Obstructive Sleep Apnea Dynamically Increases Nocturnal Plasma Free Fatty Acids, Glucose, and Cortisol During Sleep

ContextObstructive sleep apnea (OSA) is associated with diabetes and cardiovascular disease. This association may be related to metabolic changes that transpire during sleep in OSA.ObjectiveTo examine the impact of OSA, elicited by cessation of continuous positive airway pressure (CPAP), on frequent...

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Published in:	The journal of clinical endocrinology and metabolism Vol. 102; no. 9; pp. 3172 - 3181
Main Authors:	Chopra, Swati, Rathore, Aman, Younas, Haris, Pham, Luu V, Gu, Chenjuan, Beselman, Aleksandra, Kim, Il-Young, Wolfe, Robert R, Perin, Jamie, Polotsky, Vsevolod Y, Jun, Jonathan C
Format:	Journal Article
Language:	English
Published:	Washington, DC Endocrine Society 01.09.2017 Copyright Oxford University Press Oxford University Press
Subjects:	Adult Aged Apnea Biomarkers - blood Blood Glucose - analysis Blood pressure C-reactive protein Cardiovascular disease Cardiovascular diseases Cardiovascular Diseases - prevention & control Cholesterol Circadian Rhythm Clinical s Continuous positive airway pressure Continuous Positive Airway Pressure - methods Cortisol Cross-Over Studies Diabetes Diabetes mellitus Fatty acids Fatty Acids, Nonesterified - blood Female Follow-Up Studies Glucose Glucose tolerance Heart rate Hormones Humans Hydrocortisone - blood Hypoxemia Insulin Lactic acid Male Mechanical ventilation Metabolic rate Metabolism Middle Aged Oxygen Consumption - physiology Polysomnography Predictive Value of Tests Reference Values Respiratory tract Respiratory tract diseases Risk Assessment Severity of Illness Index Sleep Sleep - physiology Sleep apnea Sleep Apnea, Obstructive - blood Sleep Apnea, Obstructive - diagnosis Sleep Apnea, Obstructive - therapy Sleep disorders Treatment Outcome Triglycerides Withholding Treatment
ISSN:	0021-972X, 1945-7197, 1945-7197
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Abstract	ContextObstructive sleep apnea (OSA) is associated with diabetes and cardiovascular disease. This association may be related to metabolic changes that transpire during sleep in OSA.ObjectiveTo examine the impact of OSA, elicited by cessation of continuous positive airway pressure (CPAP), on frequently sampled nocturnal metabolic markers including plasma free fatty acids (FFAs), glucose, insulin, triglycerides (TGs), cortisol, and lactate, as well as glucose production, oral glucose tolerance, blood pressure (BP), endothelial function, cholesterol, and high-sensitivity C-reactive protein (hsCRP).Design and SettingRandomized crossover trial of CPAP vs CPAP withdrawal.PatientsThirty-one patients with moderate to severe OSA acclimated to CPAP.InterventionPatients underwent attended polysomnography while sleeping with therapeutic CPAP, or after CPAP withdrawal, in random order. Venous blood was sampled at ∼20-minute intervals on both nights. In 11 patients, we assessed glucose kinetics with an infusion of 6,6-[2H2]glucose.ResultsCPAP withdrawal caused recurrence of OSA associated with hypoxemia, sleep disruption, and heart rate (HR) elevation. CPAP withdrawal dynamically increased nocturnal FFA (P = 0.007), glucose (P = 0.028), and cortisol (P = 0.037), in proportion to respiratory event frequency, HR elevation, or sleep fragmentation. Diabetes predisposed to glucose elevation. CPAP withdrawal also increased systolic BP (P = 0.017) and augmentation index (P = 0.008), but did not affect insulin, TGs, glucose production, oral glucose tolerance, cholesterol, or hsCRP.ConclusionOSA recurrence during CPAP withdrawal increases FFA and glucose during sleep, associated with sympathetic and adrenocortical activation. Recurring exposure to these metabolic changes may foster diabetes and cardiovascular disease.We studied the overnight metabolic profile of patients during sleep, in the presence or absence of sleep apnea. Sleep apnea caused dynamic elevations of plasma FFA and glucose.
