Obesity hypoventilation syndrome

Pierce, Aaron M.; Brown, Lee K.

doi:10.1097/mcp.0000000000000210

Cited by 47 publications

(9 citation statements)

References 36 publications

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“…Hypoxemia is a critical component of respiratory diseases. Before the development of a persistent hypoxemia, a nocturnal desaturation is observed in COPD patients (Kent et al, 2011; Lewis and O’Halloran, 2016) or in patients with obesity hypoventilation syndrome (Pierce and Brown, 2015). Identifying novel therapeutic targets in these patients appear to be still necessary as they are characterized by multiple troubles leading to an increased cardiovascular risk (Kent et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Sustained Intermittent Hypoxemia Induces Adiponectin Oligomers Redistribution and a Tissue-Specific Modulation of Adiponectin Receptor in Mice

et al. 2019

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Introduction: Hypoxemia is a critical component of several respiratory diseases and is known to be involved in the processes underlying co-morbidities associated to such disorders, notably at the cardiovascular level. Circulating level of Adiponectin (Ad), known as a metabolic regulator and cardio-protective hormone was previously suggested to be reduced by hypoxia but consequences of such variation are unclear. The evaluation of the specific effect of hypoxemia on Ad forms and receptors could improve the understanding of the involvement of Ad axis in hypoxemia-related diseases.Methods: Ad-pathway components were investigated in a murine model of sustained intermittent hypoxemia (FiO2 10%, 8 h/day, 35 days).Results: Sustained intermittent hypoxemia (SIH) induced a redistribution of Ad multimers in favor of HMW forms, without change in total plasmatic level. Mice submitted to hypoxia also exhibited tissue-specific modification of adiporeceptor (AdipoR) protein level without mRNA expression change. A decreased AdipoR2 abundance was observed in skeletal muscle and heart whereas AdipoR1 level was only reduced in muscle. No change was observed in liver regarding AdipoR. Lipid profile was unchanged but glucose tolerance increased in hypoxemic mice.Conclusion: Sustained intermittent hypoxemia, per se, modify Ad oligomerization state as well as AdipoR protein abundance in a tissue-specific way. That suggests alteration in Ad-dependant pathways in pathological conditions associated to SIH. Investigation of Ad-pathway components could therefore constitute useful complementary criteria for the clustering of patients with hypoxemia-related diseases and management of co-morbidities, as well as to develop new therapeutic strategies.

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Section: Discussionmentioning

confidence: 99%

Sustained Intermittent Hypoxemia Induces Adiponectin Oligomers Redistribution and a Tissue-Specific Modulation of Adiponectin Receptor in Mice

et al. 2019

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“…Central obesity and increased neck circumference are predisposing factors for OSA [ 95 , 96 ]. The resulting reduction or interruption of airflow, which occurs despite inspiratory effort, causes poor alveolar ventilation and oxyhemoglobin desaturation and, in cases of prolonged events, a progressive increase in the arterial partial pressure of carbon dioxide [ 97 ].…”

Section: Reviewmentioning

confidence: 99%

“…Compared with eucapnic obese patients, patients with OHS have severe upper airway obstruction, restrictive pulmonary damage, decreased central respiratory drive, increased incidence of pulmonary hypertension, and increased mortality [ 100 ]. Among the possible mechanisms involved in the pathogenesis of OHS, some studies have reported damage to respiratory mechanics caused by obesity, leptin resistance leading to central hypoventilation, respiratory sleep disorders, and impaired compensatory responses to acute hypercapnia [ 97 , 100 , 102 ]. With respect to pulmonary function, patients with OHS present a reduction in chest wall compliance of approximately 2.5-fold compared to patients with eucapnic obesity, as well as increased pulmonary resistance that is likely secondary to the reduction in FRC [ 100 ].…”

Section: Reviewmentioning

confidence: 99%

Obesity: systemic and pulmonary complications, biochemical abnormalities, and impairment of lung function

Mafort

Rufino

Costa

et al. 2016

Multidiscip Respir Med

244

210

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Obesity is currently one of the major epidemics of this millennium and affects individuals throughout the world. It causes multiple systemic complications, some of which result in severe impairment of organs and tissues. These complications involve mechanical changes caused by the accumulation of adipose tissue and the numerous cytokines produced by adipocytes. Obesity also significantly interferes with respiratory function by decreasing lung volume, particularly the expiratory reserve volume and functional residual capacity. Because of the ineffectiveness of the respiratory muscles, strength and resistance may be reduced. All these factors lead to inspiratory overload, which increases respiratory effort, oxygen consumption, and respiratory energy expenditure. It is noteworthy that patterns of body fat distribution significantly influence the function of the respiratory system, likely via the direct mechanical effect of fat accumulation in the chest and abdominal regions. Weight loss caused by various types of treatment, including low-calorie diet, intragastric balloon, and bariatric surgery, significantly improves lung function and metabolic syndrome and reduces body mass index. Despite advances in the knowledge of pulmonary and systemic complications associated with obesity, longitudinal randomized studies are needed to assess the impact of weight loss on metabolic syndrome and lung function.

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“…Recently, accumulating evidence points to leptin action upstream of disordered breathing. Clinical data from individuals with obesity hypoventilation syndrome suggest that leptin resistance contributes to a reduction in HCVR and HVR likely via an impaired chemosensitivity ( 172 ). Leptin deficient ob/ob mice exhibit a disordered breathing phenotype ( 104 ), including a reduction in HCVR ( 105 ), and treating ob/ob mice with leptin improves ventilation within 3 days, before significant weight loss occurs ( 105 ).…”

Section: Leptinmentioning

confidence: 99%

The Bidirectional Relationship Between Obstructive Sleep Apnea and Metabolic Disease

Framnes

Arble

2018

Front. Endocrinol.

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Obstructive sleep apnea (OSA) is a common sleep disorder, effecting 17% of the total population and 40–70% of the obese population (1, 2). Multiple studies have identified OSA as a critical risk factor for the development of obesity, diabetes, and cardiovascular diseases (3–5). Moreover, emerging evidence indicates that metabolic disorders can exacerbate OSA, creating a bidirectional relationship between OSA and metabolic physiology. In this review, we explore the relationship between glycemic control, insulin, and leptin as both contributing factors and products of OSA. We conclude that while insulin and leptin action may contribute to the development of OSA, further research is required to determine the mechanistic actions and relative contributions independent of body weight. In addition to increasing our understanding of the etiology, further research into the physiological mechanisms underlying OSA can lead to the development of improved treatment options for individuals with OSA.

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Obesity hypoventilation syndrome

Cited by 47 publications

References 36 publications

Sustained Intermittent Hypoxemia Induces Adiponectin Oligomers Redistribution and a Tissue-Specific Modulation of Adiponectin Receptor in Mice

Sustained Intermittent Hypoxemia Induces Adiponectin Oligomers Redistribution and a Tissue-Specific Modulation of Adiponectin Receptor in Mice

Obesity: systemic and pulmonary complications, biochemical abnormalities, and impairment of lung function

The Bidirectional Relationship Between Obstructive Sleep Apnea and Metabolic Disease

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