Endothelial Dysfunction in Children Without Hypertension

Bhattacharjee, Rakesh; Kim, Jinkwan; Alotaibi, Wadha; Kheirandish‐Gozal, Leila; Capdevila, Óscar Sans; Gozal, David

doi:10.1378/chest.11-1777

Cited by 104 publications

(49 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The fact that obesity in humans is associated with decreased blood flow in response to methacholine [230], bradykinin [231, 232], substance P and acetylcholine [232], shear stress [233], and insulin [234, 235] appears to suggest that the obese condition is somehow linked causally with diminished vascular NO bioavailability; a multitude of studies showing similar results lends support to this hypothesis [120, 236-247]. However, the question remains: Is loss of NO production somehow due to excess adiposity, or is its etiology derived from those conditions commonly associated with obesity?…”

Section: No Bioavailability Is Diminished In Obese and Diabetic Stmentioning

confidence: 99%

Regulation of obesity and insulin resistance by nitric oxide

Sansbury

Hill

2014

Free Radical Biology and Medicine

220

193

View full text Add to dashboard Cite

Obesity is a risk factor for developing type 2 diabetes and cardiovascular disease and has quickly become a world-wide pandemic with few tangible and safe treatment options. While it is generally accepted that the primary cause of obesity is energy imbalance, i.e., the calories consumed are greater than are utilized, understanding how caloric balance is regulated has proven a challenge. Many “distal” causes of obesity, such as the structural environment, occupation, and social influences, are exceedingly difficult to change or manipulate. Hence, molecular processes and pathways more proximal to the origins of obesity—those that directly regulate energy metabolism or caloric intake—appear to be more feasible targets for therapy. In particular, nitric oxide (NO) is emerging as a central regulator of energy metabolism and body composition. NO bioavailability is decreased in animal models of diet-induced obesity and in obese and insulin resistant patients, and increasing NO output has remarkable effects on obesity and insulin resistance. This review discusses the role of NO in regulating adiposity and insulin sensitivity and places its modes of action into context with the known causes and consequences of metabolic disease.

show abstract

Section: No Bioavailability Is Diminished In Obese and Diabetic Stmentioning

confidence: 99%

Regulation of obesity and insulin resistance by nitric oxide

Sansbury

Hill

2014

Free Radical Biology and Medicine

220

193

View full text Add to dashboard Cite

show abstract

“…Similar to adults, OSA is associated with all such predisposing risk factors, but in children, the relationships are not as overtly established. Our group has published extensively on the obesity-independent association between OSA in childhood and endothelial dysfunction, a risk factor for atherogenesis: blunting of postocclusive hyperemia has been reported in both nonobese and obese school-age children with OSA 324–326. Pediatric data regarding endothelial dysfunction have been gathered in prepubertal school-age children; no study of which we are aware has examined endothelial dysfunction in association with OSA in adolescents.…”

Section: Obstructive Sleep Apnea and Cardiometabolic Riskmentioning

confidence: 99%

Role of sleep quality in the metabolic syndrome

Koren¹,

Dumin²,

Gozal³

2016

DMSO

Self Cite

151

View full text Add to dashboard Cite

Emerging evidence has assigned an important role to sleep as a modulator of metabolic homeostasis. The impact of variations in sleep duration, sleep-disordered breathing, and chronotype to cardiometabolic function encompasses a wide array of perturbations spanning from obesity, insulin resistance, type 2 diabetes, the metabolic syndrome, and cardiovascular disease risk and mortality in both adults and children. Here, we critically and extensively review the published literature on such important issues and provide a comprehensive overview of the most salient pathophysiologic pathways underlying the links between sleep, sleep disorders, and cardiometabolic functioning.

show abstract

“…Analogously, abnormal endothelial cell function when assessed by post-occlusive hyperemic responses is only present in a subset of children with OSA (Bhattacharjee et al, 2012 ). It is now well established that the post-occlusive hyperemic response constitutes an endothelial nitric oxide synthase (eNOS)-dependent phenomenon.…”

Section: Psdb Morbidity and The Epigenomementioning

confidence: 99%

Genotype–phenotype interactions in pediatric obstructive sleep apnea

Kheirandish‐Gozal¹,

Gozal²

2013

Respiratory Physiology & Neurobiology

Self Cite

View full text Add to dashboard Cite

Pediatric sleep disordered breathing (PSDB) is not only a very frequent condition affecting 2–4% of all children, but is also associated with an increased risk for a variety of manifestations underlying end-organ injury and dysfunction that impose both immediate and potentially long-term morbidities and corresponding inherent elevations in healthcare costs. One of the major problems with the creation of valid algorithms aiming to stratify diagnostic and treatment prioritization lies in our current inability to predict and identify those children who are most at-risk for PSDB-induced adverse consequences. Thus, improved our understanding of the mechanisms governing phenotype variance in PSDB is essential. Here, we examine some of the potential underpinnings of phenotypic variability in PSDB, and further propose a conceptual framework aimed at facilitating the process of advancing knowledge in this frequent disorder.

show abstract

Endothelial Dysfunction in Children Without Hypertension

Cited by 104 publications

References 49 publications

Regulation of obesity and insulin resistance by nitric oxide

Regulation of obesity and insulin resistance by nitric oxide

Role of sleep quality in the metabolic syndrome

Genotype–phenotype interactions in pediatric obstructive sleep apnea

Contact Info

Product

Resources

About