Decreased Delta-Sleep and Plasma Delta-Sleep-Inducing Peptide in Patients with Cushing Syndrome

Friedman, Theodore C.; Garcı́a-Borreguero, Diego; Hardwick, Donna; Akuete, C N; Doppman, John L.; Dorn, Lorah D.; Barker, Charles; Yanovski, Jack A.; Chrousos, George P.

doi:10.1159/000126806

Cited by 26 publications

(12 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The REM latency in normal individuals is around 103 min (34). Moreover, the absence of HC resulted in a decrease in sleep continuity, while HC replacement resulted in a more consolidated sleep pattern.…”

Section: Sleep Disturbancesmentioning

confidence: 99%

Inadequacies of glucocorticoid replacement and improvements by physiological circadian therapy

Debono

Ross²,

Newell‐Price

2009

European Journal of Endocrinology

114

View full text Add to dashboard Cite

Patients with adrenal insufficiency need lifelong glucocorticoid replacement, but many suffer from poor quality of life, and overall there is increased mortality. Moreover, it appears that use of glucocorticoids at the higher end of the replacement dose range is associated with increased risk for cardiovascular and metabolic bone disease. These data highlight some of the inadequacies of current regimes.The cortisol production rate is estimated to be equivalent to 5.7-7.4 mg/m 2 per day, and a major difficulty for replacement regimes is the inability to match the distinct circadian rhythm of circulating cortisol levels, which are low at the time of sleep onset, rise between 0200 and 0400 h, peaking just after waking and then fall during the day. Another issue is that current dose equivalents of glucocorticoids used for replacement are based on anti-inflammatory potency, and few data exist as to doses needed for equivalent cardiovascular and bone effects. Weight-adjusted, thrice-daily dosing using hydrocortisone (HC) reduces glucocorticoid overexposure and represents the most refined regime for current oral therapy, but does not replicate the normal cortisol rhythm. Recently, proof-of-concept studies have shown that more physiological circadian glucocorticoid therapy using HC infusions and newly developed oral formulations of HC have the potential for better biochemical control in patients with adrenal insufficiency. Whether such physiological replacement will have an impact on the complications seen in patients with adrenal insufficiency will need to be analysed in future clinical trials.

show abstract

Section: Sleep Disturbancesmentioning

confidence: 99%

Inadequacies of glucocorticoid replacement and improvements by physiological circadian therapy

Debono

Ross²,

Newell‐Price

2009

European Journal of Endocrinology

114

View full text Add to dashboard Cite

show abstract

“…Because these disorders are associated with high levels of cortisol, it follows that SWS should be diminished in the sleep of these patients. Indeed, Friedman et al (1994) demonstrated that patients with Cushing's syndrome spent much less time in SWS than did healthy controls. REM sleep, however, was not significantly different between groups in this study.…”

Section: The Role Of Cortisolmentioning

confidence: 99%

Sleep, dreams, and memory consolidation: The role of the stress hormone cortisol

Payne¹,

Nadel²

2004

Learn. Mem.

