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)

A single intravenous injection of four hypothalamic releasing hormones-corticotropin-, growth hormone-, gonadotropin- and thyrotropin-releasing hormones-was administered to normal subjects. Except for the plasma adrenocorticotropic hormone (ACTH) level, a statistically significant increase in all anterior pituitary hormone levels occurred. Transient flushing was the only consistent side effect. In the same persons, results were compared with those obtained with insulin-induced hypoglycemia and a single-dose overnight metyrapone test. Growth hormone and cortisol responses to insulin-induced hypoglycemia were similar but prolactin increment was less than that obtained by the peptide injection. ACTH increments from both tests were substantially less than those obtained by the overnight metyrapone test. We conclude that pituitary function can be effectively studied in normal subjects by the combination of a metyrapone test with a triple bolus of growth hormone-, thytropin- and gonadotropin-releasing hormones, but not by a quadruple bolus of the hypothalamic peptides. Compared with insulin-induced hypoglycemia, this approach yields more information with fewer side effects.
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PMID:Quadruple injection of hypothalamic peptides to evaluate pituitary function in normal subjects. 391 7

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

Studies have been made on the hypophysectomy-induced changes in antinociceptive and temperature responses to morphine and the effects various anterior pituitary hormones have on these altered responses under both acute and chronic conditions. Hypophysectomy altered the slope of the dose-response curve for morphine antinociception without significantly changing the ED50. It also induced an upward shift in the temperature-response curve. Treatment of hypophysectomized animals with s.c. adrenocorticotropic hormone decreased responsiveness to the antinociceptive and the hyperthermic actions of morphine. Administration of triiodothyronine increased the antinociceptive response and normalized the upward shift in the temperature response; however, these effects required approximately 3 weeks of hormone treatment. Both of these treatments normalized the altered antinociceptive dose-response curve slope. Growth hormone, luteinizing hormone and prolactin had no effects on acute morphine responses. Further experiments examined the effects of anterior pituitary hormones during chronic treatment with morphine. Adrenocorticotropic hormone, when administered 30 min before morphine, showed reproducible but statistically nonsignificant suppression of tolerance development. Growth hormone, which had no effects on acute morphine responses, was more effective than adrenocorticotropic hormone at suppressing tolerance. In studies with animals bearing growth hormone/prolactin secreting tumors, significant suppression of tolerance was seen for both responses to morphine. These results add further support to previous findings from our laboratory that the adrenal and thyroid systems are involved in modulation of acute opiate actions and also indicate that growth hormone can inhibit the development of opiate tolerance.
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PMID:Endocrine influences on the actions of morphine. II. Responses to pituitary hormones. 682 55

Growth hormone (GH) and beta-endorphin (beta-EP) responses to clonidine stimulation were examined in 18 male heroin addicts, 9 with and 9 without previous histories of attention deficit disorder with hyperactivity (ADD-H) and conduct disorder (CD). Ten psychophysically healthy volunteers were used as controls. ADD-H/CD addicts had blunted GH and beta-EP responses as compared to controls while those of non-ADD-H/CD addicts were normal. This suggests that postsynaptic adrenoceptor sensitivity is decreased and, possibly, that presynaptic noradrenaline secretion is increased in ADD-H/CD patients with heroin addiction.
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PMID:Alpha-2-adrenoceptor sensitivity in heroin addicts with and without previous attention deficit disorder/hyperactivity and conduct disorder. 796 53

Previous studies have failed to demonstrate a block of the endocrine response to upper abdominal surgery by thoracic epidural analgesia. To clarify the bases for this failure, we compared the effects of epidural analgesia of different dermatome levels up to C8-T2 or C3-4. The patients who received general anesthesia alone showed significant increases of adrenocorticotropic hormone (ACTH) and arginine vasopressin (AVP) immediately after skin incision. The patients with C8-T2 blocked developed significant increases in these hormones, not after the skin incision, but after the intraabdominal procedure. Of the eight patients with C3-4 block, six developed no such responses throughout the study period. The responses of oxytocin (OXT) and prolactin (PRL) were more susceptible to epidural analgesia and were blocked at the C8-T2 level. Growth hormone (GH) showed no correlation with surgical procedures and epidural block. These findings indicate that the nociceptive neural information during upper abdominal surgery is conveyed by the sensory fibers included in both the thoracic and lumbar spinal nerves that innervate the abdominal wall and the intraabdominal viscera, and by the phrenic nerves that innervate the diaphragm. The rationale for postulating the involvement of the phrenic nerves can be referred to the embryonal descent of the diaphragm from the C3-5 myotomes that serves as the upper wall of the abdominal cavity.
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PMID:The role of the phrenic nerves in stress response in upper abdominal surgery. 863 94

