Serum from obstructive sleep apnea patients induces inflammatory responses in coronary artery endothelial cells

Zychowski, Katherine E.; Sanchez, Bethany; Pedrosa, Rodrigo Pinto; Lorenzi-Filho, Geraldo; Drager, Luciano F.; Polotsky, Vsevolod Y.; Campen, Matthew J.

doi:10.1016/j.atherosclerosis.2016.09.017

Cited by 46 publications

(29 citation statements)

References 60 publications

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“…Experimental sleep restriction results in decreased glucose clearance and postprandial glucose elevation (193,201), decrease in glucose effectiveness, and variable decrease in insulin sensitivity (190,192,202). OSA may influence glycemic regulation in individuals with diabetes; in adults with type continuous positive airway pressure has been associated with improvement in the glycemic profile (203), decreased A1C, and improvement in insulin sensitivity indices (204) as well as inflammation (205) (206,207). The prevalence of PCOS is significantly higher in adolescent girls with obesity compared with adolescent girls without overweight/ obesity (208), but the prevalence in adolescent girls with type 2 diabetes is not well studied.…”

Section: Prevention and Management Of Diabetes Complicationsmentioning

confidence: 99%

Evaluation and Management of Youth-Onset Type 2 Diabetes: A Position Statement by the American Diabetes Association

et al. 2018

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Although all types of diabetes result in hyperglycemia, the pathophysiology of each type of diabetes is different. These guidelines summarize available data specific to the comprehensive care of youth with type 2 diabetes. The objective is to enrich the recognition of type 2 diabetes in youth, its risk factors, its pathophysiology, its management, and the prevention of associated complications. PATHOPHYSIOLOGY Glucose homeostasis is maintained by a balance between insulin secretion from the pancreatic b-cells and sensitivity to insulin in skeletal muscle, adipose tissue, and liver (1). When insulin sensitivity declines, insulin secretion must increase to maintain glucose tolerance, and, in most youth, decreased insulin sensitivity due to puberty and/or obesity is compensated by increased insulin secretion. However, when b-cells cannot secrete sufficient insulin to compensate for insulin resistance, abnormalities in glucose homeostasis ensue, potentially progressing to prediabetes and type 2 diabetes as b-cell function deteriorates further (2-9). The relationship between b-cell function and insulin sensitivity in adults and youth has been demonstrated to be a hyperbolic function and can be described mathematically as the product of insulin sensitivity and b-cell function, called the disposition index (DI) (1). The DI essentially expresses the amount of insulin being secreted relative to the degree of insulin resistance and is a constant for a given degree of glucose tolerance in any one individual. Overweight and obesity are major acquired contributors to the development of insulin resistance, particularly in the face of the physiologic insulin resistance characteristic of puberty. Robust pancreatic b-cell compensatory insulin secretion maintains normal glucose homeostasis. However, in adolescents with obesity who develop type 2 diabetes, there is severe peripheral and hepatic insulin resistance, with ;50% lower peripheral insulin sensitivity than peers with obesity without diabetes, along with increased fasting hepatic glucose production and inadequate firstand second-phase insulin secretion, resulting in ;85% lower DI (2). Additional abnormalities in youth with type 2 diabetes include impaired glucose sensitivity of insulin secretion, lower serum adiponectin concentrations, and reduced incretin effect (3,9-13). While upregulation of a-cell function with hyperglucagonemia has been implicated in the pathophysiology of type 2 diabetes in adults (14,15), there are limited data in youth with type 2 diabetes, with studies showing either hyperglucagonemia or no difference from control subjects without diabetes (3,11,16,17). Cross-sectional and longitudinal studies in youth with obesity along the spectrum of glycemia from normoglycemia to prediabetes to type 2 diabetes show, as in adults, that b-cell failure with declining insulin secretion relative to insulin sensitivity results in prediabetes and type 2 diabetes in high-risk youth (5-9,18-21). Importantly, however, prior to reaching the American Diabetes Association (...

