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)

Phosphatidylcholine (PC) synthesis in cultured fetal rabbit lung cells was studied after exposure to various pituitary peptides. Because of reports of an association between lung maturation and prolactin, 2 different preparations of ovine prolactin were studied in concentrations ranging from 0.1 to 10.0 microgram/ml. Increased saturated phosphatidylcholine (SPC) synthesis without an increase in synthesis of total PC, and increased SPC/PC, was observed after exposure to Sigma prolactin. NIH prolactin in the same concentrations had no effect on synthesis of either PC or SPC. Adrenocorticotropic hormone, luteinizing hormone and thyroid stimulating hormone increased synthesis of both PC and SPC, but none increased the SPC/PC ratio. A cold ethanol extraction of Sigma prolactin yielded fractions with no demonstrable biologic activity, and other initial attempts to characterize the active factor in the Sigma prolactin samples were unsuccessful. We concluded that prolactin per se has no direct effect on PC or SPC synthesis in the lung, but that certain other pituitary peptides have a direct effect on lung synthesis of PC and SPC.
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PMID:Pituitary oligopeptide regulation of phosphatidylcholine synthesis by fetal rabbit lung cells: lack of effect with prolactin. 626 36

The effects of neuroadenolysis on plasma titres of beta-endorphin, beta-lipotropin, ACTH, TSH and prolactin have been investigated in five patients with metastatic cancer who responded to the treatment and have been in remission for more than four years and in five others who were undergoing the treatment for the first time for pain due to cancer metastases. beta-Endorphin, beta-lipotropin and ACTH titres were within the normal ranges of values in both categories of patients but post-neuroadenolysis titres of these peptides were higher than those before the treatment. The ability to secrete TSH and prolactin and to respond to thyroid stimulating hormone releasing hormone (TRH) remains intact following the treatment. However, whereas basal TSH titres and response to TRH was lower in the majority of patients, no such effect was observed on prolactin secretion. Plasma titres of prolactin and TSH were below the sensitivity of the method in the five patients who are in remission for more than four years. These preliminary findings suggest that neuroadenolysis probably affects some mechanism(s) associated with the control of beta-endorphin, beta-lipotropin and ACTH synthesis.
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PMID:Some aspects of pituitary function after neuroadenolysis in patients with metastatic cancer. 627 71

The avidin-biotin-peroxidase complex (ABC) method was applied to semithin (0.5-1 micron) plastic-embedded sections of intact male rat pituitaries with the use of techniques previously developed for the peroxidase-antiperoxidase complex (PAP) method. Stains for adrenocorticotropin (ACTH), thyroid stimulating hormone (TSH), luteinizing hormone (LH), and follicle stimulating hormone (FSH) were cleaner, more reliable, and more efficient. The ABC method allowed the use of the same high dilutions of primary antisera used with the PAP method. Incubation time was cut to a third of the time used for the PAP stain. Furthermore, if the incubation time matched that used with the PAP method, (24-48 hr), the antisera could be diluted 2- to 4-fold further. This enhanced specific staining and allowed the use of dilutions similar to those used in the radioimmunoassay. In agreement with Hsu and Raine (J Histochem Cytochem 29:1349, 1981), the ABC method produced staining after only a 1-4 hr incubation in primary antibody that was diluted optimally for the PAP complex method. The stain was weak, however, and cell counts showed that it was restricted to the fraction of the specific cell population which stored the most hormone. Our tests showed that the most convenient incubation times for optimal staining were 12-16 hr. Furthermore, the ABC method appeared to stabilize greatly the reaction for FSH and thus improved its precision and reliability.
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PMID:Application of the avidin-biotin-peroxidase complex (ABC) method to the light microscopic localization of pituitary hormones. 628 53

The Wulzen's cone of the bovine adenohypophysis presents a variable development and general arrangement. It is joined to the pars intermedia with no intervening connective tissue. It is covered by a single layer of cubical cell epithelium on the side of the hypophysial cleft. Immunofluorescence reveals the presence of different glandular cell types. The most abundant cells are those demonstrated by an anti-oPRL antibody and are either isolated or clustered. Other cells react with anti-hGH, anti-bLH, anti-beta aLH or anti-beta hTSH antibodies. Some cells react simultaneously with anti-beta MSH, anti-1-24ACTH, anti-17-39ACTH, anti-beta LPH and anti-beta endorphin antibodies. Cell types other than the numerous prolactin cells appear only as isolated elements. We did not observe cells reacting with anti-leu-enkephalin, anti-met-enkephalin or anti-calcitonin antibodies either in the Wulzen's cone or in the pars distalis or pars intermedia.
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PMID:Immunocytochemical study of Wulzen's cone of the bovine pituitary. 629 24

