Leptin and hunger levels in young healthy adults after one night of sleep loss.

Short-term sleep curtailment associated with activation of the stress system in healthy, young adults has been shown to be associated with decreased leptin levels, impaired insulin sensitivity, and increased hunger and appetite. To assess the effects of one night of sleep loss in a less stressful environment on hunger, leptin, adiponectin, cortisol and blood pressure/heart rate, and whether a 2-h mid-afternoon nap reverses the changes associated with sleep loss, 21 young healthy individuals (10 men, 11 women) participated in a 7-day sleep deprivation experiment (four consecutive nights followed by one night of sleep loss and two recovery nights). Half of the subjects were randomly assigned to take a mid-afternoon nap (14:00-16:00 hours) the day following the night of total sleep loss. Serial 24-h blood sampling and hunger scales were completed on the fourth (predeprivation) and sixth day (postdeprivation). Leptin levels were significantly increased after one night of total sleep loss, whereas adiponectin, cortisol levels, blood pressure/heart rate, and hunger were not affected. Daytime napping did not influence the effects of sleep loss on leptin, adiponectin, or hunger. Acute sleep loss, in a less stressful environment, influences leptin levels in an opposite manner from that of short-term sleep curtailment associated with activation of the stress system. It appears that sleep loss associated with activation of the stress system but not sleep loss per se may lead to increased hunger and appetite and hormonal changes, which ultimately may lead to increased consumption of 'comfort' food and obesity.

Alexithymia and its association with burnout, depression and family support among Greek nursing staff.

BACKGROUND: Few studies have examined the relation between alexithymia (i.e. the inability to recognize and verbalize emotions) and professional burnout. Considering the absence of relevant studies in the Greek scientific literature, the aim of this work was to examine the associations of alexithymia with the three facets of professional burnout, the perception of family support and depression in nursing personnel. METHODS: The study was performed in one of the largest hospitals in Greece and included 95 nurses. Assessments of alexithymia, burnout, depression and family support were made by means of the Toronto Alexithymia Scale, the Maslach Burnout Inventory, the Beck Depression Inventory and the Julkunen Family Support Scale, respectively. Student's t-test, Pearson's correlation and stepwise linear regression were used for the evaluation of data. RESULTS: Alexithymia was correlated positively with depression, emotional exhaustion and depersonalization, and negatively with sense of family support and personal achievement. Additionally, family support was correlated positively with personal achievement and negatively with depression. CONCLUSION: In the scientific literature there is a debate as to whether alexithymia is a stable personality characteristic or if it is dependent on symptoms of mental disorders. We tried to interpret the associations of alexithymia with professional burnout, depressive symptoms and family support. From this study it appears very likely that alexithymia is directly associated with depression and personal achievement, but also indirectly with the sense of family support.

CRH Receptors in Human Reproduction.

BACKGROUND: Corticotropin releasing hormone (CRH), the main peptide-mediator of stress, has been found in the female reproductive system. OBJECTIVE: Herein, the role of CRH receptors in the female reproductive system is presented. RESULTS: It is clear that CRH receptors are involved in the regulation of the hypothalamic-pituitaryovarian axis, while locally are associated with decidualization, embryonic implantation, early fetal development and triggering of parturition. CONCLUSION: Abnormal CRH signaling may contribute to obstetrical pathophysiology, such as preeclampsia, abnormal placenta invasion, endometrial growth retardation and preterm delivery.

Plasma interleukin 6 levels are elevated in polycystic ovary syndrome independently of obesity or sleep apnea.

Premenopausal women with polycystic ovary syndrome (PCOS) are at a much higher risk for excessive daytime sleepiness, fatigue, and insulin resistance than control women. Elevated levels of interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) are presumably part of the pathogenesis of these clinical manifestations. Forty-two obese women with PCOS, 17 body mass index-comparable obese controls, and 15 normal-weight controls free from apnea participated in the study that included one 8-hour nighttime polysomnography, single morning cytokine plasma concentrations, and insulin resistance indices. Women with PCOS exhibited higher plasma concentrations of IL-6 than obese controls, who had intermediate values, or normal-weight controls, who had the lowest values (4.75 +/- 0.5 vs 3.65 +/- 0.4 vs 1.84 +/- 0.3 pg/mL, P < .01). Tumor necrosis factor alpha values were higher in PCOS and obese controls compared with normal-weight controls, but the difference was not statistically significant (4.05 +/- 0.3 vs 3.79 +/- 0.2 vs 3.14 +/- 0.2 pg/mL, P = .103). Based on backward regression analysis, IL-6 levels had a stronger association with the PCOS group than with the obese group, and the sleep or hypoxia variables did not make a significant contribution to either IL-6 or TNF-alpha. Both IL-6 and TNF-alpha correlated positively with body mass index (P < .01) in obese controls but not in women with PCOS. Furthermore, within the PCOS group, IL-6 and TNF-alpha correlated more strongly with indices of insulin resistance than obesity. We conclude that IL-6 levels are elevated in obese women with PCOS independently of obesity or sleep apnea and may represent a pathophysiologic link to insulin resistance.

