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)

Hyperprolactinemia can reduce the LH secretion in rats, but the mechanism of the effect of PRL is not clear. We have investigated the actions of PRL on the secretion of LHRH and LH and the interaction among PRL, beta-endorphin (beta-EP), and LHRH. The effects of PRL on LHRH and LH secretion were studied in ovariectomized female rats after transplanting four anterior pituitaries to the right kidney capsule of each ovariectomized rat for 2-3 weeks. The level of PRL in rats with pituitary transplants was approximately 5 times higher than that in control rats. The concentration of LHRH in pituitary portal plasma of hyperprolactinemic rats was approximately 4 times lower than that in control rats. Hyperprolactinemic animals also showed lower plasma LH levels than the controls. Since beta-EP inhibits the secretion of LHRH, we have tested whether the reduced secretion of LHRH in hyperprolactinemic ovariectomized rats is associated with an increase in beta-EP activity. This was studied by measuring the concentration of beta-EP in pituitary portal plasma and the response of LHRH and LH to the opiate antagonist naloxone. The level of beta-EP-like immunoreactivity in pituitary portal plasma was significantly higher in hyperprolactinemic rats than in control animals. Naloxone (10 mg/kg, sc) increased both LHRH and LH concentrations in hyperprolactinemic rats, but not in control rats. The present results demonstrate that hyperprolactinemia can reduce LHRH release and suggest a possible involvement of beta-EP in the PRL inhibitory action on LHRH.
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PMID:Hyperprolactinemia decreases the luteinizing hormone-releasing hormone concentration in pituitary portal plasma: a possible role for beta-endorphin as a mediator. 315 64

The authors determined in 1984 by radioimmunoassay (INEP kit) the serum prolactin concentration in 76 multiple sclerosis patients (33 males and 34 females) aged from 21 to 53 years, with disease duration from 2 to 30 years. The control group comprised 110 healthy subjects. Normal prolactin values were 150-750 mIU/ml in females and 150-500 mIU/ml in males. In about one-third of the patients raised prolactin level was found which failed to correlate with the age of the patients and with increased beta-endorphin level in them. The authors suppose that hyperprolactinaemia may be of importance in certain clinical signs of multiple sclerosis. Further investigations on prolactin are conducted with reference to the circadian rhythm of prolactin secretion and dynamic tests.
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PMID:[Prolactin in the blood serum of patients with multiple sclerosis]. 367 May 26

Hypophysectomized male rats, tested 7 days after removal of the pituitary, showed a reduced sensitivity to small doses of apomorphine. In these rats, subcutaneous (s.c.) treatment with apomorphine (25, 100 or 250 micrograms/kg) did not elicit any reduction in locomotor activity measured 5 min after injection in contrast to that observed in sham-operated control rats. The enhancement of locomotor activity and stereotyped behavior, 20 min after the s.c. administration of apomorphine, was similar in hypophysectomized rats and in control animals. Prolactin does not seem to be implicated in this altered sensitivity, since hyperprolactinaemia induced by pituitary homografts under the kidney capsule did not change the response to apomorphine in hypophysectomized rats. Chronic treatment with desenkephalin-gamma-endorphin (DE gamma E), a beta-endorphin fragment with neuroleptic-like properties, administered s.c. twice a day for 7 days at the dose of 10 micrograms/rat, restored the sensitivity to small doses of apomorphine in the hypophysectomized rats. The data suggest that removal of the pituitary leads to impaired sensitivity of presumably presynaptically located dopamine receptors mediating the effects of small doses of apomorphine without altering the sensitivity of postsynaptically located dopamine receptors that mediate the hypermotility and stereotypy induced by apomorphine. This impaired sensitivity to low doses of apomorphine could be restored by DE gamma E but not by prolactin, supporting the conclusions from previous experiments that DE gamma E and prolactin may selectively interfere with pre- and postsynaptic dopamine receptors respectively.
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PMID:Desenkephalin-gamma-endorphin restores the impaired sensitivity of hypophysectomized rats to small doses of apomorphine. 379 42

