tolerance capacity and/or insulin sensitivity.” The findings confirm our understanding of how sleep impacts glycemic indices, in

© 2014 Ruijin Hospital, Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd

Commentary

this case not relying on self-reported sleep duration, but directly measuring and quantifying sleep architecture. Stage N3 is generally considered the “restorative” period of sleep with diminished sympathetic nervous system activity and cortisol secretion. Stages N1 and N2 are “lighter” sleep, associated with more arousals and therefore less sleep efficiency. With a relatively robust sample size and detailed polysomnography in a sleep lab, this is one of the best and largest studies to date to assess the relationship between the details of sleep quality and glycemic parameters in healthy young subjects. Its findings have important implications to all populations and I expect this study to be cited frequently. Lecube et al. also explore relatively new territory, examining the acute effects of glycemic control on lung function with lessons both for possible central nervous system regulation of glucose and for the lung as a potential target of glycemic control.6 People with T2DM have been shown to have increased nocturnal episodes of oxygen desaturation of varying degrees. The degree of dysglycemia is positively correlated with the degree of desaturations. What Lecube demonstrated is that a relatively brief 5 days improvement in glycemic control, independent of weight loss, reduced the extent of desaturations. The rapidity of improvement suggests a central mechanism, but this has yet to be proven. These findings have important implications for examining other organs not usually considered targets for damage from dysglycemia and for examining acute glycemic effects as clues for predicting long-term impact of glycemic control. The central regulation of glycemic control is increasingly an area of interest. The studies in this issue of the Journal of Diabetes confirm and advance our understanding of the relationship between sleep, insulin resistance, and glycemic control. Each offers a unique addition to the literature and will likely be the basis of many more studies. These studies confirm that healthy sleep is a key part of lifestyle in the prevention and management of diabetes. In light of our understanding of the many other co-morbidities associated with pre-diabetes and diabetes, including cardiovascular disease, cancer, depression, and many other conditions, the implications of these sleep studies appear to be of great importance.

Disclosure ZB declares that he is the speaker and consultant for Merck, Novo Nordisk, Jansen, and AstraZeneca, the speaker for Santarus, holding stocks in Pfizer, Hospira, Zoetis and St Jude Medical, and the consult for St Jude Medical.

References 1. Zhang R, Guo X, Guo L, Lu J, Zhou X, Ji L. Prevalence and associated factors of Obstructive sleep apnea in hospitalized patients with Type 2 diabetes in Beijing, China. J Diabetes. 2015; 7: 16–23. doi: 10.1111/1753-0407.12180. 2. Guidelines for the Management of Diabetes. 2015. American Association of Clinical Endocrinologists/American College of Endocrinology, Endocrine Practice (in development). 3. Erman MK, Stewart D, Einhorn D, Gordon N, Casal E. Validation of the ApneaLink for the screening of sleep apnea: A novel and simple single-channel recording device. J Clin Sleep Med. 2007; 3: 387–92. 4. Zheng Y, Wang A, Pan C et al. impact of night sleep duration on glycemic and triglyceride levels in Chinese with different glycemic status. J Diabetes. 2015; 7: 24–30. doi: 10.1111/1753-0407.12186. 5. Zhu Y, Li AM, Au CT et al. Association between sleep architecture and glucose tolerance in children and adolescents. J Diabetes. 2015; 7: 10–15. doi: 10.1111/17530407.12138. 6. Lecube A, Ciudin A, Sampol G, Valladares S, Hernández C, Simó R. Effect of Glycemic control on nocturnal arterial oxygen saturation. a case-control study in Type 2 diabetic patients. J Diabetes. 2015; 7: 133–8. doi: 10.1111/ 1753-0407.12197.

© 2014 Ruijin Hospital, Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd

Daniel Einhorn Associate Editor Scripps Whittier Diabetes Institute La Jolla, CA, USA Email: [email protected] Zachary T. Bloomgarden Editor-in-Chief Mount Sinai School of Medicine New York, NY, USA Email: [email protected]

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Advances in sleep research.

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