Abstract
Serum amyloid A (SAA) was recently associated with metabolic endotoxemia, obesity and insulin resistance. Concurrently, insufficient sleep adversely affects metabolic health and is an independent predisposing factor for obesity and insulin resistance. In this study we investigated whether sleep loss modulates SAA production. The serum SAA concentration increased in C57BL/6 mice subjected to sleep restriction (SR) for 15 days or to paradoxical sleep deprivation (PSD) for 72 h. Sleep restriction also induced the upregulation of Saa1.1/Saa2.1 mRNA levels in the liver and Saa3 mRNA levels in adipose tissue. SAA levels returned to the basal range after 24 h in paradoxical sleep rebound (PSR). Metabolic endotoxemia was also a finding in SR. Increased plasma levels of SAA were also observed in healthy human volunteers subjected to two nights of total sleep deprivation (Total SD), returning to basal levels after one night of recovery. The observed increase in SAA levels may be part of the initial biochemical alterations caused by sleep deprivation, with potential to drive deleterious conditions such as metabolic endotoxemia and weight gain.
Highlights
Obesity is reaching pandemic proportions across much of the world and its consequences includes unprecedented health, social and economic issues
Sleep loss induces metabolic and endocrine alterations, such as decreased glucose tolerance, decreased insulin sensitivity, increased concentrations of cortisol and ghrelin, decreased levels of leptin, and increased hunger and appetite [2]. These metabolic and endocrine alterations are frequently used to support a causal relationship between sleep loss and obesity/insulin resistance, it is still missing the identification of a triggering factor for weight gain in sleep disorders
Mice subjected to sleep restriction (SR) for 21 h daily during 15 days lost weight (Figure 1A)
Summary
Obesity is reaching pandemic proportions across much of the world and its consequences includes unprecedented health, social and economic issues. Sleep loss induces metabolic and endocrine alterations, such as decreased glucose tolerance, decreased insulin sensitivity, increased concentrations of cortisol and ghrelin, decreased levels of leptin, and increased hunger and appetite [2]. These metabolic and endocrine alterations are frequently used to support a causal relationship between sleep loss and obesity/insulin resistance, it is still missing the identification of a triggering factor for weight gain in sleep disorders. The difficulty of translating findings directly from animal models to humans and the challenge of finding an experimental model that leads to weight gain are some of the elements that prevent new discoveries regarding the mechanisms involved in weight gain led by sleep loss. Using the multiple platform sleep restriction (SR) experimental model, we were able to link a past history of sleep restriction to subsequent complications arising from a high-fat diet [3]
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