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

The mechanisms that control lipolysis in intra-abdominal fat cells from various primate species, the marmoset (Callithrix jacchus), the baboon (Papio papio), and the macaque (Macaca fascicularis), were compared to those of human intraabdominal fat cells. Selective beta 1- or beta 2-adrenoceptor agonists induced lipolysis in all species. Selective beta 3-agonists (BRL 37344, CL 316243, and SR 58611) acted as partial agonists in marmoset but were inefficient in other primates, including humans. alpha 2-Adrenoceptor number ([3H]RX 8210002 binding) equalized (baboon) or exceeded (other primates) beta 1/beta 2-adrenoceptors ([3H]CGP 12177 binding). Baboon fat cell membranes expressed similar amounts of coupled beta- and alpha 2-adrenoceptors. In all species, norepinephrine- or epinephrine-induced lipolysis did not reach the lipolytic effect of isoproterenol but their effects were enhanced after alpha 2-adrenoceptor blockade. N6-phenylisopropyladenosine (PIA) induced a full antilipolytic effect in baboon, macaque, and human adipocytes through adenosine receptors ([3H]DPCPX binding). Peptide YY (PYY) weakly inhibited lipolysis in baboon. Adrenocorticotropic hormone (ACTH) was inactive whereas parathyroid hormone (PTH) partially stimulated lipolysis in primates. Histamine was partially lipolytic in marmoset only. This study emphasizes the similarities of the mechanisms controlling the lipolysis in nonhuman primate and in human adipocytes and suggests that the baboon and the macaque should provide unique models for the study of the regulation of lipolysis.
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PMID:Control of lipolysis in intra-abdominal fat cells of nonhuman primates: comparison with humans. 777 57

Histamine H3 receptors have been identified in rat and guinea-pig pituitary glands and in the mouse pituitary tumor cell line, AtT-20. Histamine H3 receptor agonists are reported to stimulate adrenocorticotropic hormone (ACTH) release from AtT-20 cells, an effect blocked by histamine H3 but not H1 or H2 receptor antagonists. To determine whether negative feedback regulation of the histamine H3 receptor-mediated effect might occur, we tested the effects of steroid treatment upon binding of the agonist [3H]N alpha-methylhistamine to AtT-20 cell membranes. Consistent with feedback regulation, steroid treatment of the cells reduced [3H]N alpha-methylhistamine binding. The effect was dose-dependent and was greatest for glucocorticoids among the steroids tested. As the duration of steroid treatment increased, the amount of [3H]N alpha-methylhistamine binding decreased, to 15% of control at 36 h. However, the effect was not specific for histamine H3 receptors. Somatostatin inhibits ACTH release from these cells and its binding was similarly reduced by steroid treatment. Because steroids have been reported to modulate levels of guanine nucleotide-binding proteins, the lack of receptor specificity could reflect an indirect effect of steroids upon agonist binding and, in fact, we show that [3H]N alpha-methylhistamine binding to these cells, like somatostatin, is pertussis toxin-sensitive. However, steroid treatment does not alter the apparent levels of pertussis toxin substrate in these cells. Whether steroid treatment affects histamine H3 receptors of these cells directly or through some more subtle effect upon the guanine nucleotide-binding proteins to which they couple, the result is a negative feedback loop that attenuates [3H]N alpha-methylhistamine binding to these cells.
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PMID:Steroid-sensitivity of agonist binding to pituitary cell line histamine H3 receptors. 808 74

Stress stimulates the secretion of the pro-opiomelanocortin (POMC) derived peptides ACTH and beta-endorphin (beta-END) as well as prolactin (PRL) from the adenohypophysis. The regulation of adenohypophysial hormone secretion is complex and includes a variety of neuropeptides and neuroamines. Histamine (HA) seems to participate as a neurotransmitter in the central regulation of adenohypophysial secretion and is involved in stress-induced release of these hormones. However, the effect of HA on POMC and PRL secretion is indirect and may involve activation of hypothalamic neurons subsequently releasing hypophysiotropic factors that in turn regulate adenohypophysial hormone secretion. In addition to the major hypothalamic factors regulating POMC and PRL secretion, corticotropin-releasing hormone and dopamine, the neurohypophysial peptides arginine-vasopressin (AVP) and oxytocin (OT) may serve such a regulatory role in adenohypophysial hormone secretion. We investigated this hypothesis at two different levels by a series of experiments presented in this review. The experiments aimed at studying: 1) the possible role of HA as a neuroendocrine regulator of AVP and OT secretion and neuronal activation, and 2) the possible involvement of AVP and OT in physiological regulation of POMC derived peptide and PRL secretion. In the first part of the study we found HA to be an important regulator of vasopressinergic and oxytocinergic neuronal activity and of AVP and OT secretion. The effect of HA is mediated via activation of both HA H1- and H2-receptors. The regulatory role of HA on the neuronal AVP and OT system is of physiological relevance since it is important for the adequate AVP and OT response to physiological stimuli such as dehydration and suckling. In the second part of the study we found that secretion of POMC derived peptides and PRL in response to stress and HA is transmitted via AVP but not via OT. The effect of AVP in HA- and stress-induced POMC and PRL secretion is both mediating and permissive and the AVP-receptors involved differ with respect to these two actions as well as with type of adenohypophysial hormone secreted.
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PMID:Neurohypophysial peptides. Histaminergic regulation and function in adenohypophysial secretion. 896 Aug 13