AbstractList	Abstract Obstructive sleep apnea (OSA) is associated with diabetes and cardiovascular disease. This association may be related to metabolic changes that transpire during sleep in OSA. To examine the impact of OSA, elicited by cessation of continuous positive airway pressure (CPAP), on frequently sampled nocturnal metabolic markers including plasma free fatty acids (FFAs), glucose, insulin, triglycerides (TGs), cortisol, and lactate, as well as glucose production, oral glucose tolerance, blood pressure (BP), endothelial function, cholesterol, and high-sensitivity C-reactive protein (hsCRP). Randomized crossover trial of CPAP vs CPAP withdrawal. Thirty-one patients with moderate to severe OSA acclimated to CPAP. Patients underwent attended polysomnography while sleeping with therapeutic CPAP, or after CPAP withdrawal, in random order. Venous blood was sampled at ∼20-minute intervals on both nights. In 11 patients, we assessed glucose kinetics with an infusion of 6,6-[2 H2 ]glucose. CPAP withdrawal caused recurrence of OSA associated with hypoxemia, sleep disruption, and heart rate (HR) elevation. CPAP withdrawal dynamically increased nocturnal FFA (P = 0.007), glucose (P = 0.028), and cortisol (P = 0.037), in proportion to respiratory event frequency, HR elevation, or sleep fragmentation. Diabetes predisposed to glucose elevation. CPAP withdrawal also increased systolic BP (P = 0.017) and augmentation index (P = 0.008), but did not affect insulin, TGs, glucose production, oral glucose tolerance, cholesterol, or hsCRP. OSA recurrence during CPAP withdrawal increases FFA and glucose during sleep, associated with sympathetic and adrenocortical activation. Recurring exposure to these metabolic changes may foster diabetes and cardiovascular disease. We studied the overnight metabolic profile of patients during sleep, in the presence or absence of sleep apnea. Sleep apnea caused dynamic elevations of plasma FFA and glucose. Obstructive sleep apnea (OSA) is associated with diabetes and cardiovascular disease. This association may be related to metabolic changes that transpire during sleep in OSA.ContextObstructive sleep apnea (OSA) is associated with diabetes and cardiovascular disease. This association may be related to metabolic changes that transpire during sleep in OSA.To examine the impact of OSA, elicited by cessation of continuous positive airway pressure (CPAP), on frequently sampled nocturnal metabolic markers including plasma free fatty acids (FFAs), glucose, insulin, triglycerides (TGs), cortisol, and lactate, as well as glucose production, oral glucose tolerance, blood pressure (BP), endothelial function, cholesterol, and high-sensitivity C-reactive protein (hsCRP).ObjectiveTo examine the impact of OSA, elicited by cessation of continuous positive airway pressure (CPAP), on frequently sampled nocturnal metabolic markers including plasma free fatty acids (FFAs), glucose, insulin, triglycerides (TGs), cortisol, and lactate, as well as glucose production, oral glucose tolerance, blood pressure (BP), endothelial function, cholesterol, and high-sensitivity C-reactive protein (hsCRP).Randomized crossover trial of CPAP vs CPAP withdrawal.Design and SettingRandomized crossover trial of CPAP vs CPAP withdrawal.Thirty-one patients with moderate to severe OSA acclimated to CPAP.PatientsThirty-one patients with moderate to severe OSA acclimated to CPAP.Patients underwent attended polysomnography while sleeping with therapeutic CPAP, or after CPAP withdrawal, in random order. Venous blood was sampled at ∼20-minute intervals on both nights. In 11 patients, we assessed glucose kinetics with an infusion of 6,6-[2H2]glucose.InterventionPatients underwent attended polysomnography while sleeping with therapeutic CPAP, or after CPAP withdrawal, in random order. Venous blood was sampled at ∼20-minute intervals on both nights. In 11 patients, we assessed glucose kinetics with an infusion of 6,6-[2H2]glucose.CPAP withdrawal caused recurrence of OSA associated with hypoxemia, sleep disruption, and heart rate (HR) elevation. CPAP withdrawal dynamically increased nocturnal FFA (P = 0.007), glucose (P = 0.028), and cortisol (P = 0.037), in proportion to respiratory event frequency, HR elevation, or sleep fragmentation. Diabetes predisposed to glucose elevation. CPAP withdrawal also increased systolic BP (P = 