Obstructive sleep apnoea and type 2 diabetes mellitus
Authors:
Andrea Plíhalová 1,2; Kateřina Westlake 1,3; Jan Polák 1,2
Authors‘ workplace:
II. interní klinika 3. LF UK a FN Královské Vinohrady Praha
1; Centrum pro výzkum diabetu, metabolizmu a výživy 3. LF UK, Praha
2; Diabetologická ambulance Diabetologie Praha, s. r. o.
3
Published in:
Vnitř Lék 2016; 62(Suppl 4): 79-84
Category:
Reviews
Overview
Obstructive sleep apnoea syndrome (OSA) is a disease very frequently occurring in people with type 2 diabetes, that significantly increases cardiovascular morbidity and mortality. In a number of studies, OSA has been identified as an independent risk factor for the development of insulin resistance, glucose intolerance and type 2 diabetes mellitus. Disorders of glucose homeostasis in patients with OSA are probably mediated by chronic intermittent hypoxia and/or sleep fragmentation through activation of the sympathetic nervous system, the hypothalamic-pituitary-adrenal stress axis, pro-inflammatory paths or oxidative stress. Despite the high prevalence of OSA among patients with type 2 diabetes as well as the proven benefit of the continuous positive airway pressure (CPAP) therapy on reduction of mortality, most patients with OSA remain undiagnosed. Active OSA screening should therefore be performed in all patients with type 2 diabetes, ideally through home monitoring of oxygen saturation and breathing during sleep. Although the effect of CPAP therapy on the improvement in diabetes control (decrease in glycated hemoglobin) has not been clearly proven in patients with type 2 diabetes so far, promising outcomes have been observed during the treatment of patients with prediabetes.
Key words:
CPAP – diabetes mellitus – glycemic control – intermittent hypoxia – obstructive sleep apnoea – screening – sleep fragmentation
Sources
1. Jennum P, Riha RL. Epidemiology of sleep apnoea/hypopnoea syndrome and sleep-disordered breathing. Eur Respir J 2009; 33(4): 907–914. Dostupné z DOI: <http://dx.doi.org/10.1183/09031936.00180108>.
2. Young T, Skatrud J, Peppard PE. Risk factors for obstructive sleep apnea in adults. Jama 2004; 291(16): 2013–2016.
3. Young T, Peppard PE, Taheri S. Excess weight and sleep-disordered breathing. J Appl Physiol (1985) 2005; 99(4): 1592–1599.
4. Lopez PP, Stefan B, Schulman CI et al. Prevalence of sleep apnea in morbidly obese patients who presented for weight loss surgery evaluation: more evidence for routine screening for obstructive sleep apnea before weight loss surgery. Am Surg 2008; 74(9): 834–838.
5. Aronsohn RS, Whitmore H, Van Cauter E et al. Impact of untreated obstructive sleep apnea on glucose control in type 2 diabetes. Am J Respir Crit Care Med 2010; 181(5): 507–513. Dostupné z DOI: <http://dx.doi.org/10.1164/rccm.200909–1423OC>.
6. Westlake K, Plihalova A, Pretl M et al. Screening for Obstructive Sleep Apnea Syndrome in Patients with Type 2 Diabetes Mellitus: A Prospective Study on Sensitivity of Berlin and STOP-Bang Questionnaires. Sleep Med 2016. pii: S1389–9457(16)30113–7. Dostupné z DOI: <http://dx.doi.org/10.1016/j.sleep.2016.07.009>.
7. Peppard PE, Young T, Palta M et al. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med 2000; 342(19): 1378–1384.
8. Shahar E, Whitney CW, Redline S et al. Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study. Am J Respir Crit Care Med 2001; 163(1): 19–25.
9. Mehra R, Benjamin EJ, Shahar E et al. Association of nocturnal arrhythmias with sleep-disordered breathing: The Sleep Heart Health Study. Am J Respir Crit Care Med 2006; 173(8): 910–916.
10. Punjabi NM, Caffo BS, Goodwin JL et al. Sleep-disordered breathing and mortality: a prospective cohort study. PLoS Med 2009; 6(8): e1000132. Dostupné z DOI: <http://dx.doi.org/10.1371/journal.pmed.1000132>.
11. Seicean S, Kirchner HL, Gottlieb DJ et al. Sleep-disordered breathing and impaired glucose metabolism in normal-weight and overweight/obese individuals: the Sleep Heart Health Study. Diabetes Care 2008; 31(5): 1001–1006. Dostupné z DOI: <http://dx.doi.org/10.2337/dc07–2003>.
12. Ip MS, Lam B, Ng MM et al. Obstructive sleep apnea is independently associated with insulin resistance. Am J Respir Crit Care Med 2002; 165(5): 670–676.
