Sleep, sleep-disordered breathing and lipid homeostasis: translational evidence from murine models and children

Abstract

Impaired sleep, particularly in the context of sleep-disordered breathing (SDB), is associated with a vast array of comorbidities, including obesity. It is well known that the etiology of obesity is both complex and multifactorial. Recent trends have shown that obesity rates have risen at an alarming rate in children, and this has likely contributed to an increased prevalence of SDB in children. Like the 'chicken and the egg' hypothesis, the temporal relationship of obesity and SDB is unclear but it is speculated that these two conditions converge to promote a fundamental disruption to normal lipid homeostasis. In this review, the effect of sleep disruption and SDB on lipid homeostasis in both murine and human models will be critically examined, with the intent of demonstrating that disrupted sleep in children is itself a precursor to obesity via disordered lipid homeostasis.

Figure 1. The circular model of sleep restriction, obstructive sleep apnea syndrome and obesity, emphasizing the central role of disrupted lipid metabolism

CRP: C-reactive protein; OSAS: Obstructive sleep apnea syndrome.

Figure 2. Lipid metabolism interactome in visceral adipose tissue of mouse, comprised of differentially expressed genes in response to intermittent hypoxia during sleep, as a model for obstructive sleep apnea syndrome

Colored in red are selected high-density network nodes, such as leptin, PPARGC1A, SREBF1 and SREBF2, which may represent regulators of adipocyte metabolic responses during intermittent hypoxia. Reproduced with permission from [93].