0.017) and augmentation index (P = 0.008), but did not affect insulin, TGs, glucose production, oral glucose tolerance, cholesterol, or hsCRP.ResultsCPAP withdrawal caused recurrence of OSA associated with hypoxemia, sleep disruption, and heart rate (HR) elevation. CPAP withdrawal dynamically increased nocturnal FFA (P = 0.007), glucose (P = 0.028), and cortisol (P = 0.037), in proportion to respiratory event frequency, HR elevation, or sleep fragmentation. Diabetes predisposed to glucose elevation. CPAP withdrawal also increased systolic BP (P = 0.017) and augmentation index (P = 0.008), but did not affect insulin, TGs, glucose production, oral glucose tolerance, cholesterol, or hsCRP.OSA recurrence during CPAP withdrawal increases FFA and glucose during sleep, associated with sympathetic and adrenocortical activation. Recurring exposure to these metabolic changes may foster diabetes and cardiovascular disease.ConclusionOSA recurrence during CPAP withdrawal increases FFA and glucose during sleep, associated with sympathetic and adrenocortical activation. Recurring exposure to these metabolic changes may foster diabetes and cardiovascular disease. CONTEXT:Obstructive sleep apnea (OSA) is associated with diabetes and cardiovascular disease. This association may be related to metabolic changes that transpire during sleep in OSA. OBJECTIVE:To examine the impact of OSA, elicited by cessation of continuous positive airway pressure (CPAP), on frequently sampled nocturnal metabolic markers including plasma free fatty acids (FFAs), glucose, insulin, triglycerides (TGs), cortisol, and lactate, as well as glucose production, oral glucose tolerance, blood pressure (BP), endothelial function, cholesterol, and high-sensitivity C-reactive protein (hsCRP). DESIGN AND SETTING:Randomized crossover trial of CPAP vs CPAP withdrawal. PATIENTS:Thirty-one patients with moderate to severe OSA acclimated to CPAP. INTERVENTION:Patients underwent attended polysomnography while sleeping with therapeutic CPAP, or after CPAP withdrawal, in random order. Venous blood was sampled at ~20-minute intervals on both nights. In 11 patients, we assessed glucose kinetics with an infusion of 6,6-[H2]glucose. RESULTS:CPAP withdrawal caused recurrence of OSA associated with hypoxemia, sleep disruption, and heart rate (HR) elevation. CPAP withdrawal dynamically increased nocturnal FFA (P = 0.007), glucose (P = 0.028), and cortisol (P = 0.037), in proportion to respiratory event frequency, HR elevation, or sleep fragmentation. Diabetes predisposed to glucose elevation. CPAP withdrawal also increased systolic BP (P = 0.017) and augmentation index (P = 0.008), but did not affect insulin, TGs, glucose production, oral glucose tolerance, cholesterol, or hsCRP. CONCLUSION:OSA recurrence during CPAP withdrawal increases FFA and glucose during sleep, associated with sympathetic and adrenocortical activation. Recurring exposure to these metabolic changes may foster diabetes and cardiovascular disease. ContextObstructive sleep apnea (OSA) is associated with diabetes and cardiovascular disease. This association may be related to metabolic changes that transpire during sleep in OSA.ObjectiveTo examine the impact of OSA, elicited by cessation of continuous positive airway pressure (CPAP), on frequently sampled nocturnal metabolic markers including plasma free fatty acids (FFAs), glucose, insulin, triglycerides (TGs), cortisol, and lactate, as well as glucose production, oral glucose tolerance, blood pressure (BP), endothelial function, cholesterol, and high-sensitivity C-reactive protein (hsCRP).Design and SettingRandomized crossover trial of CPAP vs CPAP withdrawal.PatientsThirty-one patients with moderate to severe OSA acclimated to CPAP.InterventionPatients underwent attended polysomnography while sleeping with therapeutic CPAP, or after CPAP withdrawal, in random order. Venous blood was sampled at ∼20-minute intervals on both nights. In 11 patients, we assessed glucose kinetics with an infusion of 6,6-[2H2]glucose.ResultsCPAP withdrawal caused recurrence of OSA associated with hypoxemia, sleep disruption, and heart rate (HR) elevation. CPAP withdrawal dynamically increased nocturnal FFA (P = 0.007), glucose (P = 0.028), and cortisol (P = 0.037), in proportion to respiratory event frequency, HR elevation, or sleep fragmentation. Diabetes predisposed to glucose