The case to be reported is that of a 72-year-old woman with isolated adrenocorticotropic hormone (ACTH) deficiency, who complained of anorexia and generalized malaise. The secretions of human growth hormone (HGH), prolactin (PRL), luteinizing hormone (LH), follicle stimulating hormone (FSH), and thyroid stimulating hormone (TSH) were all within normal limit. In spite of the extremely low level of cortisol, the plasma level of ACTH would not rise sufficiently, but a marked response of cortisol to ACTH stimulation was recognized. The postmortem examination revealed a decrease in basophilic or PAS-positive cells of the anterior pituitary gland which also showed a selective loss of ACTH-secreting cells over immunohistochemical study. Electron microscope could easily visualize somatotroph, mammotroph, thyrotroph, FSH- and LH-gonadtroph, but corticotroph was difficult to be discerned. Adrenocortical cells demonstrated atrophy and degeneration, for which the zona fasciculata and zona reticularis were narrowed. The zona glomerulosa was slightly enlarged in width.
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PMID:Isolated adrenocorticotropic hormone (ACTH) deficiency. 629 33

The chemical tools that could be used to examine the function of histamine in the brain are considered together with the evidence linking histamine specifically with the hypothalamus. The distribution of histamine and the enzymes responsible for its synthesis and metabolism is consistent with there being both mast cells and histaminergic nerve terminals within the hypothalamus. Iontophoresis, mepyramine binding and histamine-stimulated adenylate cyclase studies suggest that both histamine H1- and H2- receptors are present in the hypothalamus. In addition, intracerebroventricularly injected histamine receptor agonists and antagonists affect many functions associated with the hypothalamus such as cardiovascular control, food intake, body temperature control, and pituitary hormones whose release is mediated via the hypothalamus, such as corticotropin, growth hormone, thyroid stimulating hormone, prolactin, gonadotropins and vasopressin. However, only in the case of thyroliberin release, prolactin release, body fluid control and blood pressure control is there evidence yet that such effects are mediated via histamine receptors actually in the hypothalamus. The effects of enzyme inhibitors suggest endogenous histamine may be involved in the physiological control of thyroid stimulating hormone, growth hormone and blood pressure, and the effects of receptor antagonists support a role for endogenous histamine in prolactin control. Otherwise, there is little evidence for a physiological role for endogenous, as against exogenous, histamine whether it be from histaminergic terminals or mast cells. In addition, few studies have tried to distinguish possible effects on presynaptic receptors, postsynaptic receptors, hypothalamic blood vessels or the hypophyseal portal blood vessels. It is concluded that although there is good evidence now linking histamine and the hypothalamus more specific studies are required, for instance using microinjection or in vitro techniques and the more specific chemical tools now available, to enable a clearer understanding of the physiological role of histamine in the hypothalamus.
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PMID:Histamine and the hypothalamus. 631 74

The effects of a sustained-release implant for naloxone (NAL) on serum concentrations of prolactin (PRL), immunoreactive beta-endorphin (IR-beta-ENDO), growth hormone (GH) and thyroid stimulating hormone (TSH) were evaluated in ovariectomized female rats. After 9 days of exposure to NAL, serum levels of none of these 4 pituitary hormones were altered. However, the NAL implant antagonized the stimulatory effects of morphine (15 and 30 mg/kg body weight) on PRL and IR-beta-ENDO secretion, enhanced the stimulatory effects of morphine on GH secretion, and had no effect on morphine-induced suppression of TSH secretion. These results indicate that while chronic NAL exposure does not, by itself, persistently alter pituitary hormone secretion, it differentially effects the response of these hormones to morphine exposure. These data suggest that chronic treatment with narcotic antagonists may invoke differential compensatory mechanisms to maintain normal hormone secretion.
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PMID:The effects of chronic naloxone on pituitary hormone secretion in female rats. 632 81

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

Four hundred and thirty-four pituitary glands from an unselected autopsy series were examined to investigate the incidence and immunohistochemical nature of occult pituitary microadenomas. Fourteen tumors (3.2%) were identified. The ages of the affected patients varied from 11 to 86 yrs, with no age predominance. Males and females were similarly affected. Nine of the microadenomas were available for immunoperoxidase staining. Adrenocorticotropic hormone, follicle stimulating hormone, growth hormone, luteinizing hormone, prolactin and thyroid stimulating hormone were examined. Four of the adenomas were reactive for prolactin; one was reactive for growth hormone, with scattered positivity for adrenocorticotropic hormone, follicle stimulating hormone, luteinizing hormone and thyroid stimulating hormone; 4 were nonreactive.
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PMID:Microadenomas of the human pituitary. 760 61

A variety of neuroendocrine disturbances are observed following treatment with external radiation therapy when the hypothalamic-pituitary axis (HPA) is included in the treatment field. Radiation-induced abnormalities are generally dose dependent and may develop many years after irradiation. Growth hormone deficiency and premature sexual development can occur following doses as low as 18 Gy fractionated radiation and are the most common neuroendocrine problems noted in children. Deficiency of gonadotropins, thyroid stimulating hormone, and adrenocorticotropin are seen primarily in individuals treated with > 40 Gy HPA irradiation. Hyperprolactinemia can be seen following high-dose radiotherapy (> 40 Gy), especially among young women. Most neuroendocrine disturbances that develop as a result of HPA irradiation are treatable; patients at risk require long-term endocrine follow-up.
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PMID:Chronic neuroendocrinological sequelae of radiation therapy. 771 77


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