The first gamma knife (GK) treatment of a pituitary adenoma in 1967 was meant as an alternative to the primitive surgical approaches that prevailed at the time, with consequent unsatisfactory results. Surprisingly, pituitary adenomas still account for only 7.8% of the 27,000 cases treated in GK centers worldwide. Transnasosphenoidal surgery has greatly improved and surgeons are reluctant to give up a relatively safe and effective operative technique. Radiosurgery is not currently vying to be the primary method of "surgery", but has a definite role following failed pituitary surgery and for tumors that extend into the cavernous sinus. Of 300 patients treated in our GK service, 30 had pituitary adenomas and most had undergone surgery. To date, we have not noted any side effects in the pituitary group. Published information is also reviewed and divided, where possible, into the pre-computed tomography (CT) era and the era of CT-magnetic resonance imaging (MRI). Growth hormone (GH)-secreting adenomas and prolactinomas tend to be larger and cannot be treated with the high doses successful against corticotropin (ACTH)-secreting tumors in Cushing's disease. Radiation fall-off is steep in GK radiosurgery, with the 20% isodose curve being only millimeters away from the point of maximal radiation. The effective dose has mostly been decided on the basis of maintaining safe levels at the sensitive perisellar neural structures. The safety of GK treatment (with no mortality and no permanent morbidity) is compared with other radiosurgical techniques. Good patient response owes much to the cumulative experience of GK pioneers and also to recent advances in images and computers that have enabled increasingly precise stereotaxic targeting and dose planning.
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PMID:Stereotactic radiosurgery of pituitary adenomas. 876 1

We have shown recently that leukemia inhibitory factor (LIF) and oncostatin M (OSM), two members of the gp130-dependent cytokine family, stimulate murine proopiomelanocortin (POMC) transcription and adrenocorticotropin hormone (ACTH) secretion. LIF and corticotropin-releasing hormone (CRH) also synergistically induced in vivo ACTH secretion in fetal nonhuman primates. To elucidate the role of the gp130-related cytokines in human pituitary hormone regulation, we tested expression of gp130-related cytokine receptors in human fetal pituitaries. Using RT-PCR, mRNA expression of receptors for LIF, IL-6, and CRH, and the gp130 subunit, were all detected in fetal pituitaries of 18- and 31-wk gestation. Recombinant human IL-6, LIF, and OSM treatments of primary human fetal pituitary cultures (16-31 wk) increased ACTH secretion by up to 48% (P < 0.05) using doses of 1 nM, and when fetal cultures were cotreated with CRH, ACTH was induced five- to sixfold as compared to CRH alone (three- to fourfold; P = 0.01). Incubation with gp130-specific antibody suppressed basal and cytokine-stimulated ACTH secretion (alone or with CRH) from human fetal cells. Human POMC promoter -879/+6 fused to the luciferase reporter gene and transfected into AtT-20 cells, was stimulated by LIF (7-fold), which also exerted strong (22-fold) synergy with CRH on POMC transcription. Growth hormone (GH) release from fetal cultures was modestly stimulated (15-31%, P < 0.05), while other anterior pituitary hormones were not altered by these cytokines. Thus, physiologic concentrations of the gp130-related cytokines have direct effects on ACTH and GH regulation in the human pituitary, indicating that gp130-dependent signals serve as a paracrine system controlling early human pituitary function.
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PMID:Cytokine-dependent gp130 receptor subunit regulates human fetal pituitary adrenocorticotropin hormone and growth hormone secretion. 921 12