elevation. CPAP withdrawal also increased systolic BP (P = 0.017) and augmentation index (P = 0.008), but did not affect insulin, TGs, glucose production, oral glucose tolerance, cholesterol, or hsCRP.ConclusionOSA recurrence during CPAP withdrawal increases FFA and glucose during sleep, associated with sympathetic and adrenocortical activation. Recurring exposure to these metabolic changes may foster diabetes and cardiovascular disease.We studied the overnight metabolic profile of patients during sleep, in the presence or absence of sleep apnea. Sleep apnea caused dynamic elevations of plasma FFA and glucose. We studied the overnight metabolic profile of patients during sleep, in the presence or absence of sleep apnea. Sleep apnea caused dynamic elevations of plasma FFA and glucose. Obstructive sleep apnea (OSA) is associated with diabetes and cardiovascular disease. This association may be related to metabolic changes that transpire during sleep in OSA. To examine the impact of OSA, elicited by cessation of continuous positive airway pressure (CPAP), on frequently sampled nocturnal metabolic markers including plasma free fatty acids (FFAs), glucose, insulin, triglycerides (TGs), cortisol, and lactate, as well as glucose production, oral glucose tolerance, blood pressure (BP), endothelial function, cholesterol, and high-sensitivity C-reactive protein (hsCRP). Randomized crossover trial of CPAP vs CPAP withdrawal. Thirty-one patients with moderate to severe OSA acclimated to CPAP. Patients underwent attended polysomnography while sleeping with therapeutic CPAP, or after CPAP withdrawal, in random order. Venous blood was sampled at ∼20-minute intervals on both nights. In 11 patients, we assessed glucose kinetics with an infusion of 6,6-[2H2]glucose. CPAP withdrawal caused recurrence of OSA associated with hypoxemia, sleep disruption, and heart rate (HR) elevation. CPAP withdrawal dynamically increased nocturnal FFA (P = 0.007), glucose (P = 0.028), and cortisol (P = 0.037), in proportion to respiratory event frequency, HR elevation, or sleep fragmentation. Diabetes predisposed to glucose elevation. CPAP withdrawal also increased systolic BP (P = 0.017) and augmentation index (P = 0.008), but did not affect insulin, TGs, glucose production, oral glucose tolerance, cholesterol, or hsCRP. OSA recurrence during CPAP withdrawal increases FFA and glucose during sleep, associated with sympathetic and adrenocortical activation. Recurring exposure to these metabolic changes may foster diabetes and cardiovascular disease. ContextObstructive sleep apnea (OSA) is associated with diabetes and cardiovascular disease. This association may be related to metabolic changes that transpire during sleep in OSA.ObjectiveTo examine the impact of OSA, elicited by cessation of continuous positive airway pressure (CPAP), on frequently sampled nocturnal metabolic markers including plasma free fatty acids (FFAs), glucose, insulin, triglycerides (TGs), cortisol, and lactate, as well as glucose production, oral glucose tolerance, blood pressure (BP), endothelial function, cholesterol, and high-sensitivity C-reactive protein (hsCRP).Design and SettingRandomized crossover trial of CPAP vs CPAP withdrawal.PatientsThirty-one patients with moderate to severe OSA acclimated to CPAP.InterventionPatients underwent attended polysomnography while sleeping with therapeutic CPAP, or after CPAP withdrawal, in random order. Venous blood was sampled at ∼20-minute intervals on both nights. In 11 patients, we assessed glucose kinetics with an infusion of 6,6-[2H2]glucose.ResultsCPAP withdrawal caused recurrence of OSA associated with hypoxemia, sleep disruption, and heart rate (HR) elevation. CPAP withdrawal dynamically increased nocturnal FFA (P = 0.007), glucose (P = 0.028), and cortisol (P = 0.037), in proportion to respiratory event frequency, HR elevation, or sleep fragmentation. Diabetes predisposed to glucose elevation. CPAP withdrawal also increased systolic BP (P = 0.017) and augmentation index (P = 0.008), but did not affect insulin, TGs, glucose production, oral glucose tolerance, cholesterol, or hsCRP.ConclusionOSA recurrence during CPAP withdrawal increases FFA and glucose during sleep, associated with sympathetic and adrenocortical activation. Recurring exposure to these metabolic changes may foster diabetes and cardiovascular disease.