Studies were undertaken to evaluate the effects of chronic hyperprolactinemia (HYP) induced by the MtTW15 tumor on the thermoregulatory response of female rats to blockade of opiate receptors with naloxone. Both chronic administration of morphine and HYP cause a mild hyperthermia as evidenced by a 0.8-1.0 degrees C elevation in rectal temperature (Tr). Naloxone-precipitated morphine withdrawal caused a prompt increase (4.9 +/- 0.76 degrees C) in tail skin temperature (TST) and a subsequent decline in Tr (-2.8 degrees C). Similarly, naloxone administration to HYP rats caused a dramatic TST response which was coincident with the onset of severe HYP. This effect of naloxone was maximal at 7 weeks of tumor growth when a TST response of 4.8 +/- 0.3 degrees C was observed but was not evident prior to or 1 week following tumor inoculation, when serum prolactin levels were low. The TST response to naloxone in chronic HYP exhibited distinct pulses with an amplitude of 3.4 +/- 0.4 degrees C and a frequency of 2.2 +/- 0.5 pulses per 120 min. It appears that blockade of opiate receptors in HYP rats induces instability in the regulation of skin temperature as evident by recurrent episodes of TST surges. These effects of chronic HYP on the TST response to naloxone were not influenced by ovariectomy, suggesting that changes in ovarian secretions were not involved in the response. At 4 weeks of tumor growth, immunoreactive beta-endorphin concentrations in the medial basal hypothalamus, preoptic area-anterior hypothalamus and the neurointermediate lobe of the pituitary were decreased by 59, 28 and 47%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence that chronic hyperprolactinemia effects skin temperature regulation through an opioid mechanism. 609 86

The role of prolactin (PRL) in the control of the lordosis reflex of female rats was investigated. In the initial series of experiments, the normal high level of sexual receptivity observed in the ovariectomized, estrogen-progesterone (E-P) primed female rat was suppressed by intraventricular infusion of 100 ng PRL. Mating behavior remained suppressed 2, 3, and 5 hours following a single infusion of PRL into the third ventricle. In contrast, infusions of either an equal volume of the solvent vehicle (saline) or 100 ng of adrenocorticotropic hormone (ACTH) were ineffective in modulating the level of mating behavior in hormone-primed female rats. In a second series of experiments, chronic hyperprolactinemia was induced by pituitary transplants under the renal capsule in intact, normal cycle diestrus rats (N=12). A significant decrement in E-P induced mating behavior was observed at 12 and 14 weeks posttransplantation but not at 4 weeks. Sham-operated animals (N=12) displayed the characteristic pattern of behavior normally observed under exogenous E-P therapy. In summary, transient exposure as well as chronic exposure to high levels of PRL can suppress mating behavior, thus suggesting a possible role for PRL in the mediation of reproductive behavior in the female rat.
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PMID:Inhibition of lordosis behavior in the female rat by intraventricular infusion of prolactin and by chronic hyperprolactinemia. 627 47

A pituitary tumor from a patient with severe Cushing's disease and marked hyperprolactinemia was extensively studied by immunohistochemical techniques. Tissues from two separate areas of the adenoma were found to contain similar cell proportions of PRL as well as ACTH and related peptides (beta-lipotropin, beta-endorphin, and alpha MSH). The tumor was composed of approximately 70% immunoreactive PRL cells and 5% ACTH-containing cells. Double immunostaining revealed that PRL or ACTH and related peptides were found in two distinct populations of tumor cells. These results document for the first time inappropriate synthesis and secretion of an unusual combination of pituitary hormones from a mixed pituitary adenoma.
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PMID:Concurrent production of adrenocorticotropin and prolactin from two distinct cell lines in a single pituitary adenoma: a detailed immunohistochemical analysis. 628 57

A beta-endorphin (beta END)-containing pituitary adenoma was demonstrated by immunocytochemical, biochemical, and ultrastructural methods in a 43-yr-old man who had impotence, slight testicular atrophy, and an enlarged sella turcica (grade II0), but no manifestations of Cushing's disease. Preoperative hormone data revealed hyperprolactinemia (97 ng/ml), low plasma cortisol levels without circadian rhythm, undetectable plasma ACTH, and normal plasma FSH and LH levels, with an impaired response to LRH. After hypophysectomy, these hormone levels normalized and responded normally to dynamic tests. Immunocytochemically, 30% of the tumor cells reacted only with beta END antiserum. beta END immunoreactivity was the only component revealed by RIA and sodium dodecyl sulfate-polyacrylamide gel electrophoresis. A characteristic ultrastructural aspect is also described. These findings demonstrate dissociation in the secretion of the proopiomelanocortin-derived peptides and suggest a relationship between hyperprolactinemia and tumor secretion of beta END.
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PMID:A human beta-endorphin pituitary adenoma. 631 45

