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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of growth hormone (GH), prolactin (PRL), and adrenocorticotropic hormone (ACTH) in the induction of the PRL receptor was investigated in hypophysectomized male rat livers and in the livers of male rats bearing a GH secreting tumor. After 7 days of sc injections, specific binding of PRL in controls and rats treated with PRL, GH, ACTH, human chorionic gonadotropin, estradiol, or testosterone was approximately 1%. Treatment with PRL plus ACTH increased specific binding to 4%; adding estradiol to this combination produced a further increase to 8%, whereas the addition of testosterone decreased hepatic binding to 1%. Combination of GH with ACTH was most effective giving a specific binding of 33%, which is similar to the 36% observed in the liver of rats bearing a GH-secreting tumor. These results suggest that GH acts synergistically with PRL and/or ACTH to increase lactogenic binding sites in the male rat liver and that sex steroids have a modulating effect on this action.
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PMID:Induction of lactogenic receptors. II. Studies on the liver of hypophysectomized male rats and on rats bearing a growth hormone secreting tumor. 18 48

Morphine sulfate (MS) and the opioid peptide beta-endorphin beta-LPH-(61-91) stimulate prolactin and growth hormone release in steroid-primed and non-treated male rats when injected intravenously or intracisternally. On a molar basis beta-endorphin is at least 20 times more potent than MS, whereas Met5-enkephalin (beta-LPH-(61-65)) and alpha-endorphin (beta-LPH-(61-76)) are devoid of activity at the dose injected (300 mug). The in vivo stimulatory effects of beta-endorphin on prolactin secretion are reversed by the opiate antagonist naloxone. The absence of in vitro effect of MS and beta-endorphin on prolactin and growth hormone secretion by cultured rat pituitary cells suggest that they have a central nervous system site of action.
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PMID:Stimulation in vivo of the secretion of prolactin and growth hormone by beta-endorphin. 18 6

We examined whether hormones would modify the carcinogenic action of aflatoxin B1 (AFB1). Four groups of inbred Fischer rats received AFB1, 125 mug per animal, weekly per os. In three of the groups, certain hormones were administered simultaneously: One group received 1 U growth hormone (GH) sc weekly, another was given 4 U adrenocorticotropin (ACTH) weekly, and a third received 0.5 U insulin weekly sc. AFB1, ACTH, and insulin were given for 20 weeks; GH was given for only 10 weeks. The control group did not receive hormone adjuvant. In each group, 4 animals were killed at 7, 14, 21, 28, and 35 weeks; the remaining rats were killed at 77 weeks. Their livers were carefully examined and samples prepared for light and electron microscopy. Animals receiving AFB1 and ACTH failed to exhibit hepatocellular carcinoma. On the other hand, malignant lymphoma appeared at 56 weeks in 3 of the 6 surviving males on this regime. AFB1, alone or when given with insulin or GH, caused hepatocellular carcinoma in all animals; in these, lymphoma was not observed. Lymphoma comprised two cell types, each with similar neclear characteristics but differing in their nucleocytoplasmic ratios and in the amount and distribution of cytoplasmic organelles. Alterations leading to hepatocellular carcinoma were examined at various stages of development. "Basophilic hyperplasia" reflected an increase in free ribosomes. "Hyperplastic nodules" were composed of hepatocyte aggregates with characteristics similar to those encountered in the earlier stage. Both the "neoplastic nodules" and hepatocellular carcinomas were formed by cells containing large, "smooth fingerprints" and free ribosomal aggregates. These features supported the concept that AFB1 impairs ribosomal binding to endoplasmic reticulum membranes. The failure of ACTH-treated animals to develop hepatocellular carcinoma was ascribed to the effect of adrenal cortical stimulation upon membrane-polysome binding.
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PMID:Inhibition of hepatocarcinogenesis by adrenocorticotropin in aflatoxin B1-treated rats. 18 49

In the pituitary of an Amphibian (Urodela), various cell types were localized by cytoimmunological techniques: corticotrophs located in a rostral zone near the median eminence, ventral orangeophilic cells secreting a prolactin-like hormone and erythrosinophilic cells in a more dorso-caudal situation secreting growth hormone. Alpha-MSH and beta-MSH produceng cell were identified in the intermediate lobe; these cells were also labelled with antibodies against 1-24 ACTH and 17-39 ACTH. These data are in accordance with results obtained after an experimental study of the prolactin cells.
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PMID:[Cyto-immunological study of the Pleurodele pituitary gland]. 19 20

The effects of prostaglandin E1 (PGE1) and indomethacin (IDM) on the release of several pituitary hormones from the rat pituitary were investigated in vitro. An addition of 2 microng/ml of PGE1 to the medium elicited the release of growth hormone (GH) and prolactin, but not of adrenocorticotropin (ACTH) and luteinizing hormone (LH). Although the addition of 1 microng/ml of IDM alone resulted in no effect on the basal release of these hormones, IDM diminished the release of ACTH induced by crude rat hypothalamic extracts (HE) or lysine-8-vasopressin (LVP), and LH induced by HE or luteinizing hormone-releasing hormone (LH-RH). These findings implicate that a part of PGE1 action might be a direct one on the pituitary gland and PGE1 might release GH and prolactin, whereas IDM might have a direct action on the pituitary gland, and that blunt the release of these pituitary hormones induced by several stimuli.
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PMID:Effects of prostaglandin E1 and indomethacin on ACTH, prolactin, GH and LH from rat pituitary in vitro. 19 86

