Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endogenous opiates have been implicated in pain and stress experiences. In order to directly assess the relationship between endorphin activity and acute behavioral distress, beta-endorphin immunoreactivity (beta-EPI) was measured by radioimmunoassay in cerebrospinal fluid of 75 children with acute leukemia undergoing routine lumbar puncture. These data were related to four measures of behavioral distress collected during the procedure. For children 4 years of age and above, beta-EPI correlated inversely with age (r = -.31,p less than or equal to .05). All behavioral measures also inversely correlated with age (r = -.26 to -.67,p less than or equal to .05 to .001). Females had a significantly lower mean beta-EPI than males (p less than or equal to .01), and exhibited greater behavioral distress. beta-EPI and behavioral measures interacted with the use of specific antileukemia agents. L-Asparaginase was associated with lower beta-EPI (p less than or equal to .05), while prednisone was associated with lower behavioral distress on three of the four measures (p less than or equal to .05 to .01). After controlling for age, sex, and chemotherapy, beta-EPI and nurse ratings of anxiety were positively correlated (partial correlation coefficient = .31, p less than or equal to .05). Correlations between beta-EPI and other behavioral measures demonstrated positive trends. Results of this study are interpreted as support for the reactive nature of beta-EPI in cerebrospinal fluid to acute distress, and may help explain documented sex differences in distress behavior. Potential clinical implications and directions for further research are discussed.
 ...
PMID:beta-Endorphin immunoreactivity and acute behavioral distress in children with leukemia. 627 5

Acute glucoprivation profoundly stimulated hypothalamic-pituitary-adrenocortical (HPA) and adrenomedullary outflows. Whether these responses reflect a single central mechanism regulated by corticotropin-releasing hormone (CRH) has been unclear. This study examined the role of endogenous CRH in HPA and adrenomedullary responses to hypoglycemia in Sprague-Dawley rats, by using anti-CRH immune serum or a CRH antagonist (alpha-helical h/r CRH9-41, and in Lewis rats, a strain characterized by deficient hypothalamic CRH responses during stress. In conscious Sprague-Dawley rats with indwelling arterial and venous cannulas, insulin (0.3 U/kg was injected iv, and responses of serum glucose concentrations and plasma levels of corticotropin (ACTH) and catechols (including epinephrine, EPI; norepinephrine, NE; dihydroxyphenylalanine, DOPA; dihydroxyphenylglycol, DHPG; and dihydroxyphenylacetic acid, DOPAC) were assessed, with or without pretreatment with anti-CRH immune serum (0.5 or 1.0 ml iv or 10 microl icv) or alpha-helical h/r CRH9-41 (130 nmol iv or 13 nmol icv). Responses to insulin (1.0 U/kg iv) were also measured in conscious juvenile Lewis and Fischer 344/N rats. Insulin-induced hypoglycemia markedly increased plasma levels of EPI and ACTH in all groups. Pretreatment iv with 1/0 ml of anti-CRH immune serum blocked the ACTH response to insulin but failed to attenuate the EPI response. alpha-helical h/r CRH9-41, whether given iv or icv, failed to alter ACTH or EPI responses to insulin, although the antagonist did block EPI responses to icv CRH. Hypoglycemia elicited similar increments in ACTH levels in Lewis rats and Fischer 344/N control rats; and although Lewis rats had lower baseline EPI and smaller responses of NE, DHPG, DOPA, and DOPAC levels, the groups did not differ in proportionate increments in EPI levels. The results indicate that the ACTH response to hypoglycemia depends on availability of CRH outside the blood-brain barrier--presumably in the pituitary gland. The findings with icv alpha-helical h/r CRH9-41 can be explained by failure of the antagonist to reach effective concentrations at central sites of action of endogenous CRH, or by mechanisms other than CRH release determining the adrenomedullary response to hypoglycemia. Lewis rats seem to have less adrenomedullary secretion at baseline and smaller responses of NE synthesis and release during hypoglycemia than do Fischer 344/N rats. Neurochemical evidence for differential adrenomedullary and sympathoneural responses during hypoglycemia in all three rat strains is inconsistent with Cannon's view of a functionally unitary sympathoadrenal system. Lewis rats have deficient CRH responses to some stressors but not to others, or else pituitary-adrenomedullary responses in this setting depend on mechanisms other than CRH release in the brain. Both explanations are inconsistent with the doctrine of non-specificity, the main tenet of Selye's stress theory.
 ...
PMID:Role of CRH in glucopenia-induced adrenomedullary activation in rats. 868 Apr 14

