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)

Stressors generally induce a depression of the hypothalamus-pituitary-testis (HPT) system, mediated by the activated hypothalamus-pituitary-adrenocortical (HPA) system, resulting in a fall in plasma luteinising hormone (LH) and testosterone levels. Hypothalamic gonadotrophin-releasing hormone (GnRH) secretion may be suppressed by endogenous opioid peptides (EOP) and/or corticosteroids. The latter dramatically enhance the negative feedback effects of testosterone on both the hypothalamus and pituitary. Pituitary gonadotrophin secretion may be reduced by adrenocorticotrophic hormone or by EOP of hypothalamic or pituitary origin. Decreases in plasma concentrations of testosterone, independent of gonadotrophins, can be induced by corticosteroids. These hormones might reduce the number of Leydig-cell LH-receptors or occupation of LH-receptors. Testicular steroidogenesis may also be inhibited by pro-opiomelanocortin-derived (opioid) peptides secreted by the Leydig cells. There are some indications of increases in LH and testosterone during acute stress and, in dominant male animals, during the stress of social conflict. The latter finding indicates a difference in stress response between dominant and subordinate males. In subordinate males, decreased feedback sensitivity may allow hypersecretion throughout the HPA system. As a result, corticotrophin releasing hormone may induce the release of EOP from the hypothalamus, which inhibit the HPT axis. This inhibition may be enhanced by a corticosteroid-induced decrease in testosterone feedback.
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PMID:Stress and the endocrine hypothalamus-pituitary-testis system: a review. 188 89

1. Corticotropin-stimulated lipolysis in adipocytes of rats, mice, hamsters, guinea pigs and rabbits. Melanotropins elicited high lipolytic activity only in guinea pig and rabbit adipocytes. Opiate peptides were active only in rabbit adipocytes. Pituitary and chorionic gonadotropins and somatotropin were lipolytic in guinea pig adipocytes. Other hormones tested including prolactin, somatostatin, substance P, neurotensin, angiotensin II, thyrotropin releasing hormone and pancreatic polypeptide were devoid of lipolytic activity in all of the adipocytes studied. 2. In the rabbit adipocytes gamma-melanotropin was lipolytic only at high doses. At these doses the peptide inhibited the lipolytic response to a high dose of corticotropin. 3. Lipolysis stimulated by vasoactive intestinal peptide and epinephrine in rat adipocytes was antagonized by insulin. The lipolytic hormones corticotropin, epinephrine, vasoactive intestinal peptide and secretin suppressed basal and insulin-stimulated lipogenesis.
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PMID:Studies on hormonal regulation of lipolysis and lipogenesis in fat cells of various mammalian species. 196 44

Neuropeptides that have relatively narrow actions on mammalian pituitary secretion may have divergent effects on pituitary hormone secretion in ectothermal vertebrates. In turtles, secretion of both thyrotropin (TSH) and growth hormone (GH) can be stimulated in vitro by thyrotropin-releasing hormone (TRH) and by members of corticotropin-releasing hormone (CRH) and growth hormone-releasing hormone (GHRH) peptide families. To determine if these neuropeptides share common modes of action, and to study other potential regulators of the turtle pituitary, somatostatin-14 (SRIH) and monoamines were tested for direct effects on in vitro basal and neuropeptide-stimulated TSH and GH secretion. Pituitary glands from young turtles (Pseudemys scripta) were cultured in the presence of 25 nM TRH, ovine CRH, or rat GHRH with or without SRIH. Glands were incubated for several 2-hr periods in medium alone or in medium containing peptides. Preincubation for 4 hr with SRIH (6 or 60 nM) significantly reduced basal and TRH-stimulated TSH and GH output (SRIH present during entire incubation). In another experiment, basal hormone secretion was reduced when SRIH (60 nM) was present only during the 2-hr basal period; however, reduction of TSH and GH responses to TRH required the presence of SRIH (60 nM) during the basal period and the period of stimulation. TSH responses to 25 nM oCRH and rGHRH and GH responses to rGHRH were significantly reduced by preincubation with 60 nM SRIH. The biogenic amines, dopamine (DA), serotonin (5HT), and norepinephrine (NE) (50 or 500 nM) were tested for possible direct actions on basal and neuropeptide-stimulated pituitary TSH and GH secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation of neuropeptide-stimulated pituitary hormone secretion in hatchling turtles. 196 41

