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)

Plasma 16 beta-hydroxydehydroepiandrosterone (16 beta-OH-DHEA) levels were measured by radioimmunoassay in normal and pathological conditions in man. 16 beta-OH-DHEA levels in normal subjects rose sharply during adolescence and then declined slowly throughout adult life: 192 pg/ml age 7-11, 395 pg/ml age 15-19, 330 pg/ml age 20-39, 261 pg/ml age 40-59, and 124 pg/ml over 60-years-old. No marked difference was seen between male and female subjects. 16 beta OH-DHEA rose significantly (p less than .01) during adrenocorticotropin (ACTH) stimulation, declined (p less than .005) during dexamethasome suppression and during gonadal suppression, rose (p less than .05) during gonadal stimulation and following administration of WIN 24540, an inhibitor of 3 beta-o1-dehydrogenase (p less than .005). 16 beta-OH-DHEA levels in adrenal venous blood were higher than in inferior vena cava blood but the levels in hepatic venous blood were not higher than in arterial blood. These results indicate that 16 beta-OH-DHEA is secreted directly by the adrenal cortex and probably the gonads. 16 beta-OH-DHEA levels were elevated in normal pregnant women, pregnant women with toxemia and in patients with Cushing's disease, ectopic ACTH-producing tumor and congenital adrenal hyperplasia but not in patients with low-renin essential hypertension.
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PMID:Plasma 16 beta-hydroxydehydroepiandrosterone in normal and pathological conditions in man. 18 75

Two cases of small cell carcinoma of the lung associated with the ectopic production of multiple hormones are reported. Both tumors were shown to contain significant amounts of ADH, ACTH, and beta-MSH. Biologic, immunologic, and gel chromatographic properties of these ectopic hormones were found to be very similar to those of pituitary origin. The effect of excessive secretion of antidiuretic hormone (ADH) dominated the clinical manifestations in both cases, i.e., syndrome of inappropriate secretion of ADH (SIADH). The clinical manifestations of the ectopic ACTH-MSH syndrome were minimal. These data suggest that multiple hormone production without clinically overt sequelae of excess hormone is not uncommon in small cell (oat cell) carcinoma of the lung.
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PMID:Two cases of multiple hormone-producing small cell carcinoma of the lung: coexistence of tumor ADH, ACTH, and beta-MSH. 18 19

The absorption of a synthetic ACTH-peptide (alpha1-18 corticotropin, Ba 41.795) via the nasal mucosa was investigated in twelve probands. After application of 1 mg into each nostril a rapid increase of the plasma cortisol was observed which returned to the initial value only after 7 hours. In two patients with rheumatoid arthritis and two patients with bronchial asthma who had been treated with regular steroid injections an attempt was made to replace the injections by nasal application. The same therapeutic effects could be obtained, but larger doses were required than when using injection therapy.
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PMID:[Nasal application of a synthetic alpha1-18 corticotropin: an effective form of ACTH treatment (author's transl)]. 18 98

Human and rat pituitaries were investigated immunohistochemically for ACTH and alpha MSH activity by means of the enzyme-labeling technique. In rat pituitaries cells present in both the anterior and intermediate lobes were reactive with the anti-ACTH antibodies, the cells from the intermediate lobe were also reactive with anti-alpha MSH antibodies. In human pituitaries, ACTH-immunoreactivity was found in cells from the anterior lobe and cells invading the posterior lobe. In 5 out of 15 pituitaries ACTH-immunoreactive cells located at or invading the posterior lobe were also reactive with the anti-alpha MSH antibodies. It is concluded that the human pituitary cells that invade the posterior lobe represent a population which is at least immunohistochemically identical with the intermediate lobe cells of the rat. The ACTH-immunoreactivity of intermediate lobe cells may be explained by the presence of a corticotropin-like intermediate lobe peptide (CLIP) which has been suggested to be a prohormonal fragment of alpha MSH.
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PMID:The immunolocalization of ACTH and alpha MSH in human and rat pituitaries. 18 28

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

The ability of ACTH fragments and of an ACTH analogue [9-tryptophan(o-nitrophenylsulfenyl)] corticotropin-(1-24)-tetracosapeptide[Trp-(Nps)9 ACTH1-24] to stimulate adenylate cyclase in bovine adrenal cortex membranes and a crude membrane fraction from rat adrenals has been determined. Partial agonists like Trp (Nps)9 ACTH1-24 displayed intrinsic activity in the rat adrenal preparation only if tested in the presence of 5'-guanylylimidodiphosphate [Gpp(NH)p]. On the other hand, no addition of Gpp(NH)p was necessary to demonstrate intrinsic activity of Trp(Nps)9 ACTH1-24 for bovine adrenal cortex adenylate cyclase. A large decrease (15-fold) of the apparent Km values for ACTH1-24, ACTH1-23 and ACTH1-17 was observed with the rat adrenal preparation when Gpp(NH)p was added. The shift in apparent Km values for ACTH1-24 and ACTH1-23 for the bovine adrenal cortex adenylate cyclase system was small or insignificant when Gpp(NH)p was added. The observations suggest that the hormone receptor facilitates the action of guanylnucleotide sites in the membrane. When guanylnucleotide sites are occupied by Gpp(NH)p even weak interactions of the hormone receptor with e.g. partial agonists are propagated to the catalytic subunits of the adenylate cyclase complex resulting in enhanced activity. The differences in adenylate cyclase activation with hormone fragments or analogues and different target tissues may rather reflect the state of the coupling process involving guanylnucleotide binding sites of the isolated membrane fraction than differences in the receptor itself.
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PMID:Adrenal cortex adenylate cyclase. In vitro acitivity of ACTH fragments and analogues. 18 24

