scholarly journals Metabolic dysfunction in obstructive sleep apnea: A critical examination of underlying mechanisms

2014 ◽  
Vol 13 (1) ◽  
pp. 2-17 ◽  
Author(s):  
Omar A Mesarwi ◽  
Ellora V Sharma ◽  
Jonathan C Jun ◽  
Vsevolod Y Polotsky
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Critical Examination ◽  
Metabolic Dysfunction ◽  
Obstructive Sleep ◽  
Underlying Mechanisms

scholarly journals Translational approaches to understanding metabolic dysfunction and cardiovascular consequences of obstructive sleep apnea

2015 ◽  
Vol 309 (7) ◽  
pp. H1101-H1111 ◽  
Author(s):  
Luciano F. Drager ◽  
Vsevolod Y. Polotsky ◽  
Christopher P. O'Donnell ◽  
Sergio L. Cravo ◽  
Geraldo Lorenzi-Filho ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Cardiovascular Risk ◽  
Sleep Apnea ◽  
Animal Models ◽  
Metabolic Dysfunction ◽  
Significant Progress ◽  
Glucose And Lipid Metabolism ◽  
Obstructive Sleep ◽  
Underlying Mechanisms ◽  
Made In

Obstructive sleep apnea (OSA) is known to be independently associated with several cardiovascular diseases including hypertension, myocardial infarction, and stroke. To determine how OSA can increase cardiovascular risk, animal models have been developed to explore the underlying mechanisms and the cellular and end-organ targets of the predominant pathophysiological disturbance in OSA–intermittent hypoxia. Despite several limitations in translating data from animal models to the clinical arena, significant progress has been made in our understanding of how OSA confers increased cardiovascular risk. It is clear now that the hypoxic stress associated with OSA can elicit a broad spectrum of pathological systemic events including sympathetic activation, systemic inflammation, impaired glucose and lipid metabolism, and endothelial dysfunction, among others. This review provides an update of the basic, clinical, and translational advances in our understanding of the metabolic dysfunction and cardiovascular consequences of OSA and highlights the most recent findings and perspectives in the field.

scholarly journals Effects of acute intermittent hypoxia on glucose metabolism in awake healthy volunteers

2009 ◽  
Vol 106 (5) ◽  
pp. 1538-1544 ◽  
Author(s):  
Mariam Louis ◽  
Naresh M. Punjabi
Keyword(s):  
Obstructive Sleep Apnea ◽  
Insulin Secretion ◽  
Sleep Apnea ◽  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Healthy Volunteers ◽  
Intermittent Hypoxia ◽  
Metabolic Dysfunction ◽  
Glucose Effectiveness ◽  
Obstructive Sleep

Accumulating evidence suggests that obstructive sleep apnea is associated with alterations in glucose metabolism. Although the pathophysiology of metabolic dysfunction in obstructive sleep apnea is not well understood, studies of murine models indicate that intermittent hypoxemia has an important contribution. However, corroborating data on the metabolic effects of intermittent hypoxia on glucose metabolism in humans are not available. Thus the primary aim of this study was to characterize the acute effects of intermittent hypoxia on glucose metabolism. Thirteen healthy volunteers were subjected to 5 h of intermittent hypoxia or normoxia during wakefulness in a randomized order on two separate days. The intravenous glucose tolerance test (IVGTT) was used to assess insulin-dependent and insulin-independent measures of glucose disposal. The IVGTT data were analyzed using the minimal model to determine insulin sensitivity (SI) and glucose effectiveness (SG). Drops in oxyhemoglobin saturation were induced during wakefulness at an average rate of 24.3 events/h. Compared with the normoxia condition, intermittent hypoxia was associated with a decrease in SI [4.1 vs. 3.4 (mU/l)−1·min−1; P = 0.0179] and SG (1.9 vs. 1.3 min−1×10−2, P = 0.0065). Despite worsening insulin sensitivity with intermittent hypoxia, pancreatic insulin secretion was comparable between the two conditions. Heart rate variability analysis showed the intermittent hypoxia was associated with a shift in sympathovagal balance toward an increase in sympathetic nervous system activity. The average R-R interval on the electrocardiogram was 919.0 ms during the normoxia condition and 874.4 ms during the intermittent hypoxia condition ( P < 0.04). Serum cortisol levels after intermittent hypoxia and normoxia were similar. Hypoxic stress in obstructive sleep apnea may increase the predisposition for metabolic dysfunction by impairing insulin sensitivity, glucose effectiveness, and insulin secretion.

scholarly journals Impaired Glucose Metabolisms of Patients with Obstructive Sleep Apnea and Type 2 Diabetes

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Ye Zhang ◽  
Yanpeng Xing ◽  
Haibo Yuan ◽  
Xiaokun Gang ◽  
Weiying Guo ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Plasma Cortisol ◽  
Sleep Disordered Breathing ◽  
Model Assessment ◽  
Obstructive Sleep ◽  
Underlying Mechanisms ◽  
Disordered Breathing

