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Obstructive sleep apnoea and metabolic syndrome: put CPAP efficacy in a more realistic perspective
  1. Jean-Louis Pépin1,2,
  2. Renaud Tamisier1,2,
  3. Patrick Lévy1,2
  1. 1Laboratoire HP2, Hypoxie: Physiopathologies, Faculté de Médecine, Université Joseph Fourier; INSERM U 1042, Grenoble Cedex 09, France
  2. 2Pôle Locomotion, Rééducation et Physiologie, CHU de Grenoble, Grenoble Cedex 09, France
  1. Correspondence to Professor Jean Louis Pépin, Laboratoire EFCR, CHU de Grenoble, BP217X, Grenoble Cedex 09 38043, France; jpepin{at}

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Non-communicable Diseases, mainly cardiovascular diseases, cancer, diabetes and chronic respiratory diseases, are responsible for two-thirds of the 57 million annual deaths worldwide.1 Obesity and obstructive sleep apnoea (OSA) are among the key players involved in non-communicable diseases. Several studies have reported an independent association of OSA with the different components of the metabolic syndrome, particularly hypertension, insulin resistance and abnormal lipid metabolism.2 Both OSA and metabolic syndrome are associated with an increase risk in cardiovascular disease. Hence, rapidly accumulating data from both epidemiological and clinical studies3 have suggested that OSA is independently associated with alterations in glucose metabolism and with an increased risk of developing type 2 diabetes. Indeed, recent reports have indicated that more than 50% of patients with type 2 diabetes have OSA. Multiple mechanistic pathways contribute to the deteriorated plasma glucose/insulin homeostasis in OSA, the number one being sympathetic over activity,4 due to sleep fragmentation and intermittent hypoxia (figure 1). Independently of autonomic nervous system activation, in animal models intermittent hypoxia contributes to decreased glucose utilisation in oxidative muscle fibres.5 Intermittent hypoxia also seems to be responsible for increased beta-cell proliferation and cell death, the latter being due to oxidative stress.6 In fat tissue, chronic intermittent hypoxia (CIH) the hallmark of OSA exacerbate adipose tissue inflammation and lead to a dysregulated production of adipocytokines which may contribute to insulin resistance and could trigger non-alcoholic fatty liver disease (figure 1). We have demonstrated in morbid obesity that CIH is strongly associated with higher systemic inflammation (IL-6) and more severe fibrotic or inflammatory liver injuries.7 Visceral fat releases free fatty acids in the portal vein leading to accumulation of hepatic fat and development of hepatic insulin resistance. Regarding lipid abnormalities, intermittent hypoxia leads to an increase in serum cholesterol, to an up-regulation …

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  • Competing interests None.

  • Provenance and peer review Not commissioned; internally peer reviewed.

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