A 61 year old woman presented with profound hyponatremia and markedly low serum osmolality. Urine osmolality was greater than the serum osmolality, an abnormality that was corrected by water restriction, suggesting inappropriate ADH secretion. Although there were no physical signs of Cushing's syndrome, her serum potassium level was low and markedly elevated levels of plasma and urine corticosteroids were not altered by the administration of large amounts of dexamethasone, suggesting the ectopic ACTH-MSH syndrome. Plasma levels of immunoreactive ACTH and beta-MSH were elevated. At autopsy, a metastastic oat cell carcinoma of the lung, not detected antemortem by chest roentgenograms and bronchoscopy, was found. Immunoreactive ADH, ACTH and beta-MSH were detected in the primary tumor and in metastases to the liver. beta-MSH was also detected in the spleen, in which metastases were observed. This is the first documented case of the simultaneous production of ADH, ACTH and beta-MSH by neoplastic tissue associated with clinical manifestations of the syndrome of inappropriate ADH secretion and the ectopic ACTH-MSH syndrome.
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PMID:Ectopic production of antidiuretic hormone (adh), adrenocorticotrophic hormone (ACTH) and beta-melanocyte stimulating hormone (beta-MSH) by an oat cell carcinoma of the lung. 18 5

The authors have carried out research into the GH stimulating action of 0.25 mg of synthetic beta-1-24 corticotropin (Synacthen) injected intravenously into 26 healthy normally developed children. The results obtained prove the limited and irregular action of ACTH.
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PMID:[The use of synthetic beta-1-24 corticotropin as a GH stimulating factor (author's transl)]. 18 71

The adenylate cyclase responses of the human GH or ACTH producing pituitary adenomas and ectopic ACTH producing tumors to TRH, LH-RH, biogenic amines, peptides hormones, PGE1 and rat median eminence extract (MEE) have been examined. Out of 4 GH producing pituitary adenomas obtained from patients with active acromegaly at hypophysectomy two were stimulated by TRH, two by LH-RH, three by norepinephrine, one by dopamine, four by PGE1 and none by serotonin. Glucagon stimulated the adenylate cyclase in one of three and MEE in both of two tested. The positive responses of paradoxical GH release after TRH and/or LH-RH before surgery in these patients coincidentally related to the response of adenylate cyclase of each pituitary adenoma. There seems, however, to be no consistent correlation between the adenylate cyclase responses to biogenic amines and the GH release after L-Dopa or 5-hydroxytroptophan tested. The adenylate cyclase of a pituitary adenoma from case of Cushing's disease was stimulated by LH-RH, norepinephrine glucagon and MEE but not by TRH. Plasma levels of ACTH, beta-MSH and cortisol increased after LH-RH but not after TRH in this patient before hypophysectomy. The adenylate cyclase of two ectopic ACTH producing tumors (gastric carcinoid and malignant thymoma) was activated by TRH, LH-RH, norepinephrine, epinephrine, serotonin, PGE1 and MEE. These results indicate the presence of multiple hormone receptors in GH or ACTH producing pituitary adenomas and ectopic ACTH producing tumors, and suggest that the paradoxical GH or ACTH release after TRH and/or LH-RH injection in acromegaly and Cushing's syndrome might be caused by an alteration of the cellular membrane receptors of the pituitary adenomas.
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PMID:Adenylate cyclase of GH and ACTH producing tumors of human: activation by non-specific hormones and other bioactive substances. 19 Feb 56

The peptides alpha-MSH and MSH/ACTH 4-10 were degraded by rat brain extracts and serum to yield free amino acids among the end-products. Breakdown of these two peptides was double that of a related synthetic hexapeptide Met (0)-Glu-His-Phe-D-Lys-Phe. No significant breakdown of the hexapeptide occurred after incubation with human serum; it also had almost negligible pigmentary effects in vivo and in vitro when compared to alpha-MSH. The patterns of amino acid release indicate possible endopeptidase cleavage at Phe-Arg in alpha-MSH followed by secondary exopeptidase action to release free amino acids. For the hexapeptide, the primary cleavage point occurred at the -His3-Phe4 bond. The stability of this analog in human sera, coupled with its lower rate of degradation in the CNS, may contribute to its more potent behavioral actions in vivo.
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PMID:Biodegradation of alpha-MSH and derived peptides by rat brain extracts, and by rat and human serum. 19 Nov 54


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