Aims. Obstructive sleep apnea (OSA) is a very common disorder which is associated with metabolic comorbidities. The aims of this study were to analyze clinical data of patients with OSA and evaluate influence of sleep-disordered breathing on glycometabolism and its underlying mechanisms. Methods. We designed a cross-sectional study involving 53 OSA patients in The First Hospital of Jilin University from March 2015 to March 2016. They underwent a full-night polysomnography, measurement of fasting blood glucose and blood lipid profiles. Besides, we chose 20 individuals with type 2 diabetes mellitus (T2DM) as a subgroup for an in-depth study. This group additionally underwent a steamed bread meal test and measurement of HbA1c, C-reactive protein, tumor necrosis factor-α, interleukin 6, morning plasma cortisol, and growth hormone. Results. The two groups which with or without T2DM showed no significant differences in baseline characteristics. As for OSA patients with T2DM, the severe OSA group had higher homeostasis model assessment of insulin resistance (HOMA-IR) (P=0.013) than the mild-to-moderate OSA group, whereas had lower morning plasma cortisol levels (P=0.005) than the mild-to-moderate OSA group. AHI was positive correlated with HOMA-IR (r=0.523, P=0.018), yet negative correlated with morning plasma cortisol (r=−0.694, P=0.001). However, nadir SpO2 was positive correlated with morning plasma cortisol (rs=0.646, P=0.002), while negative correlated with HOMA-IR (rs=−0.489, P=0.029). Conclusions. Our study showed that sleep-disordered breathing exerted negative influence on glucose metabolisms. The impairment of hypothalamic-pituitary-adrenal axis activity may be one of the underlying mechanisms of the glycometabolic dysfunctions in OSA with T2DM patients.

scholarly journals Underlying Mechanisms for Coexisting Central and Obstructive Sleep Apnea: Nocturnal PaCO2 and Poor Sleep Quality Are Key Issues

Respiration ◽  
2015 ◽  
Vol 89 (5) ◽  
pp. 416-419 ◽  
Author(s):  
Olivier Contal ◽  
Jean Louis P�pin ◽  
Jean Christian Borel ◽  
Fabrice Espa ◽  
Stephen Perrig ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Sleep Quality ◽  
Poor Sleep ◽  
Poor Sleep Quality ◽  
Obstructive Sleep ◽  
Key Issues ◽  
Underlying Mechanisms

scholarly journals Association Between Obstructive Sleep Apnea, Its Treatment, and Alzheimer's Disease: Systematic Mini-Review

2021 ◽  
Vol 12 ◽  
Author(s):  
Chih-Yun Kuo ◽  
Hung-Ta Hsiao ◽  
Ing-Hsien Lo ◽  
Tomas Nikolai
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
The Elderly ◽  
Protein Levels ◽  
Obstructive Sleep ◽  
Increased Risk ◽  
Osa Treatment ◽  
Underlying Mechanisms

Obstructive sleep apnea (OSA) and Alzheimer's disease (AD) are common in the elderly population. Obstructive sleep apnea that may cause significant changes in the cerebrospinal fluid β-amyloid and T-tau and/or P-tau protein levels is often identified as a risk factor for development of AD. Although the underlying mechanisms of AD are still not fully understood, a hypothesis associating OSA with AD has been already proposed. In this systematic mini-review, we first discuss the recent findings supporting the association of OSA with an increased risk of AD and then provide evidence suggesting the positive effect of OSA treatment on a reduced risk of AD.

Impact Of Obstructive Sleep Apnea On Metabolic Dysfunction In Severe Obesity

2011 ◽  
Author(s):  
Mercè Gasa ◽  
Neus Salord ◽  
Ana Maria Fortuna ◽  
Mercè Mayos ◽  
Nuria Vilarrasa ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Severe Obesity ◽  
Metabolic Dysfunction ◽  
Obstructive Sleep

scholarly journals Atrial Arrhythmias in Obstructive Sleep Apnea: Underlying Mechanisms and Implications in the Clinical Setting

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
David Filgueiras-Rama ◽  
Miguel A. Arias ◽  
Ángel Iniesta ◽  
Eduardo Armada ◽  
José L. Merino ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Current Knowledge ◽  
Upper Airway ◽  
Atrial Arrhythmias ◽  
Therapeutic Implications ◽  
Obstructive Sleep ◽  
Cardiovascular Morbidity And Mortality ◽  
Young Subjects ◽  
Underlying Mechanisms

Obstructive sleep apnea (OSA) is a common disorder characterized by repetitive interruption of ventilation during sleep caused by recurrent upper airway collapse, which leads to intermittent hypoxia. The disorder is commonly undiagnosed despite its relationship with substantial cardiovascular morbidity and mortality. Moreover, the effects of the disorder appear to be particularly dangerous in young subjects. In the last decade, substantial clinical evidence has identified OSA as independent risk factor for both bradyarrhythmias and tachyarrhythmias. To date the mechanisms leading to such arrhythmias have not been completely understood. However, recent data from animal models and new molecular analyses have increased our knowledge of the field, which might lead to future improvement in current therapeutic strategies mainly based on continuous positive airway pressure. This paper aims at providing readers a brief and specific revision of current knowledge about the mechanisms underlying atrial arrhythmias in OSA and their clinical and therapeutic implications.

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