The effects of chronic haloperidol treatment on pro-opiomelanocortin (POMC) synthesis, processing, and release in the anterior (AL) and intermediate (IL) lobes of the rat pituitary were studied. In the IL, 14 days of haloperidol administration promoted an increase in the level of POMC mRNA, and a corresponding elevation of levels of beta-endorphin (beta E), alpha-melanocyte-stimulating hormone (MSH), and gamma 3 MSH. In the AL, a reduction of POMC mRNA as well as immunoreactive beta E, adrenocorticotropin (ACTH), and gamma 3 MSH was observed. Column chromatography revealed that this treatment promoted an apparent alteration of POMC processing in AL: the conversion of larger, precursor-sized peptides to smaller, more-processed forms was relatively inhibited. Circulating levels of both N-acetyl-beta E and corticosterone were elevated following haloperidol challenge in drug-naive animals. Resting plasma levels of both, however, were not changed following chronic haloperidol treatment. Pituitary culture studies demonstrated that chronic haloperidol treatment increased the releasability of IL-derived products, while simultaneously decreasing the releasability of those products from the AL. These results suggest that pituitary POMC biosynthesis, processing and release are under at least partial dopaminergic control in both the IL and the AL of the pituitary, but by different mechanisms; chronic haloperidol treatment upregulates the POMC system in IL, but downregulates it in AL, despite similarities of the responses of both lobes to acute haloperidol challenge.
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PMID:Differential effects of haloperidol on the rat pituitary: decreased biosynthesis, processing and release of anterior lobe pro-opiomelanocortin. 210 73

Activation of serotonergic neurotransmission has been shown to increase plasma beta-endorphin-like immunoreactivity (beta-End-LI). To study the mechanism(s) of this action, we measured the effects of 3 potent serotonin (5-HT) agonists with different structures and 5-HT receptor binding profiles in conscious unrestrained Sprague-Dawley rats in vivo and in dispersed anterior pituicytes in vitro. The 5-HT1A agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), the 5-HT1C agonist, m-chlorophenylpiperazine (m-CPP), and the 5-HT2 agonist, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI), all markedly increased beta-End-LI in plasma in vivo. All 3 responses were blocked by dexamethasone pretreatment. Pituitary stalk transection (PST), as well as pretreatment with rabbit serum hyperimmune against rat corticotropin-releasing hormone (CRH, TS-6) completely abolished beta-End-LI response to 8-OH-DPAT and attenuated the responses by about 60% to DOI. Responses to m-CPP were markedly attenuated in PST rats, but pretreatment with TS-6 had no significant effect. To examine whether vasopressin (AVP) might be involved in the CRH neutralizing antibody-resistant beta-End-LI responses after m-CPP and DOI, we measured AVP concentrations after each agonist, m-CPP, but not DOI or 8-OH-DPAT, significantly elevated circulating AVP levels. As a proof of direct pituitary effect, DOI markedly stimulated beta-End-LI release from the anterior pituitary cell culture preparation in vitro. It was approximately as potent as CRH in the picomolar range, m-CPP was much less effective than DOI, while 8-OH-DPAT did not stimulate beta-End-LI release in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beta-endorphin responses to different serotonin agonists: involvement of corticotropin-releasing hormone, vasopressin and direct pituitary action. 215 Jul 76

Corticotropin-releasing hormone (CRH) has been found in both hypothalamic and extrahypothalamic sites of the brain and also in the adrenal medulla. To study the timing and location of delayed glucocorticoid action in rats, we measured the effects of 2-day and 7-day cortisol treatment on immunoreactive CRH concentrations in hypothalamus, cerebral cortex, hippocampus, cerebellum, and adrenal gland. The activity of the hypothalamo-pituitary-adrenal (HPA) axis and the sympathoadrenal system were also measured. Studies were carried out both in the afternoon and/or in the morning, to get information about possible circadian changes. CRH contents were not changed in any brain areas studied, except there was a trend of decrease in the hypothalamus compared to vehicle in the afternoon due to the lack of circadian increase after 7-day cortisol treatment. Pituitary ACTH content decreased significantly after 7-day treatment, while beta-endorphin did not. Plasma levels of ACTH, corticosterone, norepinephrine and epinephrine and adrenal ACTH and beta-endorphin contents decreased after 2-day, adrenal CRH content after 7-day treatment with cortisol. Our findings suggest, that chronic cortisol treatment inhibits the circadian activation of the HPA axis at all levels but has variable effects on baseline measures because it causes different changes in release and synthesis at different sites.
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PMID:Effects of cortisol treatment on brain and adrenal corticotropin-releasing hormone (CRH) content and other parameters regulated by CRH. 217 9

Pituitary adenomas from 15 patients with Cushing's disease were studied histopathologically. The tumors were examined for the presence of neural axons by the Bodian silver impregnation technique and a specific immunohistologic technique based on a monoclonal antibody to axonal neurofilaments. Axons were not seen in any of the surgical specimens. This finding suggests that most, if not all, adrenocorticotropin-secreting pituitary adenomas are of anterior lobe origin.
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PMID:Pituitary adenomas in Cushing's disease: do they arise from the intermediate lobe? 245 24