136

101

View full text Add to dashboard Cite

We discuss the relationship between sleep, dreams, and memory, proposing that the content of dreams reflects aspects of memory consolidation taking place during the different stages of sleep. Although we acknowledge the likely involvement of various neuromodulators in these phenomena, we focus on the hormone cortisol, which is known to exert influence on many of the brain systems involved in memory. The concentration of cortisol escalates over the course of the night's sleep, in ways that we propose can help explain the changing nature of dreams across the sleep cycle.There is currently no convincing explanation for why we dream or what we dream about. In this article we propose an approach to dreaming that focuses on the relationship between sleep and memory. We suggest that dreams reflect a biological process of long-term memory consolidation, serving to strengthen the neural traces of recent events, to integrate these new traces with older memories and previously stored knowledge, and to maintain the stability of existing memory representations in the face of subsequent experience (Winson 1985(Winson , 2002(Winson , 2004Kali and Dayan 2004).It is generally assumed that long-term memory consolidation involves interactions among multiple brain systems, modulated by various neurotransmitters and neurohormones. We propose that the characteristics of dreams are best understood in the context of this neuromodulatory impact on the brain systems involved in memory consolidation. Although a number of neurotransmitters and neurohormones are likely involved, we focus our attention in particular on the stress hormone cortisol, which has widespread effects on memory during waking life through its impact on many of the critical brain structures implicated in memory function.Our hypothesis, briefly stated, is that variations in cortisol (and other neurotransmitters) determine the functional status of hippocampal ↔ neocortical circuits, thereby influencing the memory consolidation processes that transpire during sleep. The status of these circuits largely determines the phenomenology of dreams, providing an explanation for why we dream and of what. As a corollary, dreams can be thought of as windows onto the inner workings of our memory systems, at least those of which we can become conscious.In addition to exploring these ideas in more detail, we provide some background concerning (1) the states of sleep and the role of various neurotransmitters in switching from one sleep state to another, (2) how the characteristics of dreams vary as a function of sleep state, (3) the memory content typically associated with dreaming in different dream states, and (4) the role of sleep in the consolidation of memory.

show abstract

“…In the pituitary of vertebrates DSIP‐LI co‐localizes with such peptides as corticotrophin‐like intermediate lobe peptide (CLIP), adrenocorticotropic hormone (ACTH), melanocyte‐stimulating hormone (MSH), thyreotropic hormone (TSH) and melanin‐concentrating hormone (MCH), and it co‐localizes with adrenaline and noradrenaline in the adrenal medulla (Table 2). The human pituitary does not appear to be the site of synthesis of plasma DSIP‐LI (Friedman et al . 1994a).…”

Section: Structure Of Delta Sleep‐inducing Peptide (Dsip) and Dermorpmentioning

confidence: 99%

Delta sleep‐inducing peptide (DSIP): a still unresolved riddle

Kovalzon

Strekalova

2006

Journal of Neurochemistry

View full text Add to dashboard Cite

Delta sleep-inducing peptide (DSIP) was isolated from rabbit cerebral venous blood by Schoenenberger-Monnier group from Basel in 1977 and initially regarded as a candidate sleep-promoting factor. However, the link between DSIP and sleep has never been further characterized, in part because of the lack of isolation of the DSIP gene, protein and possible related receptor. Thus the hypothesis regarding DSIP as a sleep factor is extremely poorly documented and still weak. Although DSIP itself presented a focus of study for a number of researchers, its natural occurrence and biological activity still remains obscure. DSIP structure is different from any other known representative of the various peptide families. In this mini-review we hypothesize the existence of a DSIP-like peptide(s) that is responsible (at least partly) for DSIP-like immunoreactivity and DSIP biological activity. This assumption is based on: (i) a highly specific distribution of DSIP-like immunoreactivity in the neurosecretory hypothalamic nuclei of various vertebrate species that are not particularly relevant for sleep regulation, as revealed by the histochemical studies of the Geneva group (Charnay et al.); (ii) a large spectrum of DSIP biological activity revealed by biochemical and physiological studies in vitro; (iii) significant slow-wave sleep (SWS) promoting activity of certain artificial DSIP structural analogues (but not DSIP itself!) in rabbits and rats revealed by our early studies; and (iv) significant SWS-promoting activity of a naturally occurring dermorphin-decapeptide that is structurally similar to DSIP (in five of the nine positions) and the sleep-suppressing effect of its optical isomer, as revealed in rabbits. Potential future studies are outlined, including natural synthesis and release of this DSIP-like peptide and its role in neuroendocrine regulation.

show abstract

Decreased Delta-Sleep and Plasma Delta-Sleep-Inducing Peptide in Patients with Cushing Syndrome

Cited by 26 publications

References 31 publications

Inadequacies of glucocorticoid replacement and improvements by physiological circadian therapy

Inadequacies of glucocorticoid replacement and improvements by physiological circadian therapy

Sleep, dreams, and memory consolidation: The role of the stress hormone cortisol

Delta sleep‐inducing peptide (DSIP): a still unresolved riddle

Contact Info

Product

Resources

About