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Section: Prevention and Management Of Diabetes Complicationsmentioning

confidence: 99%

Evaluation and Management of Youth-Onset Type 2 Diabetes: A Position Statement by the American Diabetes Association

et al. 2018

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“…In a study by Zychowski et al[ 36 ], human coronary endothelial cells were incubated with 5% serum, of control and OSA patients for 4 h. They then, performed qPCR to evaluate for endothelial inflammatory markers. OSA serum induced much more endothelial cell expression of VCAM1, ICAM1, IL8, SELP and CCL5 mRNA.…”

Section: Correlations Between Ms and Osamentioning

confidence: 99%

“…OSA serum induced much more endothelial cell expression of VCAM1, ICAM1, IL8, SELP and CCL5 mRNA. This suggested another molecular role of endothelial activation and dysfunction in patients with OSA[ 36 ].…”

Section: Correlations Between Ms and Osamentioning

confidence: 99%

Correlation between metabolic syndrome and sleep apnea

Castañeda¹,

Jauregui-Maldonado²,

Ratnani

et al. 2018

WJD

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The so-called “metabolic syndrome” (MS), constitutes a cluster of metabolic and cardiovascular abnormalities, including fasting glucose, blood pressure, triglycerides, high density lipoprotein cholesterol (HDL-C), and waist circumference that arise from insulin resistance. Obstructive sleep apnea (OSA) syndrome is characterized by recurrent episodes of partial or complete obstruction of the upper airway, involving cessation or significant decreased airflow, with intermittent hypoxemia, frequent arousals from sleep and recurrent oxyhemoglobin desaturations that interfere with normal sleep patterns generating difficulty falling asleep, unrefreshing sleep and loud snoring. The relation between these two entities is known as “Syndrome Z”, and there is no question about the impact of these risk factors on health and disease. This clinical condition presents a growing epidemic Worldwide, affecting approximately 60% of the general population with both MS and OSA due to the constant increase of body mass index in humans. This article presents evidence-based data that focuses on the direct relationship between MS and OSA.

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“…The expression of P-selectin, as well as proatherogenic cytokines characteristic for endothelium, increased after stimulation with OSA patients' serum. These molecules activate platelets in a positive feedback mechanism ( 101 ). Platelet P-selectin is involved in atherosclerotic lesions formation and their further maturation and progression ( 100 ).…”

Section: Platelets As Immune Cells Mediating Cvdmentioning

confidence: 99%

Obstructive Sleep Apnea: From Intermittent Hypoxia to Cardiovascular Complications via Blood Platelets

et al. 2018

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Obstructive sleep apnea is a chronic condition characterized by recurrent episodes of apneas or hypopneas during sleep leading to intermittent hypoxemia and arousals. The prevalence of the sleep disordered breathing is estimated that almost 50% of men and 24% of women suffer from moderate to severe form of the disorder. Snoring, collapse of upper airways and intermittent hypoxia are main causes of smoldering systemic inflammation in patients suffering from obstructive sleep apnea. The systematic inflammation is considered one of the key mechanisms leading to significant cardiovascular complications. Blood platelets, formerly not even recognized as cells, are currently gaining attention as crucial players in the immune continuum. Platelet surface is endowed with receptors characteristic for cells classically belonging to the immune system, which enables them to recognize pathogens, immune complexes, and interact in a homo- and heterotypic aggregates. Platelets participate in the process of transcellular production of bioactive lipids by delivering both specific enzymes and substrate molecules. Despite their lack of nucleus, platelets synthetize proteins in a stimuli-dependent manner. Atherosclerosis and consequent cardiovascular complications result from disruption in homeostasis of both of the platelet roles: blood coagulation and inflammatory processes modulation. Platelet parameters, routinely evaluated as a part of complete blood count test, were proposed as markers of cardiovascular comorbidity in patients with obstructive sleep apnea. Platelets were found to be excessively activated in this group of patients, especially in obese subjects. Persistent activation results in enhanced spontaneous aggregability and change in cytokine production. Platelet-lymphocyte ratio was suggested as an independent marker for cardiovascular disease in obstructive sleep apnea syndrome and continuous positive air pressure therapy was found to have an impact on platelet parameters and phenotype. In this literature review we summarize the current knowledge on the subject of platelets involvement in obstructive sleep apnea syndrome and consider the possible pathways in which they contribute to cardiovascular comorbidity.

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Serum from obstructive sleep apnea patients induces inflammatory responses in coronary artery endothelial cells

Cited by 46 publications

References 60 publications

Evaluation and Management of Youth-Onset Type 2 Diabetes: A Position Statement by the American Diabetes Association

Evaluation and Management of Youth-Onset Type 2 Diabetes: A Position Statement by the American Diabetes Association

Correlation between metabolic syndrome and sleep apnea

Obstructive Sleep Apnea: From Intermittent Hypoxia to Cardiovascular Complications via Blood Platelets

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