Sleep and vascular disorders

Plante, Gérard E.

doi:10.1016/j.metabol.2006.07.013

Cited by 25 publications

(14 citation statements)

References 33 publications

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“…Obesity, in addition to increasing the vascular risk of diabetes, hypertension, and hyperlipidemia, is also associated with sleep apnea [44][45][46]60,125], as mentioned above. Childhood obesity is associated with hypertension, impaired vascular function, dyslipidemia, atheroma formation, the metabolic syndrome, type 2 diabetes, systemic inflammation and oxidative stress resulting in premature death and disability in adulthood [126].…”

Section: Body Mass Index (Bmi)mentioning

confidence: 93%

Environmental vascular risk factors: New perspectives for stroke prevention

Bernal-Pacheco

Román

2007

Journal of the Neurological Sciences

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Section: Body Mass Index (Bmi)mentioning

confidence: 93%

Environmental vascular risk factors: New perspectives for stroke prevention

Bernal-Pacheco

Román

2007

Journal of the Neurological Sciences

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“…This trend toward shorter sleep times has occurred over the same time period as the dramatic increases in the prevalence of obesity and diabetes. Current evidence suggests a close relationship among endocrine, metabolic, cardiovascular, and immune functions and sleep disturbances (149,183). In studies of healthy young adults subjected to recurrent partial sleep restriction, increased hunger and appetite leading to overeating and weight gain were observed and were correlated with a decrease in glucose tolerance and insulin sensitivity as well as a decrease in circulating levels of the anorexigenic hormone leptin and a concomitant increase in levels of the orexigenic hormone ghrelin (169,183).…”

Section: Glucocorticoids Play An Important Role In Insulin Resistancementioning

confidence: 99%

Adrenocortical dysregulation as a major player in insulin resistance and onset of obesity

Roberge¹,

Carpentier²,

Langlois³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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The aim of this review is to explore the dysregulation of adrenocortical secretions as a major contributor in the development of obesity and insulin resistance. Disturbance of adipose tissue physiology is one of the primary events in the development of pathologies associated with the metabolic syndrome, such as obesity and type 2 diabetes. Several studies indicate that alterations in metabolism of glucocorticoids (GC) and androgens, as well as aldosterone in excess, are involved in the emergence of metabolic syndrome. Cross talk among adipose tissue, the hypothalamo-pituitary complex, and adrenal gland activity plays a major role in the control of food intake, glucose metabolism, lipid storage, and energy balance. Perturbation of this cross talk induces alterations in the regulatory mechanisms of adrenocortical steroid synthesis, secretion, degradation, and/or recycling, at the level of the zonae glomerulosa (aldosterone), fasciculata (GC and GC metabolites), and reticularis (androgens and androgen precursors DHEA and DHEAS). As a whole, these adrenocortical perturbations contribute to the development of metabolic syndrome at both the paracrine and systemic level by favoring the physiological dysregulation of organs responsive to aldosterone, GC, and/or androgens, including adipose tissue. adrenal gland; adipocytes; angiotensin II; adrenocorticotropic hormone; adrenal steroids INSULIN RESISTANCE (IR), which is characterized by an insufficiency in insulin action, is associated with pathologies related to the metabolic syndrome, such as central obesity, hypertension, and dyslipidimia, and leads to increased risk of type 2 diabetes and cardiovascular diseases. Common forms of obesity and type 2 diabetes are polygenic diseases, resulting from complex interactions between genetic predispositions and environmental factors (18, 42), with particular importance of dietary fat intake (114,146). Current data converge to indicate that dysregulation in adipose tissue physiology is one of the primary events in the development of insulin resistance (52, 109, 111), although other insulin-and glucocorticoid-responsive organs such as skeletal muscles and liver may also play a primary role (144, 168). Several publications and reviews also point to glucocorticoids (GC) (151,190) and the renin-angiotensin system (RAS) as key players in controlling adipose tissue physiology (187). However, several reports indicate cross-talk relationships among the hypothalamo-pituitary-adrenal (HPA) axis, the melanocortin pathways, and the adipose tissue. Combination of certain gene variants with environmental factors, such as overheating, sedentarity, and chronic stress, appears to alter this cross talk, hence inducing perturbations in the regulatory mechanisms of adrenocortical steroid synthesis, secretion, degradation, and/or recycling. The aim of the present review is to explore the dysregulation of adrenocortical secretions as a major contributor in the development of obesity and insulin resistance. Structure and Functions of the Adrenal Cortex...

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“…Epidemiological studies have revealed that chronic hypoxia, whether constant (e.g., resulting from pulmonary diseases or living at high altitude, hereafter denoted by CCH) or intermittent (e.g., such as in sleep apnea, denoted by CIH) is a major cause of cardiovascular and cerebrovascular disease, a most common ailment of industrialized societies (e.g., Covello and Simon 2004;Dursunoglu and Dursunoglu 2006;Jain 2007;Parati et al 2007;Park et al 2007;Plante 2006;Teran Santos et al 2006;Venardos and Kaye 2007). The more than 140 million residents of high altitude (>2,500 m above the sea), for example, have pulmonary hypertension and right ventricular hypertrophy (Penaloza and Arias-Stella 2007), a condition characterizing also animals subjected to CCH (e.g., Abe et al 2006;de Frutos et al 2007;Fan et al 2005;Morecroft et al 2007;Paddenberg et al 2007).…”

Section: Introductionmentioning

confidence: 99%

Integrated transcriptomic response to cardiac chronic hypoxia: translation regulators and response to stress in cell survival

Iacobaş

Fan

Iacobaş

et al. 2008

Funct Integr Genomics

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Complementary deoxyribonucleic acid microarray data from 36 mice subjected for 1, 2, or 4 weeks of their early life to normal atmospheric conditions (normoxia) or chronic intermittent (CIH) or constant (CCH) hypoxia were analyzed to extract organizational principles of the developing heart transcriptome and determine the integrated response to oxygen deprivation. Although both CCH and CIH regulated numerous genes involved in a wide diversity of processes, the changes in maturational profile, expression stability, and coordination were vastly different between the two treatments, indicating the activation of distinct regulatory mechanisms of gene transcription. The analysis focused on the main regulators of translation and response to stress because of their role in the cardiac hypertrophy and cell survival in hypoxia. On average, the expression of each heart gene was tied to the expression of about 20% of other genes in normoxia but to only 8% in CCH and 9% in CIH, indicating a strong decoupling effect of hypoxia. In contrast to the general tendency, the interlinkages among components of the translational machinery and response to stress increased significantly in CIH and much more in CCH, suggesting a coordinated response to the hypoxic stress. Moreover, the transcriptomic networks were profoundly and differently remodeled by CCH and CIH.

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Sleep and vascular disorders

Cited by 25 publications

References 33 publications

Environmental vascular risk factors: New perspectives for stroke prevention

Environmental vascular risk factors: New perspectives for stroke prevention

Adrenocortical dysregulation as a major player in insulin resistance and onset of obesity

Integrated transcriptomic response to cardiac chronic hypoxia: translation regulators and response to stress in cell survival

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