In response to stressors involving tissue injury, pituitary corticotroph secretion of immunoreactive beta-endorphin (iB-END) could be either due to release of hypothalamic factors such as corticotropin-releasing factor (CRF) or to release of a tissue factor from the periphery. In the present experiments, we investigated whether inflamed tissue releases a factor which evokes pituitary secretion of iB-END. In an initial experiment, rats with an inflamed hindpaw due to carrageenan injection had significantly greater levels of circulating iB-END as compared to rats with saline-injected paws. Removal of afferent input, by hindlimb denervation, failed to block the carrageenan-induced increase in iB-END levels. Subcutaneous perfusates were then collected from inflamed and control hindlimbs and applied to rat anterior pituitary cell cultures. Pituitary release of iB-END due to administration of perfusate from inflamed paws was significantly greater than iB-END release due to perfusate from saline-injected paws or to basal release. The releasing activity in the perfusates was blocked in calcium-free medium and was not due to a direct action of carrageenan, bradykinin, substance P or calcitonin gene-related peptide. The results indicate that inflamed tissue releases a CRF-like factor which stimulates iB-END release both in the denervated rat and cultured pituitary cells.
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PMID:Release from inflamed tissue of a substance with properties similar to corticotropin-releasing factor. 252 75

It is well-known that prenatal chronic intermittent stress affects the reproductive system of both sexes. Investigating the effects of an acute maternal stress on the fetal neuroendocrine system, parameters such as hypothalamic catecholamines. CRF, GRF, LH-RH, beta-endorphin, hypophysial beta-endorphin and beta-LPH as well as plasma LH, corticosterone and androstenedione were measured. Pregnant rats of Wistar strain were exposed to restraint stress at day 22 of gestation or to forced immobilization at day 20 of gestation, respectively, and were sacrificed before stress and 10, 30, 60, and 120 min after starting stress. A decrease of fetal hypothalamic catecholamines and an increase of LH-RH content of the hypothalamus as well as of plasma catecholamines were observed under stress on day 22 of gestation. On day 20 of gestation hypothalamic beta-endorphin was depleted in male and unchanged in female fetuses under stress. A depletion of hypothalamic CRF was observed in male fetuses, whereas female fetuses showed an increase of hypothalamic CRF. An increase of GRF was found in fetuses of both sexes. Pituitary opioid content increased in fetuses of both sexes initially, but was depleted secondarily in male fetuses. The LH plasma level was markedly reduced in male, the corticosterone level was elevated in fetuses of both sexes as well as the androstenedione level in female fetuses. A simultaneous treatment of mother animals with tyrosine--a catecholamine precursor--prevented the depletion of hypothalamic and pituitary beta-endorphin as well as in part the reduction of plasma LH levels in male fetuses. Hypothalamic GRF content does not increase under tyrosine treatment in male fetuses, whereas in female fetuses the stress-induced increase of GRF content was rather pronounced under tyrosine than attenuated. These results indicate that fetal hypothalamic neurotransmitters and neurohormones (such as LH-RH, CRF, GRF and opioids) are involved in changing circulating hypophysial and adrenal hormones in fetuses exposed to maternal stress in late pregnancy, whereby sex-specific different pathways might be effective in fetal stress processing. The prenatal administration of tyrosine prevented at least in part--those neurohormonal changes which are affecting the sex-specific brain differentiation.
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PMID:Sex-specific effects on the fetal neuroendocrine system during acute stress in late pregnancy of rat and the influence of a simultaneous treatment by tyrosine. 253 47

Progesterone is a potent hormone acting on the female reproductive tract and influencing a series of other functions. Recent studies revealed a correlation between progesterone and brain neurotransmitters and neuropeptides. Our study evaluated the possible effect of norgestimate, a new progestin, on hypothalamic and pituitary beta-endorphin (B-EP) concentration in castrated female rats. Ovariectomy was performed under ethyl ether anesthesia. Treatment was started 3 weeks after surgery. Norgestimate, estradiol benzoate or norgestimate plus estradiol benzoate were administered. The two steroids were dissolved in sesame oil and injected (s.c.) every day for 2 weeks. Pituitary and hypothalamus B-EP concentrations were measured by radioimmunoassay. Our studies showed that norgestimate increases the pituitary and hypothalamic B-EP concentration in female rats, reaching values higher than controls and estrogen-treated rats. Because B-EP has an important role in reproductive function, both modulating gonadotropin secretion and sexual behavior, the present results lead to the hypothesis that norgestimate affecting B-EP concentrations may influence central functions.
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PMID:Norgestimate increases pituitary and hypothalamic concentrations of immunoreactive beta-endorphin. 253 55


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