Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The human response to surgical stress is characterized by massive release of neuroendocrine hormones, provoking catabolism, thermogenesis, and hyperglycemia. Considering the possible adverse outcomes of excessive stress hormones, understanding various components of the stress response may improve management of postoperative morbidity. Leptin, initially described as an adipocyte-derived signaling factor, may also play an important role in regulating the hypothalamo-pituitary-adrenocortical axis. In phase I, plasma leptin and cortisol were measured in women before, during, and after total abdominal hysterectomy. The anesthetic technique was strictly controlled, balanced anesthesia. In phase II, plasma leptin and cortisol levels were measured in cardiac surgery patients. These subjects were anesthetized with a high dose opioid technique that blunts the intraoperative surgical stress response. In phase I, mean leptin levels did not change over the week before surgery, had a maximal decrease to 49% of baseline 2 h after surgery, and increased to just above baseline 24 h postoperatively. Cortisol was 176% of the baseline just before surgery, peaked at 2 h after surgery (383%), and remained elevated 24 h (200%) and 48 h (165%) after surgery. During the first 2 h of surgery, the decrease in leptin parallels the increase in cortisol. In phase II, high dose fentanyl limited both the cortisol increase and the leptin decrease; thus, the ratio of cortisol increase to leptin decrease was similar for the cardiac patients and the hysterectomy patients. These data indicate that leptin has a role in the surgically induced acute stress response in humans. Early in surgery the decrease in leptin parallels the increase in cortisol. This suggests a possible relationship between the neurobiology of these two systems, which could have important implications for regulation of the neuroendocrine response to surgical stress.
 ...
PMID:Leptin and the perioperative neuroendocrinological stress response. 1040 18

The placenta is a major source of leptin in the fetomaternal circulation, although its physiological role remains to be clarified. Leptin in the fetomaternal circulation is proposed to be a marker of acute stress in the fetus, and the fetus suffering from pre-eclampsia would be under chronic stress. In 16 pre-eclamptic placentas, the expressions of leptin, hypoxia-inducible factor 1alpha (HIF1alpha) and leptin receptor mRNAs were analyzed by semi-quantitative reverse-transcriptase-polymerase chain reaction and compared with clinical data. The co-expressions of leptin and the isoforms of the leptin receptor were observed in all the pre-eclamptic placentas. Leptin mRNA was significantly augmented in the pre-eclamptic placentas, although the level in fetal plasma was not high. The level of the expression of leptin mRNA was correlated with the placental HIF1alpha mRNA level and fetal body weight, but not with the levels of the leptin receptor isoforms in the pre-eclamptic placentas. This observation may suggest that autocrine/paracrine regulation of leptin exists in the human placenta and is upregulated in the pre-eclamptic placenta.
 ...
PMID:Augmentation of leptin and hypoxia-inducible factor 1alpha mRNAs in the pre-eclamptic placenta. 1534 62

Leptin deficiency in mice results in chronic thymic atrophy, suppressed cell-mediated immunity, and decreased numbers of total lymphocytes, suggesting a key role for the metabolic hormone leptin in regulating thymopoiesis and overall immune homeostasis. Unfortunately, the thymus is highly susceptible to stress-induced acute involution. Prolonged thymus atrophy in stress situations can contribute to peripheral T cell deficiency or inhibit immune reconstitution. Little is known, however, about specific roles for leptin signaling in the thymus or the underlying mechanisms driving thymic involution or thymic recovery after acute stress. We report here that leptin receptor expression is restricted in thymus to medullary epithelial cells. Using a model of endotoxemia-induced acute thymic involution and recovery, we have demonstrated a role for supraphysiologic leptin in protection of thymic epithelial cells (TECs). We also present data in support of our hypothesis that leptin treatment decreases in vivo endotoxemia-induced apoptosis of double positive thymocytes and promotes proliferation of double negative thymocytes through a leptin receptor isoform b-specific mechanism. Furthermore, our studies have revealed that leptin treatment increases thymic expression of interleukin-7, an important soluble thymocyte growth factor produced by medullary TECs. Taken together, these studies support an intrathymic role for the metabolic hormone leptin in maintaining healthy thymic epithelium and promoting thymopoiesis, which is revealed when thymus homeostasis is perturbed by endotoxemia.
 ...
PMID:Leptin receptor is expressed in thymus medulla and leptin protects against thymic remodeling during endotoxemia-induced thymus involution. 1958 63

Both animals and humans show a tendency toward eating more "comfort food" (high fat, sweet food) after acute stress. Such stress eating may be contributing to the obesity epidemic, and it is important to understand the underlying psychobiological mechanisms. Prior investigations have studied what makes individuals eat more after stress; this study investigates what might make individuals eat less. Leptin has been shown to increase following a laboratory stressor, and is known to regulate satiety. This study examined whether leptin reactivity accounts for individual differences in stress eating. To test this, we exposed forty women to standardized acute psychological laboratory stress (Trier Social Stress Test) while blood was sampled repeatedly for measurements of plasma leptin. We then measured food intake after the stressor. Increasing leptin during the stressor predicted lower intake of comfort food. These initial findings suggest that acute changes in leptin may be one of the factors modulating down the consumption of comfort food following stress.
 ...
PMID:Leptin concentrations in response to acute stress predict subsequent intake of comfort foods. 2257 88

Food consumption and preferences may be shaped by exposure to stressful environments during sensitive periods in development, and even small changes in consumption can have important effects on long term health. Adolescence is increasingly recognized as a sensitive period, in which adverse experiences can alter development, but the specific programming effects that may occur during adolescence remain incompletely understood. The current study seeks to explore the effects of stress during late adolescence on consumption of a palatable, high-fat, high-sugar food in adulthood-under basal conditions, as well following acute stress. Male Long-Evans rats were exposed to a regimen of variable stress for seven days in late adolescence (PND 45-51). During the stress regimen, stressed animals gained significantly less weight than control animals, but weight in adulthood was unaffected by adolescent stress. Palatable food consumption differed between experimental groups, and the direction of effect depended on context; stressed rats ate significantly more palatable food than controls upon first exposure, but ate less following an acute stressor. Leptin levels and exploratory behaviors did not differ between stressed and non-stressed groups, suggesting that other factors regulate preference for a palatable food. Altered food consumption following adolescent stress suggests that rats remain sensitive to stress during late adolescence, and that adult feeding behavior may be affected by previous adverse experiences. Such programming effects highlight adolescence as a period of plasticity, with the potential to shape long term food consumption patterns and preferences.
...
PMID:Stress during Adolescence Alters Palatable Food Consumption in a Context-Dependent Manner. 2687 68