Histamine is able to induce spontaneous-like headache attacks in migraine and cluster headache subjects. Therefore, it has been considered as a possible agent in the pathogenesis of headache. Histamine desensitization is used for the treatment of cluster and other chronic headaches like migrains with interparoxysmal headache. However, it is unknown whether desensitization plays a role in headache improvement. Since a disfunction of the opioid system has been considered responsible for idiopathic headache and since low beta-endorphin levels have been demonstrated in some idiopathic headaches, particularly in migraine with interparoxysmal headache, we planned this study to verify if histamine therapy is able to modify serum beta-endorphin concentrations. For this purpose, we studied 24 healthy control subjects and 36 patients suffering from migraine with interparoxysmal headache refractory to conventional therapies. Patients showed baseline serum beta-endorphin levels significantly lower than healthy control subjects and treatment with histamine for 15 days increased their beta-endorphin concentrations. We believe that histamine treatment can activate the opioid endogenous system. However, the therapeutic effect of histamine remains to be verified by evaluating the correlation between beta-endorphin levels and headache improvement.
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PMID:Serum beta-endorphin increase after intravenous histamine treatment of chronic daily headache. 927 Feb 92

Peripheral corticotropin-releasing hormone (CRH) is an important regulator of localized inflammatory responses. The aim of this study is to define the pathological signaling pathways in which peripheral CRH receptor-mediated responses reside. We report that PECAM-1-expressing synovial membrane endothelial cells are the principal source of CRH receptor subtype 1alpha in chronically inflamed synovial tissue (ST). Analysis of ST from an early arthritis patient cohort (n = 9) established that expression of CRH-R1alpha significantly (P < 0.03) colocalized with PECAM-1 and E-selectin expression in vivo. Freshly excised ST explants released a mediator(s) that acts to promote CRH-R1alpha mRNA to levels present in inflamed human synovium (n = 8). We tested the ability of conditioned medium and individual inflammatory mediators to modulate CRH-R1alpha expression. Histamine selectively induced the expression of CRH-R1alpha, and these effects were mediated through the histamine receptor type 1. Ectopic expression of CRH-R1alpha in normal human endothelial and synoviocyte cells resulted in the induction of the orphan receptor NR4A2 through the reconstitution of cAMP/protein kinase A/cAMP response element-binding protein signaling and identified a role for CRH in modulating nuclear factor kappaB transcriptional activity. CRH enhanced the expression of nitric-oxide synthase (NOS III) to promote NO production from CRH-R1alpha-expressing cells. These data establish a role for CRH receptor-mediated responses in regulating vascular changes associated with chronic synovitis.
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PMID:A role for type 1alpha corticotropin-releasing hormone receptors in mediating local changes in chronically inflamed tissue. 1732 94

Cell populations of Tetrahymena pyriformisGL were kept in nutrient-free (Losina) milieu and treated with different (10(-6)-10(-21)M) concentrations of serotonin, histamine or insulin for 30 min. Following that the hormone (serotonin and adrenocorticotropin (ACTH) content of the cells were measured by immunocytochemical flow cytometric method. Serotonin reduced histamine when applied in 10(-12) and 10(-15)M concentrations, while elevated ACTH levels when applied in 10(-6), 10(-9) and 10(-21)M concentrations. Histamine reduced serotonin concentration at 10(-9)-10(-21)M concentrations and increased ACTH in 10(-6)M. Insulin elevated both hormones' content in each concentration except at 10(-12)M. The results demonstrate that (1) in nutrient-free conditions the hormonal effects differ from that of nutrient-rich (tryptone+yeast) condition; (2) there is an optimal hormone concentration, which causes the strongest effect and this is different for each hormones; (3) the hormone receptors of Tetrahymena are very sensitive; as they react to zeptomolar concentrations. Such small concentration is even more effective than higher ones. Since hormones must become highly diluted in the natural environment of Tetrahymena, it seems that such low concentrations are the actual physiological concentrations.
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PMID:Effect of different concentrations of serotonin, histamine and insulin on the hormone (serotonin and ACTH) production of Tetrahymena in nutrient-free physiological milieu. 2174 Sep 2


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