13. Pamidi S, Tasali E. Obstructive sleep apnea and type 2 diabetes: is there a link? Front Neurol 2012; 3: 126. eCollection 2012.
14. Punjabi NM, Shahar E, Redline S et al. Sleep-disordered breathing, glucose intolerance, and insulin resistance: the Sleep Heart Health Study. Am J Epidemiol 2004; 160(6): 521–530.
15. Borel AL, Monneret D, Tamisier R et al. The severity of nocturnal hypoxia but not abdominal adiposity is associated with insulin resistance in non-obese men with sleep apnea. PloS One 2013; 8(8): e71000. Dostupné z DOI: <http://dx.doi.org/10.1371/journal.pone.0071000>.
16. Al-Delaimy WK, Manson JE, Willett WC et al. Snoring as a risk factor for type II diabetes mellitus: a prospective study. Am J Epidemiol 2002; 155(5): 387–393.
17. Polotsky VY, Li J, Punjabi NM et al. Intermittent hypoxia increases insulin resistance in genetically obese mice. The Journal of physiology 2003; 552(Pt 1): 253–264.
18. Polak J, Shimoda LA, Drager LF et al. Intermittent hypoxia impairs glucose homeostasis in C57BL6/J mice: partial improvement with cessation of the exposure. Sleep 2013; 36(10): 1483–1490; 1490a-1490b. Dostupné z DOI: <http://dx.doi.org/10.5665/sleep.3040>.
19. Drager LF, Li J, Reinke C et al. Intermittent hypoxia exacerbates metabolic effects of diet-induced obesity. Obesity (Silver Spring) 2011; 19(11): 2167–2174. Dostupné z DOI: <http://dx.doi.org/10.1038/oby.2011.240>.
20. Iiyori N, Alonso LC, Li J et al. Intermittent hypoxia causes insulin resistance in lean mice independent of autonomic activity. Am J Respir Crit Care Med 2007; 175(8): 851–857.
21. Xu J, Long YS, Gozal D et al. Beta-cell death and proliferation after intermittent hypoxia: role of oxidative stress. Free Radic Biol Med 2009; 46(6): 783–790. Dostupné z DOI: <http://dx.doi.org/10.1016/j.freeradbiomed.2008.11.026>.
22. Wang N, Khan SA, Prabhakar NR et al. Impairment of pancreatic beta-cell function by chronic intermittent hypoxia. Exp Physiol 2013; 98(9): 1376–1385. Dostupné z DOI: <http://dx.doi.org/10.1113/expphysiol.2013.072454>.
23. Ko SH, Ryu GR, Kim S et al. Inducible nitric oxide synthase-nitric oxide plays an important role in acute and severe hypoxic injury to pancreatic beta cells. Transplantation 2008; 85(3): 323–330. Dostupné z DOI: <http://dx.doi.org/10.1097/TP.0b013e31816168f9>.
24. Louis M, Punjabi NM. Effects of acute intermittent hypoxia on glucose metabolism in awake healthy volunteers. J Appl Physiol (1985) 2009; 106(5): 1538–1544. Dostupné z DOI: <http://dx.doi.org/10.1152/japplphysiol.91523.2008>.
25. Drager LF, Jun JC, Polotsky VY. Metabolic consequences of intermittent hypoxia: relevance to obstructive sleep apnea. Best Pract Res Clin Endocrinol Metab 2010; 24(5): 843–851. Dostupné z DOI: <http://dx.doi.org/10.1016/j.beem.2010.08.011>.
26. Xing T, Pilowsky PM, Fong AY. Mechanism of sympathetic activation and blood pressure elevation in humans and animals following acute intermittent hypoxia. Prog Brain Res 2014; 209: 131–146. Dostupné z DOI: <http://dx.doi.org/10.1016/B978–0-444–63274–6.00007–2>.
27. Jun J, Polotsky VY. Sleep disorder breathing and metabolic effects: evidence from animal models. Sleep Med Clin 2007; 2(2): 263–277.
28. Lafontan M, Langin D. Lipolysis and lipid mobilization in human adipose tissue. Prog Lipid Res 2009; 48(5): 275–297. Dostupné z DOI: <http://dx.doi.org/10.1016/j.plipres.2009.05.001>.
29. Samuel VT, Petersen KF, Shulman GI. Lipid-induced insulin resistance: unravelling the mechanism. Lancet 2010; 375(9733): 2267–2277. Dostupné z DOI: <http://dx.doi.org/10.1016/S0140–6736(10)60408–4>.
30. Giacca A, Xiao C, Oprescu AI et al. Lipid-induced pancreatic beta-cell dysfunction: focus on in vivo studies. American journal of physiology Endocrinology and metabolism 2011; 300(2): E255-E262.