Author	Gu, Chenjuan Jun, Jonathan C Rathore, Aman Younas, Haris Polotsky, Vsevolod Y Pham, Luu V Kim, Il-Young Chopra, Swati Beselman, Aleksandra Wolfe, Robert R Perin, Jamie
AuthorAffiliation	1Division of Pulmonary and Critical Care, Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21224 2Department of Respiratory Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China 3Department of Pharmacy Services, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224 4Center for Translational Research in Aging & Longevity, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205 5School of Public Health, Johns Hopkins University, Baltimore, Maryland 21205
AuthorAffiliation_xml	– name: 1Division of Pulmonary and Critical Care, Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21224 2Department of Respiratory Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China 3Department of Pharmacy Services, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224 4Center for Translational Research in Aging & Longevity, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205 5School of Public Health, Johns Hopkins University, Baltimore, Maryland 21205 – name: 1Division of Pulmonary and Critical Care, Department of Medicine (S.C., A.R., H.Y., L.P., V.Y.P., J.C.J), Johns Hopkins University, Baltimore, MD; Department of Pharmacy Services (A.B.), Johns Hopkins University School of Medicine, Baltimore, MD; Center for Translational Research in Aging & Longevity (I.-Y.K., R.R.W.), The University of Arkansas for Medical Sciences; School of Public Health (J.P.), Johns Hopkins University, Baltimore, MD; Department of Respiratory Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine (C.J.G)
Author_xml	– sequence: 1 givenname: Swati surname: Chopra fullname: Chopra, Swati organization: 1Division of Pulmonary and Critical Care, Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21224 – sequence: 2 givenname: Aman surname: Rathore fullname: Rathore, Aman organization: 1Division of Pulmonary and Critical Care, Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21224 – sequence: 3 givenname: Haris surname: Younas fullname: Younas, Haris organization: 1Division of Pulmonary and Critical Care, Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21224 – sequence: 4 givenname: Luu V surname: Pham fullname: Pham, Luu V organization: 1Division of Pulmonary and Critical Care, Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21224 – sequence: 5 givenname: Chenjuan surname: Gu fullname: Gu, Chenjuan organization: 2Department of Respiratory Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China – sequence: 6 givenname: Aleksandra surname: Beselman fullname: Beselman, Aleksandra organization: 3Department of Pharmacy Services, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224 – sequence: 7 givenname: Il-Young surname: Kim fullname: Kim, Il-Young organization: 4Center for Translational Research in Aging & Longevity, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205 – sequence: 8 givenname: Robert R surname: Wolfe fullname: Wolfe, Robert R organization: 4Center for Translational Research in Aging & Longevity, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205 – sequence: 9 givenname: Jamie surname: Perin fullname: Perin, Jamie organization: 5School of Public Health, Johns Hopkins University, Baltimore, Maryland 21205 – sequence: 10 givenname: Vsevolod Y surname: Polotsky fullname: Polotsky, Vsevolod Y organization: 1Division of Pulmonary and Critical Care, Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21224 – sequence: 11 givenname: Jonathan C surname: Jun fullname: Jun, Jonathan C email: jjun2@jhmi.edu organization: 1Division of Pulmonary and Critical Care, Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21224
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Snippet	ContextObstructive sleep apnea (OSA) is associated with diabetes and cardiovascular disease. This association may be related to metabolic changes that... CONTEXT:Obstructive sleep apnea (OSA) is associated with diabetes and cardiovascular disease. This association may be related to metabolic changes that... Obstructive sleep apnea (OSA) is associated with diabetes and cardiovascular disease. This association may be related to metabolic changes that transpire... Abstract Obstructive sleep apnea (OSA) is associated with diabetes and cardiovascular disease. This association may be related to metabolic changes that... We studied the overnight metabolic profile of patients during sleep, in the presence or absence of sleep apnea. Sleep apnea caused dynamic elevations of plasma...
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SubjectTerms	Adult Aged Apnea Biomarkers - blood Blood Glucose - analysis Blood pressure C-reactive protein Cardiovascular disease Cardiovascular diseases Cardiovascular Diseases - prevention & control Cholesterol Circadian Rhythm Clinical s Continuous positive airway pressure Continuous Positive Airway Pressure - methods Cortisol Cross-Over Studies Diabetes Diabetes mellitus Fatty acids Fatty Acids, Nonesterified - blood Female Follow-Up Studies Glucose Glucose tolerance Heart rate Hormones Humans Hydrocortisone - blood Hypoxemia Insulin Lactic acid Male Mechanical ventilation Metabolic rate Metabolism Middle Aged Oxygen Consumption - physiology Polysomnography Predictive Value of Tests Reference Values Respiratory tract Respiratory tract diseases Risk Assessment Severity of Illness Index Sleep Sleep - physiology Sleep apnea Sleep Apnea, Obstructive - blood Sleep Apnea, Obstructive - diagnosis Sleep Apnea, Obstructive - therapy Sleep disorders Treatment Outcome Triglycerides Withholding Treatment
Title	Obstructive Sleep Apnea Dynamically Increases Nocturnal Plasma Free Fatty Acids, Glucose, and Cortisol During Sleep
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