In a series of 250 pituitary adenomas, 72 (28.8%) were nonsecreting and 178 (71.2%) produced a hypersecretion syndrome: human growth hormone (83), prolactin (59), and adrenocorticotropic hormone (ACTH) (36). One-fifth had received prior treatment and one-fourth had visual impairment. The technical aspects of the transsphenoidal procedure are given with separate consideration of microadenomas and larger tumors. The results are provided in summary form with emphasis on the favorable outcome following removal of microadenomas. There was one postoperative death, and the complications observed after operation are presented.
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PMID:Transsphenoidal microsurgical removal of 250 pituitary adenomas. 20 36

While an attempt was being made to identify the source of the growth hormone releasing factor present in cerebral spinal fluid of man, it was discovered that cells of the rat amygdaloid nucleus, grown in tissue culture, produce a material that is immunologically and chromatographically identical to growth hormone found in the pituitary. Immunoperoxidase staining revealed dense accumulation of the peroxidase-antibody to growth hormone complex in amygdala cells. Significant amounts of growth hormone and adrenocorticotropin could be extracted from this limbic structure. Extracts containing immunoequivalent amounts of growth hormone were measured by bioassay in hypophysectomized rats. Stimulation of the growth of epiphyseal cartilage by extracts of the amygdala was comparable to the stimulation by extracts of anterior pituitary glands. The stimulatory effect of amygdala extracts on adrenal and gonadal size and weight and on growth of thyroid follicular epithelium was also comparable to that of pituitary extracts.
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PMID:Biologically active pituitary hormones in the rat brain amygdaloid nucleus. 20 34

Cases of seven different types of surgically resected pituitary adenoma are described. Included are tumours secreting prolactin or growth hormone or both, and nonfunctioning tumours--undifferentiated and oncocytic tumours, and one tumour with cells of the adrenocorticotropin-melanocyte-stimulating hormone type. The final interpretation of a case of pituitary adenoma should include an assessment of thorough morphologic studies, using not only routine staining and light microscopy but also immunostaining and electron microscopy, to complement the biochemical, radiologic and clinical evaluation.
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PMID:A new look at pituitary adenomas: structure elucidating function. 20 3

GH4C1 cells are a clonal strain of rat pituitary tumor cells which synthesize and secrete prolactin and growth hormone. Somatostatin, a hypothalamic tetradecapeptide, inhibits the release of growth hormone and, under certain circumstances, also prolactin from normal pituitary cells. We have prepared [125I-Tyr1]somatostatin (approximately 2200 C1/mmol) and have shown that this ligand binds to a limited number of high affinity sites on GH4C1 cells. Half-maximal binding of somatostatin occurred at a concentration of 6 x 10(-10) M. A maximum of 0.11 pmol of [125I-Tyr1]somatostatin was bound per mg of cell protein, equivalent to 13,000 receptor sites per cell. The rate constant for binding (kon) was 8 x 10(7) M(-1) min(-1). The rate constant for dissociation (koff) was determined by direct measurement to be 0.02 min(-1) both in the presence and absence of excess nonradioactive somatostatin. Binding of [125I-Tyr1]somatostatin was not inhibited by 10(-7) M thyrotropin-releasing hormones. Substance P, neurotensin, luteinizing hormone-releasing hormone, calcitonin, adrenocorticotropin, or insulin. Of seven nonpituitary cell lines tested, none had specific receptors for somatostatin. Somatostatin was shown to inhibit prolactin and growth hormone production by CH4C1 cells. The dose-response characteristics for binding and the biological actions of somatostatin were essentially coincident. Furthermore, among several clonal pituitary cell strains tested, only those which had receptors for somatostatin showed a biological response to the hormone. We conclude that the characterized somatostatin receptor is necessary for the biological actions of somatostatin on GH4C1 cells.
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PMID:Characterization of functional receptors for somatostatin in rat pituitary cells in culture. 21 Jan 85

Systematic pituitary evaluation was performed in four patients suspected of having Sheehan's syndrome. A sequential pituitary stimulation test, consisting of insulin-induced hypoglycemia followed by stimulation of gonadotropin-(GnRH) and thyroid-releasing hormone (TRH), a metyrapone test, and adrenocorticotropic hormone (ACTH) stimulation test, was performed. All four patients failed to develop a normal increase in serum growth hormone, cortisol, and prolactin (PRL) following insulin-induced hypoglycemia. All patients demonstrated a blunted PRL, follicle-stimulating hormone, and luteinizing hormone response to the combination of GnRH and TRH. Although thyroid stimulating hormone (TSH) response was impaired in all patients, two patients had normal T3 resin uptake and thyroxine, demonstrating minimal TSH reserve maintaining normal baseline free thyroxine index. Metyrapone administration was followed by no increase in 11-deoxycortisol or 17-ketogenic steroids, thereby adding no additional information to the hypoglycemia stimulation. ACTH infusion revealed normal adrenal cortisol response. In conclusion, in patients with suspected postpartum hypopituitarism, a complete pituitary function investigation can be done in a short time by using the described pituitary sequential stimulation test.
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PMID:Diagnosis of Sheehan's syndrome using a sequential pituitary stimulation test. 21 51


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