Interactions between sleep, stress, and metabolism: From physiological to pathological conditions

TL;DR: Short term sleep fragmentation enhances anxiety-related behavior in rats, which could be partly mediated by the observed hormonal changes presented in the current study in form of testosterone, estradiol and progesterone depletion.

TL;DR: In this article, a review summarizes the literature on sleep and cognition in Addison's disease and the role that cortisol concentrations play in the relationship between the two, and provides support for existing theoretical frameworks which postulate that disrupted sleep is an important biological mechanism that underlies, at least partially, the memory impairments that patients frequently report experiencing.

TL;DR: It is concluded that biasing RAS network activity to optimize sleep efficiency and enhance mood by electrically modulating TSNC activity through its afferent inputs holds tremendous potential for optimizing mental health and human performance.

TL;DR: Surprisingly, most studies revealed the presence of a stress response following sleep deprivation, however, the origin and the impact of the stress response during sleep deprivation remain somewhat unclear.

TL;DR: Differences in leptin and ghrelin are likely to increase appetite, possibly explaining the increased BMI observed with short sleep duration, and changes in appetite regulatory hormones with sleep curtailment may contribute to obesity.

TL;DR: In this study, 12 young, healthy, normal-weight men exhibited reductions in the satiety hormone leptin, increases in the hunger hormone ghrelin, and increases in hunger after 2 nights of only 4 hours of sleep compared with after two nights of 10 hours ofSleep, suggesting inadequate sleep seems to influence the hormones that regulate satiety and hunger.

TL;DR: In this article, a meta-analysis was carried out to assess whether the evidence supports the presence of a relationship between short sleep duration and obesity at different ages, and to obtain a quantitative estimate of the risk in order to assess the consistency and potential public health relevance.

TL;DR: Increased adipocyte 11β HSD-1 activity may be a common molecular etiology for visceral obesity and the metabolic syndrome.