We validated the use of urine to monitor changes in the activity of both the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS) in swine. Ten pregnant sows were fitted with venous catheters 3 wk after mating. In the early (wk 6), middle (wk 9), and late (wk 14) stages of gestation, blood and urine were collected over 24 h to monitor diurnal changes in plasma cortisol, urinary cortisol, and urinary catecholamines (norepinephrine [NE] and epinephrine [EPI]). Dexamethasone suppression tests (DST) and ovine corticotropin-releasing hormone (CRH) challenge tests were also performed at each stage of gestation. All plasma and urinary values changed markedly around the clock. Diurnal variations of urinary cortisol were comparable to those in plasma, with a late nocturnal peak and a trough occurring in the evening. During the dark period, urinary catecholamines were lower than during the light period. Norepinephrine increased sharply after lights came on and peaked after meal time. Epinephrine began to rise at the end of the dark period and peaked just before meal time. Average plasma cortisol increased with the stage of gestation, due to higher levels during daylight hours. Dexamethasone at 2000 (20 microg/kg i.v.) decreased plasma cortisol at 0830 and nocturnal cortisol excretion. The magnitude of the decrease in plasma ACTH and urinary cortisol after DST was lower in late than in early and midgestation, indicating increased feedback resistance at that stage. The CRH (1 microg/kg i.v.) increased plasma and urinary cortisol. Peak levels occurred 30 min and 2 to 3 h after the injection, respectively. Catecholamines and cortisol in urine produced during the night (2000 to 0800) and the early morning (0400 to 0800 and 0800 to 0900) were highly correlated with their 24-h excretion rate. These results indicate that it is possible to monitor changes in the HPA axis and SNS activity through urinary measurements in pigs.
 ...
PMID:Assessment of hypothalamic-pituitary-adrenal axis and sympathetic nervous system activity in pregnant sows through the measurement of glucocorticoids and catecholamines in urine. 1070 34

This paper discusses the hypothesis that a 'drive for activity" in the presence of physiological and endocrine changes consistent with starvation is a characteristic symptom of acute anorexia nervosa (AN). This 'drive for movement', along with alertness and lack of fatigue, so unlike the motor slowing and loss of energy observed in simple starvation has been recognized in AN throughout history, but has received little attention in the past fifty years. Clinical reports and experimental evidence suggest that 'restlessness' and a 'drive for activity' vary in intensity, they appears to be starvation-dependent and to wane with food intake. Central nervous system (CNS) systems known to be involved in mediating activity and arousal levels that are altered by the negative energy expenditure in AN are reviewed. Among these, the corticotropin-releasing hormone (CRH) system, the melanocyte stimulating hormone/agouti-related protein (MSH/AGRP) system and the norepinephrine/epinephrine (NE/EPI) and dopamine (DA) system may contribute to the 'drive for activity' and alertness in AN. AN appears to represent a disorder of gene/environment interaction. Future research will reveal whether in individuals predisposed to AN, the 'drive for activity' reflects the reactivation of mechanisms important in food scarcity, controlled by one or more evolutionary conserved genes including those regulating foraging behavior. Recognition of the 'drive for activity' as a diagnostic symptom of AN and its assessment prior to re-nutrition would permit clarification of its role in the etiology of AN.
 ...
PMID:The 'drive for activity' and "restlessness" in anorexia nervosa: potential pathways. 1644 3