The pituitary gland plays a key role in the regulation of growth, differentiation and function of all cells in the body, including immunocytes. Immune reactions are generated through the proliferation of antigen-specific lymphocyte clones. Growth hormone and prolactin are required for the development of mature lymphocytes and for the maintenance of immunocompetence. These hormones enable lymphocytes to respond to antigen, which is delivered as an adherence signal in the context of major histocompatibility surface molecules of antigen-presenting cells. Numerous other adhesion molecules play a role in the regulation of lymphocyte activation. The activation process is completed by cytokine signalling, after which lymphocyte proliferation, differentiation and functional maturation take place. Interleukins, hormones and growth factors may all function as cytokines. Many lymphocytes exist in the body in a quiescent state, with minimal metabolic activities. These cells are maintained by competence hormones and insulin-like growth factor 1, which are present in the systemic and local environment. Apparently, some steroid hormones, opioid peptides and catecholamines are capable of modulating delivery of the signal from the lymphocyte membrane receptor to the nucleus. Steroid and thyroid hormones control nuclear transcription factors as their receptors, and thus are powerful regulators of lymphocyte signalling at the nuclear level. The bioactive forms of thyroid hormone and of several steroid hormones are generated locally by immunocytes. These important hormonal immunoregulators function both at systemic and local levels. Glucocorticoids are major regulators of cytokine production, and alpha-melanocyte-stimulating hormone functions as a powerful cytokine antagonist. The hormones secreted or regulated by the pituitary gland therefore regulate every level of immune activity, including the competence of lymphocytes to respond to immune/inflammatory stimuli, signal transduction, gene activation, the production and activity of cytokines and other immune effector functions.
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PMID:Pituitary hormones and immune function. 940 45

Administration of steroid hormones was demonstrated to modulate the sleep electroencephalogram (EEG) and sleep-associated hormonal secretion in specific ways. The present study was conducted to compare the effects of mifepristone (Mif), a mixed glucocorticoid (GR) and progesterone receptor (PR) antagonist, and megestrol acetate (Meg), a PR agonist. Nine healthy men were pretreated with either placebo or 200 mg Mif or 320 mg Meg, or a combination of both. Changes in plasma adrenocorticotropic hormone (ACTH), cortisol, and growth hormone concentrations were registered every 30 min; sleep EEG recordings were obtained continuously. Administration of Mif increased the morning plasma ACTH and cortisol surges, whereas Meg had the opposite effect. Growth hormone secretion was lowered by Mif pretreatment and enhanced by Meg. Simultaneous administration of both compounds led to largely compensated effects. The sleep EEG changes induced by Mif were a slight increase in the time awake and a delayed onset of slow-wave sleep. Meg led to a reduction of rapid-eye-movement sleep. Simultaneous administration of Mif and Meg showed a synergism in increasing time awake and shallow sleep: it therefore may be concluded that the sleep EEG effects are mediated by an interaction of GR and PR in unknown mechanisms.
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PMID:Sleep-endocrine effects of mifepristone and megestrol acetate in healthy men. 945 59

Administration of hormones to humans and animals results in specific effects on the sleep electroencephalogram (EEG) and nocturnal hormone secretion. Studies with pulsatile administration of various neuropeptides in young and old normal controls and in patients with depression suggest they play a key role in sleep-endocrine regulation. Growth hormone (GH)-releasing hormone (GHRH) stimulates GH and slow wave sleep (SWS) and inhibits cortisol, whereas corticotropin-releasing hormone (CRH) exerts opposite effects. Changes in the GHRH:CRH ratio contribute to sleep-endocrine aberrations during normal ageing and acute depression. In addition, galanin and neuropeptide Y promote sleep, whereas, in the elderly, somatostatin impairs sleep. The rapid eye movement (REM)-nonREM cycle is modulated by vasoactive intestinal polypeptide. Cortisol stimulates SWS and GH, probably by feedback inhibition of CRH. Neuroactive steroids exert specific effects on the sleep EEG, which can be explained by gamma-aminobutyric acid(A) receptor modulation.
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PMID:Effects of hormones on sleep. 955 Jan 12


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