Implantation of the PRL, ACTH, beta-endorphin (beta-EP), and beta-lipotropin (beta-LPH)-secreting transplantable rat pituitary tumor 7315a resulted in a suppression of the PRL and the ACTH content of the anterior pituitary gland and also of the beta-EP/beta-LPH content of the neurointermediate (NI) lobe. Treatment with bromocriptine further diminished the anterior lobe PRL content, whereas haloperidol partially inhibited this tumor-mediated diminution. The administration of these drugs did not influence the suppressed ACTH content of the anterior pituitary lobe. The diminished beta-EP/beta-LPH content of the NI lobe of tumor-bearing rats became completely normal after treatment with haloperidol, whereas bromocriptine administration further diminished the NI lobe beta-EP/beta-LPH content. There was a close correlation between the anterior pituitary lobe PRL content and the beta-EP/beta-LPH content of the NI lobe in all four groups of rats taken together (including nontumor-bearing controls, control tumor rats, and tumor rats treated with bromocriptine or haloperidol; P less than 0.01). Implantation of the pure PRL-secreting pituitary tumor 7315b resulted in hyperprolactinemia and a suppression of the PRL content of the anterior lobe and the beta-EP/beta-LPH content of the NI lobe, without affecting the ACTH content of the anterior pituitary lobe. There was a negative correlation between the level of the circulating PRL concentration and the beta-EP/beta-LPH content of the NI lobe. These results suggest a possible relationship between the synthesis of PRL by the anterior pituitary lactotroph and of the hormones of the NI lobe. The level of the circulating PRL concentration may play, directly or indirectly, a role in the regulation of both systems.
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PMID:Hyperprolactinemia exerts a negative effect on the beta-endorphin content of the rat neurointermediate pituitary lobe. 632 44

A 37-year-old woman presented with acute psychosis and cognitive impairment. Skull x-ray showed an enlarged sella turcica with erosion of the floor. Endocrinologic workup suggested the diagnosis of Cushing's disease and hyperprolactinemia. She had no cushingoid feature, and the only physical sign was mild generalized obesity. She showed a paradoxic response to dexamethasone suppression, and underwent trans-sphenoidal resection of a pituitary macroadenoma. Electron microscopy showed the tumor to be a Crooke's cell adenoma. Results of immunohistochemical staining were positive only for ACTH and beta-endorphin. The neuropsychiatric manifestations resolved after surgery.
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PMID:Occult Cushing's disease presenting with acute psychosis. 671 82

A case report is presented of the need for both bromocriptine and human menopausal gonadotropin (hMG) for induction of ovulation in a patient who developed partial hypopituitarism and persistent hyperprolactinemia even after a transsphenoidal pituitary microadenectomy. The patient, a 27-year old white female, initially presented in 1979 with a history of amenorrhea and galactorrhea after discontinuing oral contraceptives (OCs). Her menstrual cycles had been regular since her menarch at age 13 until she began taking OCs at age 20. Preoperative endocrine evaluation in 1979 revealed serum luteinizing hormone (LH), 9.1 mIU/ml; serum follicle stimulating hormore (FSH), 6.4 mIU/ml; serum thyroid stimulating hormone (TSH), 3.8 mIU/ml; serum prolactine (PRL), 300 ng/ml; serum thyroxine (T4), 6.4 mcg/dl; and an attenuated PRL response to thyrotropin releasing hormone (TRH). Radiographic studies revealed a pituitary tumor of approximately 1 cm in diameter. In July 1979 a transsphenoidal hypophysectomy was performed. Pathologic examination revealed a pituitary adenoma with a monomorphic basophilic cell population with fibrosis and chronic inflammation. The patient required prednisone therapy postoperatively for 3 months secondary to compromised adrenal status. Prednisone therapy was discontinued in October 1979 after a normal cortisol (F) response to induced hypoglycemia was documented. The patient's serum PRL levels remained elevated at 111 ng/ml in August 1979 and 269 ng/ml in October 1979. Her amenorrhea and galactorrhea persisted. Bromocriptine therapy, 2.5 mg 3 times daily, was instituted in October 1979. She became normoprolactinemic, with a serum PRL of 6 ng/ml, and the galactorrhea disappeared but the amenorrhea persisted. In February 1981 she was referred for further consultation on her fertility status. Bromocriptine therapy was discontinued. In April 1981 she underwent a thorough endocrine evaluation. The results indicate that GnRH stimulation was unable to elicit a pituitary gonadotropin response anywhere near normal levels of FSH and LH, thus suggesting pituitary hypogonadotropism. Growth hormone release was subnormal in response to the insulin induced hypoglycemia and L-dopa ingestion. Hyperprolactinemia was obvious but the patient's serum TSH, T4, and adrenocorticotropin (ACTH) levels were normal. A diagnosis of hyperprolactinemia with partial hypopituitarism and gonadotropin deficiency was made. Bromocriptine therapy was reinstituted at 2.5 mg twice daily in June 1981, with good results. In November 1981 her serum PRL was normal, and as she was desirous of pregnancy, ovulation induction with bromocriptine and Pergonal was carried out. The patient is now 6 months pregnant and doing well. This case illustrates the poor functional results for surgery for pituitary microplactinomas.
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PMID:Partial hypopituitarism and hyperprolactinemia: successful induction of ovulation with bromocriptine and human menopausal gonadotropins. 681 37


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