Beneficial effects of severe sleep apnea therapy on nocturnal glucose control in persons with type 2 diabetes mellitus

Pallayová, Mária; Donič, Viliam; Tomori, Z

doi:10.1016/j.diabres.2008.03.012

Cited by 60 publications

(29 citation statements)

References 15 publications

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“…In patients with T2D, CPAP has also been shown to reduce nocturnal [37,38] and postprandial peaks of interstitial glycaemia [39]. However, the effect of CPAP on HbA 1c levels has been investigated only in small, non-randomized studies that had divergent results [37,39,40].…”

Section: Discussionmentioning

confidence: 97%

Intermittent hypoxia is an independent marker of poorer glycaemic control in patients with uncontrolled type 2 diabetes

Torrella

Castells

Giménez-Pérez

et al. 2015

Diabetes & Metabolism

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Section: Discussionmentioning

confidence: 97%

Intermittent hypoxia is an independent marker of poorer glycaemic control in patients with uncontrolled type 2 diabetes

Torrella

Castells

Giménez-Pérez

et al. 2015

Diabetes & Metabolism

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“…At least part of the variability in results may be accounted for by the sensitivity of methods to detect IR, especially if one considers the peculiar condition of OSA patients who develop respiratory events only at night. For example, acute CPAP application in diabetic patients was found to decrease glucose level variability, as assessed by continuous glucose monitoring [152,153]. Similarly, glycosylated haemoglobin (HbA1c) could be a sensitive marker of altered glucose metabolism in OSA in patients with [154] or without diabetes [155], or with the MetS [156].…”

Section: Ir and Mets In Osamentioning

confidence: 99%

Adipose tissue in obesity and obstructive sleep apnoea

Bonsignore¹,

McNicholas²,

Montserrat³

et al. 2011

European Respiratory Journal

113

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A European Respiratory Society research seminar on ''Metabolic alterations in obstructive sleep apnoea (OSA)'' was jointly organised in October 2009 together with two EU COST actions (Cardiovascular risk in the obstructive sleep apnoea syndrome, action B26, and Adipose tissue and the metabolic syndrome, action BM0602) in order to discuss the interactions between obesity and OSA.Such interactions can be particularly significant in the pathogenesis of metabolic abnormalities and in increased cardiovascular risk in OSA patients. However, studying the respective role of OSA and obesity is difficult in patients, making it necessary to refer to animal models or in vitro systems. Since most OSA patients are obese, their management requires a multidisciplinary approach.This review summarises some aspects of the pathophysiology and treatment of obesity, and the possible effects of sleep loss on metabolism. OSA-associated metabolic dysfunction (insulin resistance, liver dysfunction and atherogenic dyslipidaemia) is discussed from the perspective of both obesity and OSA in adults and children.Finally, the effects of treatment for obesity or OSA, or both, on cardio-metabolic variables are summarised. Further interdisciplinary research is needed in order to develop new comprehensive treatment approaches aimed at reducing sleep disordered breathing, obesity and cardiovascular risk.

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“…Third, most studies involve IH exposures lasting days to weeks in an effort to simulate the chronic IH of OSA. However, brief and reversible changes in metabolism occur during IH (39,47,52,77), high-altitude hypoxia (45,78), and OSA (18,59). To place chronic effects of IH in their proper context, these acute changes and their mechanisms must first be understood.…”

mentioning

confidence: 99%

“…For example, OSA is associated with diabetes in cross-sectional studies (64), and OSA increases risks of developing diabetes in longitudinal studies (12,16,53). Furthermore, core features of diabetes, such as insulin resistance (29, 32, 76) and hyperglycemia (4,17,18,59), are improved by treatment of OSA with continuous positive airway pressure (57). Mechanisms by which OSA might induce metabolic impairment are poorly understood.…”

mentioning

confidence: 99%

Intermittent hypoxia-induced glucose intolerance is abolished by α-adrenergic blockade or adrenal medullectomy

Jun

Shin

Devera

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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Obstructive sleep apnea causes intermittent hypoxia (IH) during sleep and is associated with dysregulation of glucose metabolism. We developed a novel model of clinically realistic IH in mice to test the hypothesis that IH causes hyperglycemia, glucose intolerance, and insulin resistance via activation of the sympathetic nervous system. Mice were exposed to acute hypoxia of graded severity (21, 14, 10, and 7% O2) or to IH of graded frequency [oxygen desaturation index (ODI) of 0, 15, 30, or 60, SpO2 nadir 80%] for 30 min to measure levels of glucose fatty acids, glycerol, insulin, and lactate. Glucose tolerance tests and insulin tolerance tests were then performed under each hypoxia condition. Next, we examined these outcomes in mice that were administered phentolamine (α-adrenergic blockade) or propranolol (β-adrenergic blockade) or that underwent adrenal medullectomy before IH exposure. In all experiments, mice were maintained in a thermoneutral environment. Sustained and IH induced hyperglycemia, glucose intolerance, and insulin resistance in a dose-dependent fashion. Only severe hypoxia (7% O2) increased lactate, and only frequent IH (ODI 60) increased plasma fatty acids. Phentolamine or adrenal medullectomy both prevented IH-induced hyperglycemia and glucose intolerance. IH inhibited glucose-stimulated insulin secretion, and phentolamine prevented the inhibition. Propranolol had no effect on glucose metabolism but abolished IH-induced lipolysis. IH-induced insulin resistance was not affected by any intervention. Acutely hypoxia causes hyperglycemia, glucose intolerance, and insulin resistance in a dose-dependent manner. During IH, circulating catecholamines act upon α-adrenoreceptors to cause hyperglycemia and glucose intolerance.

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Beneficial effects of severe sleep apnea therapy on nocturnal glucose control in persons with type 2 diabetes mellitus

Cited by 60 publications

References 15 publications

Intermittent hypoxia is an independent marker of poorer glycaemic control in patients with uncontrolled type 2 diabetes

Intermittent hypoxia is an independent marker of poorer glycaemic control in patients with uncontrolled type 2 diabetes

Adipose tissue in obesity and obstructive sleep apnoea

Intermittent hypoxia-induced glucose intolerance is abolished by α-adrenergic blockade or adrenal medullectomy

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