Corticotropin-releasing hormone (CRH) and immunotolerance of the fetus.

The hypothalamic neuropeptide corticotropin-releasing hormone (CRH) is produced by several tissues of the female reproductive system, including the endometrial glands and decidualized stroma, as well as the trophoblast, syncytiotrophoblast, and placental decidua. CRH is also secreted at inflammatory sites and possesses potent pro-inflammatory properties influencing both innate and acquired immune processes. Recent experimental findings show that uterine CRH participates in local immune phenomena associated with early pregnancy, such as differentiation of endometrial stroma to decidua and protection of the fetus from the maternal immune system. CRH induces the expression of apoptotic Fas ligand (FasL) on invasive extravillous trophoblast and maternal decidual cells at the fetal-maternal interface. Furthermore, CRH increases the apoptosis of activated T lymphocytes through FasL induction, participating in the processes of both implantation and early pregnancy tolerance.

Stress neuropeptides in the human endometrium: paracrine effects on cell differentiation and apoptosis.

Human endometrium exhibits characteristics of a neuroendocrine-like stress organ in addition to its classical role as the main target of ovarian steroid hormones. Indeed, the epithelial cells of human endometrium express the stress-associated neuropeptide genes corticotropin-releasing hormone (CRH), proopiomelanocortin, proenkephalin and prodynorphin. Furthermore, endometrium stroma cells also express CRH when they differentiate into decidual cells. Multiple lines of evidence suggest that the stress-associated neuropeptides of human endometrium are under the endocrine control of gonadal steroids as well as under an autocrine/paracrine regulation by prostanoids and interleukins. Endometrial stress-associated neuropeptides appear to exert their biological effect locally, i.e. within the uterus since human endometrium and myometrium also express the relevant receptors. More specifically, recent data suggest that endometrial CRH participates in the regulation of intrauterine inflammatory processes taking place in early pregnancy including stroma decidualization, blastocyst implantation and early maternal tolerance. Similarly, endometrial opioids participate in the regulation of uterine tissue remodeling via their effect on endometrial cell apoptosis. Thus, endometrial stress neuropeptides act as paracrine regulators of uterine cell differentiation and tissue remodeling as well as modulators of local immune responses.

The role of stress in female reproduction and pregnancy: an update.

Life exists by establishing a balanced equilibrium, called homeostasis, constantly challenged by adverse stimuli, called stressors. In response to these stimuli, a complex neurohormonal reaction exerted by the activation of the so-called stress system is initiated. The latter is activated in a coordinated fashion, leading to behavioral and peripheral changes that improve the ability of the organism to adjust homeostasis and increase its chance for survival. The stress system suppressive effects on female reproduction involve suppression of the hypothalamic-pituitary-ovarian axis at the hypothalamic, pituitary, ovarian, and uterine levels. Experimental and human data suggest that adverse prenatal stimuli, of either maternal or fetal origin, acting in the developing embryo in utero, can lead to the development of short- and long-term health disorders. These include preterm birth of the offspring, low birth weight, and the development of adult diseases ranging from the metabolic syndrome to several neurodevelopmental disorders.

Chronic administration of an angiotensin II receptor antagonist resets the hypothalamic-pituitary-adrenal (HPA) axis and improves the affect of patients with diabetes mellitus type 2: preliminary results.

Diabetes mellitus type 2 (DM type 2) is associated with depressive symptomatology and intermittent hyperfunction of the hypothalamic-pituitary-adrenal (HPA) axis. DM type 2 is also accompanied by increased tissue levels of angiotensin II (Ang II), which stimulates the HPA axis through the Ang II type 1 receptors (AT1). We investigated the effect of candesartan, an angiotensin receptor blocker (ARB) that crosses the blood brain barrier, on the activity of the HPA axis and on the affect of 17 patients with DM type 2, aged 40-65 years, who were treated with 4 mg/day candesartan per os for at least 3 months. Before and after candesartan administration, a corticotropin-releasing hormone (CRH) stimulation test and psychological tests were performed. In response to hCRH, time-integrated secretion of ACTH was not altered by candesartan administration, however, the cortisol response was decreased significantly compared to baseline (mean +/- SEM, 2327 +/- 148.3 vs. 1943 +/- 131.9 microg/dl, P = 0.005) suggesting reduced sensitivity of the adrenals to ACTH. In parallel, there was a significant improvement in interpersonal sensitivity (0.91 +/- 0.16 vs. 0.70 +/- 0.15, P = 0.027) and depression scores (0.96 +/- 0.15 vs. 0.71 +/- 0.10, P = 0.026). We suggest that candesartan resets the HPA axis of patients with DM type 2 and improves their affect.