31. Weiszenstein M, Musutova M, Plihalova A et al. Adipogenesis, lipogenesis and lipolysis is stimulated by mild but not severe hypoxia in 3T3-L1 cells. Biochem Biophys Res Commun 2016; 478(2): 727–732. Dostupné z DOI: <http://dx.doi.org/10.1016/j.bbrc.2016.08.015>.
32. Weiszenstein M, Pavlikova N, Elkalaf M et al. The Effect of Pericellular Oxygen Levels on Proteomic Profile and Lipogenesis in 3T3-L1 Differentiated Preadipocytes Cultured on Gas-Permeable Cultureware. PloS One 2016; 11(3): e0152382. Dostupné z DOI: <http://dx.doi.org/10.1371/journal.pone.0152382>.
33. Weiszenstein M, Shimoda LA, Koc M et al. Inhibition of Lipolysis Ameliorates Diabetic Phenotype in a Mouse Model of Obstructive Sleep Apnea. Am J Respir Cell Mol Biol 2016; 55(2): 299–307. Dostupné z DOI: <http://dx.doi.org/10.1165/rcmb.2015–0315OC>.
34. Yokoe T, Alonso LC, Romano LC et al. Intermittent hypoxia reverses the diurnal glucose rhythm and causes pancreatic beta-cell replication in mice. Journal Physiol 2008; 586(3): 899–911.
35. Morton NM. Obesity and corticosteroids: 11beta-hydroxysteroid type 1 as a cause and therapeutic target in metabolic disease. Mol Cell Endocrinol 2010; 316(2): 154–164. Dostupné z DOI: <http://dx.doi.org/10.1016/j.mce.2009.09.024>.
36. Rosmond R. Stress induced disturbances of the HPA axis: a pathway to Type 2 diabetes? Med Sci Monit 2003; 9(2): Ra35-Ra39.
37. da Rosa DP, Forgiarini LF, Baronio D et al. Simulating sleep apnea by exposure to intermittent hypoxia induces inflammation in the lung and liver. Mediators Inflamm 2012; 2012: 879419. Dostupné z DOI: <http://dx.doi.org/10.1155/2012/879419>.
38. Phillips BG, Kato M, Narkiewicz K et al. Increases in leptin levels, sympathetic drive, and weight gain in obstructive sleep apnea. Am J Physiol Heart Circ Physiol 2000; 279(1): H234-H237.
39. Briançon-Marjollet A, Weiszenstein M, Henri M et al. The impact of sleep disorders on glucose metabolism: endocrine and molecular mechanisms. Diabetol Metab Syndr 2015; 7: 25. Dostupné z DOI: <http://dx.doi.org/1186/s13098–015–0018–3>.
40. Stamatakis KA, Punjabi NM. Effects of sleep fragmentation on glucose metabolism in normal subjects. Chest 2010; 137(1): 95–101. Dostupné z DOI: <http://dx.doi.org/10.1378/chest.09–0791>.
41. Gonnissen HK, Hursel R, Rutters F et al. Effects of sleep fragmentation on appetite and related hormone concentrations over 24 h in healthy men. Br J Nutr 2013; 109(4): 748–756. Dostupné z DOI: <http://dx.doi.org/10.1017/S0007114512001894>.
42. Tasali E, Leproult R, Ehrmann DA et al. Slow-wave sleep and the risk of type 2 diabetes in humans. Proc Natl Acad Sci U S A 2008; 105(3): 1044–1049. Dostupné z DOI: <http://dx.doi.org/10.1073/pnas.0706446105>.
43. Buxton OM, Cain SW, O’Connor SP et al. Adverse metabolic consequences in humans of prolonged sleep restriction combined with circadian disruption. Sci Transl Med 2012; 4(129): 129ra43. Dostupné z DOI: <http://dx.doi.org/10.1126/scitranslmed.3003200>.
44. Marin JM, Carrizo SJ, Vicente E et al. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet 2005; 365(9464): 1046–1053.
45. Martinez-Garcia MA, Campos-Rodriguez F, Catalan-Serra P et al. Cardiovascular mortality in obstructive sleep apnea in the elderly: role of long-term continuous positive airway pressure treatment: a prospective observational study. Am J Respir Crit Care Med 2012; 186(9): 909–916. Dostupné z DOI: <http://dx.doi.org/10.1164/rccm.201203–0448OC>.
46. Jennum P, Tonnesen P, Ibsen R et al. All-cause mortality from obstructive sleep apnea in male and female patients with and without continuous positive airway pressure treatment: a registry study with 10 years of follow-up. Nat Sci Sleep 2015; 7: 43–50. eCollection 2015. Dostupné z DOI: <http://dx.doi.org/10.2147/NSS.S75166>.
