Obstructive sleep apnoea syndrome impairs insulin sensitivity independently of anthropometric variables

Tassone, F.; Lanfranco, Fabio; Gianotti, Laura; Pivetti, S; Navone, F; Rossetto, Ruth; Grottoli, Silvia; Gai, V; Ghigo, Ezio; Maccario, Mauro

doi:10.1046/j.1365-2265.2003.01859.x

Cited by 90 publications

(49 citation statements)

References 30 publications

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“…Similar data have been obtained in samples of OSA patients (tables 3 and 4) [64][65][66][67][68][69][70][71][72][73][74][75][76][77][78][79][80], with a large prevalence of positive [63,[64][65][66][67][68][69][70][71][72][73][74][75][76][77][78][79] rather than negative [78][79][80] studies. In clinical populations, OSA patients characterised by full-PSG were significantly more likely to have impaired glucose tolerance (IGT) and diabetes than subjects free of OSA syndrome (OSAS) [71].…”

Section: Physiological and Clinical Datasupporting

confidence: 65%

Sleep, sleep-disordered breathing and metabolic consequences

Lévy¹,

Bonsignore²,

Eckel³

2009

European Respiratory Journal

293

187

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Sleep profoundly affects metabolic pathways. In healthy subjects, experimental sleep restriction caused insulin resistance (IR) and increased evening cortisol and sympathetic activation. Increased obesity in subjects reporting short sleep duration leads to speculation that, during recent decades, decreased sleeping time in the general population may have contributed to the increasing prevalence of obesity. Causal inference is difficult due to lack of control for confounders and inconsistent evidence of temporal sequence.In the general population, obstructive sleep apnoea (OSA) is associated with glucose intolerance. OSA severity is also associated with the degree of IR. However, OSA at baseline does not seem to significantly predict the development of diabetes. Prevalence of the metabolic syndrome is higher in patients with OSA than in obese subjects without OSA. Treatment with continuous positive airway pressure seems to improve glucose metabolism both in diabetic and nondiabetic OSA but mainly in nonobese subjects.The relative role of obesity and OSA in the pathogenesis of metabolic alterations is still unclear and is intensively studied in clinical and experimental models. In the intermittent hypoxia model in rodents, strong interactions are likely to occur between haemodynamic alterations, systemic inflammation and metabolic changes, modulated by genetic background. Molecular and cellular mechanisms are currently being investigated.

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Section: Physiological and Clinical Datasupporting

confidence: 65%

Sleep, sleep-disordered breathing and metabolic consequences

Lévy¹,

Bonsignore²,

Eckel³

2009

European Respiratory Journal

293

187

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“…Several studies have reported on the relationship between OSA and glucose metabolism [2,3,5,25,26,28,29]. The prevalence of OSA in our cohort was higher than the prevalence reported in the Wisconsin Sleep Cohort Study [4].…”

Section: Discussioncontrasting

confidence: 53%

Metabolically Healthy and Unhealthy Obesity Phenotypes in the General Population: The FIN-D2D Survey

Ahima¹

2016

Obesity Epidemiology, Pathogenesis, and Treatment

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Context: Sleep abnormalities, including obstructive sleep apnea (OSA), have been associated with insulin resistance.Objective: To determine the relationship between sleep, including OSA, and glucose parameters in a prospectively assembled cohort of chronically sleep-deprived obese subjects.Design: Cross-sectional evaluation of a prospective cohort study. Setting: Tertiary Referral Research Clinical Center.Main Outcome Measure(s): Sleep duration and quality assessed by actigraphy, sleep diaries and questionnaires, OSA determined by a portable device; glucose metabolism assessed by oral glucose tolerance test (oGTT), and HbA 1 c concentrations in 96 obese individuals reporting sleeping less than 6.5 h on a regular basis.Results: Sixty % of subjects had an abnormal respiratory disturbance index (RDI$5) and 44% of these subjects had abnormal oGTT results. Severity of OSA as assessed by RDI score was associated with fasting glucose (R = 0.325, p = 0.001) and fasting insulin levels (r = 0.217, p = 0.033). Subjects with moderate to severe OSA (RDI.15) had higher glucose concentrations at 120 min than those without OSA (RDI,5) (p = 0.017). Subjects with OSA also had significantly higher concentrations of plasma ACTH (p = 0.009). Several pro-inflammatory cytokines were higher in subjects with OSA (p,0.050). CRP levels were elevated in this sample, suggesting increased cardiovascular risk.Conclusions: OSA is associated with impaired glucose metabolism in obese, sleep deprived individuals. Since sleep apnea is common and frequently undiagnosed, health care providers should be aware of its occurrence and associated risks.

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“…mostraram que os pacientes com SAOS (n = 30) apresentam menor sensibilidade à insulina, calculada pelo ISI, do que o grupo controle sem AOS (n = 27), mesmo após ajuste para idade, IMC e relação cintura-quadril (21).…”

Section: Resistência à Insulina (Ri) E Saosunclassified

Interações entre síndrome da apnéia obstrutiva do sono e resistência à insulina

Carneiro

Filho

Togeiro

et al. 2007

Arq Bras Endocrinol Metab

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RESUMOEstudos anteriores mostraram que pacientes com Apnéia Obstrutiva do Sono (AOS) apresentam maior risco para doenças cardiovasculares. Entretanto, permanece controverso se essa associação depende da obesidade ou se ocorre devido a alterações fisiológicas decorrentes da desordem do sono, como ativação do sistema nervoso simpático, da inflamação e desordens do eixo corticotrófico e somatotrófico, que predispõem a danos vasculares. Além disso, muitos fatores de risco para doenças cardiovasculares (DCV) estão fortemente associados ao distúrbio respiratório, entre eles hipertensão, obesidade, resistência à insulina e diabetes tipo 2 (DM2). Neste artigo, vamos discutir a interação entre resistência à insulina e AOS e os possíveis mecanismos fisiopatológicos que contribuem para suas co-morbidades. Previous studies have shown Obstructive Sleep Apnea (OSA) as a risk factor for development of cardiovascular and cerebrovascular disease. However, controversies remain as to whether these changes are consequences of the associated obesity or OSA itself results in endocrine and metabolic changes, including impairment of insulin sensitivity, growth hormone, secretion inflammatory cytokines alterations, activation of peripheral sympathetic activity, and hipothalamic-pituitary-adrenal (HPA) axis, that may predispose to vascular disease. Furthermore many cardiovascular risk factors, such as hypertension, obesity, insulin resistance and type 2 diabetes, are strongly associated with OSA. In this article, we will review the evidence and discuss possible mechanisms underlying these links and the pathophysiology of OSA morbidities.

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Obstructive sleep apnoea syndrome impairs insulin sensitivity independently of anthropometric variables

Cited by 90 publications

References 30 publications

Sleep, sleep-disordered breathing and metabolic consequences

Sleep, sleep-disordered breathing and metabolic consequences

Metabolically Healthy and Unhealthy Obesity Phenotypes in the General Population: The FIN-D2D Survey

Interações entre síndrome da apnéia obstrutiva do sono e resistência à insulina

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