47. Pallayova M, Donic V, Tomori Z. Beneficial effects of severe sleep apnea therapy on nocturnal glucose control in persons with type 2 diabetes mellitus. Diabetes Res Clin Pract 2008; 81(1): e8-e11. Dostupné z DOI: <http://dx.doi.org/10.1016/j.diabres.2008.03.012>.
48. Babu AR, Herdegen J, Fogelfeld L et al. Type 2 diabetes, glycemic control, and continuous positive airway pressure in obstructive sleep apnea. Arch Intern Med 2005; 165(4): 447–452.
49. West SD, Nicoll DJ, Wallace TM et al. Effect of CPAP on insulin resistance and HbA1c in men with obstructive sleep apnoea and type 2 diabetes. Thorax 2007; 62(11): 969–974.
50. Shaw JE, Punjabi NM, Naughton MT et al. The Effect of Treatment of Obstructive Sleep Apnea on Glycemic Control in Type 2 Diabetes. Am J Respir Crit Care Med 2016; 194(4): 486–492. Dostupné z DOI: <http://dx.doi.org/10.1164/rccm.201511–2260OC>.
51. Feng Y, Zhang Z, Dong ZZ. Effects of continuous positive airway pressure therapy on glycaemic control, insulin sensitivity and body mass index in patients with obstructive sleep apnoea and type 2 diabetes: a systematic review and meta-analysis. NPJ Prim Care Respir Med 2015; 25: 15005. Dostupné z DOI: <http://dx.doi.org/10.1038/npjpcrm.2015.5>.
52. Pamidi S, Wroblewski K, Stepien M et al. Eight Hours of Nightly Continuous Positive Airway Pressure Treatment of Obstructive Sleep Apnea Improves Glucose Metabolism in Patients with Prediabetes. A Randomized Controlled Trial. Am J Respir Crit Care Med 2015; 192(1): 96–105. Dostupné z DOI: <http://dx.doi.org/10.1164/rccm.201408–1564OC>.
53. Weinstock TG, Wang X, Rueschman M et al. A controlled trial of CPAP therapy on metabolic control in individuals with impaired glucose tolerance and sleep apnea. Sleep 2012; 35(5): 617b-625b. Dostupné z DOI: <http://dx.doi.org/10.5665/sleep.1816>.
54. Iftikhar IH, Khan MF, Das A et al. Meta-analysis: continuous positive airway pressure improves insulin resistance in patients with sleep apnea without diabetes. Ann Am Thorac Soc 2013; 10(2): 115–120. Dostupné z DOI: <http://dx.doi.org/10.1513/AnnalsATS.201209–081OC>. Erratum in Ann Am Thorac Soc 2013; 10(3): 279.
55. Botros N, Concato J, Mohsenin V et al. Obstructive sleep apnea as a risk factor for type 2 diabetes. Am J Med 2009; 122(12): 1122–1127. Dostupné z DOI: <http://dx.doi.org/10.1016/j.amjmed.2009.04.026>.
56. Young T, Evans L, Finn L et al. Estimation of the clinically diagnosed proportion of sleep apnea syndrome in middle-aged men and women. Sleep 1997; 20(9): 705–706.
57. Chung F, Subramanyam R, Liao P et al. High STOP-Bang score indicates a high probability of obstructive sleep apnoea. Br J Anaesth 2012; 108(5): 768–775. Dostupné z DOI: <http://dx.doi.org/10.1093/bja/aes022>.
58. Pataka A, Daskalopoulou E, Kalamaras G et al. Evaluation of five different questionnaires for assessing sleep apnea syndrome in a sleep clinic. Sleep Med 2014; 15(7): 776–781. Dostupné z DOI: <http://dx.doi.org/10.1016/j.sleep.2014.03.012>.
59. Erman MK, Stewart D, Einhorn D et al. Validation of the ApneaLink for the screening of sleep apnea: a novel and simple single-channel recording device. J Clin Sleep Med 2007; 3(4): 387–392.
60. Westlake K, Polak J. Screening for Obstructive Sleep Apnea in Type 2 Diabetes Patients – Questionnaires Are Not Good Enough. Front Endocrinol (Lausanne) 2016; 7:124. Dostupné z DOI: <http://dx.doi.org/10.3389/fendo.2016.00124>.
Labels
Diabetology Endocrinology Internal medicineArticle was published in
Internal Medicine
2016 Issue Suppl 4
Most read in this issue
- Congenital hyperinsulinism: Loss of B-cell self-control
- Gestational Diabetes Mellitus
- Growth hormone, axis GH-IGF1 and glucose metabolism
- Education of a patient with diabetes – an integral part of complex therapy