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 young man presented with rapidly developing Cushing's syndrome which was due to the ectopic secretion of ACTH and beta-MSH-like material from hepatic tumour deposits, possibly originating from biliary radicals. This association of the ectopic ACTH syndrome has not previously been described. During the 22 month course of the illness the plasma immunoreactive ACTH and 'beta-MSH' concentrations rose by logarithmic progression. The plasma calcitonin concentration was also raised but did not change during the last 12 months. At any stage of the illness the plasma concentration of the ecotopically produced hormones was stable except that after hydrocortisone there were inconstant variations. During the course of the illness the ectopic ACTH became biologically less potent. This ineffectural ACTH was present in the plasma, in the tumour, and in the medium in which the tumour was cultured, in a large molecular weight form. This 'big ACTH' differed from the normal ACTH found in the patient's pituitary and from authentic ACTH in its immunochemical character: the C-terminal antigenic determinant (33-39 region of ACTH) was masked in the large molecular weight form but was uncovered after extraction in neutral buffer and this 'big ACTH' was more readily extracted from the tumour at pH 7.0. The tumour tissue also contained immunoreactive beta-MSH-like material and immunoreactive calcitonin which resembled calcitonin M chromatographically.
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PMID:'Big ACTH' and calcitonin in an ectopic hormone secreting tumour of the liver. 19 56

Daily, for 14 days, rabbits of one group were injected with corticotropin, i.e. ACTH-zinc-phosphate (10 units/kg), whereas rabbits of another group were given (in addition) sodium ribonucleate (40 mg/kg) through a tube into the stomach. Formation of lysyl-tRNA, leucyl-tRNA, and alanyl-tRNA in the liver and the skeletal muscles proved to be significantly greater in the animals which received ACTH together with sodium ribonucleate, as compared to that in the animals given the hormone alone. Hyperglycemia, hepatomegaly, and emaciation were less pronounced in the animals given both the preparations.
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PMID:[Effect of enteral administration of sodium ribonucleate on the synthesis of amino acyl t RNA in the liver and skeletal muscles of rabbits in experimental hypercorticism]. 19 79

The ability of cytochalasin B to inhibit the steroidogenic response of mouse adrenal tumor cells (Y-1) to adrenocorticotropin (ACTH) was examined with two aims: to consider the specificity of the inhibitor and to determine at what point(s) in the steroidogenic pathway it acts. Cytochalasin B did not inhibit protein synthesis or transport of [3H]-cholesterol into the cells nor did it alter total cell concentration of ATP. Together with previous evidence, this suggests that the effects of cytochalasin observed are relatively specific in these cells. Cytochalasin inhibits the increase in conversion of [3H]cholesterol to 20alpha-[3H]dihydroprogesterone (20alpha-hydroxypregn-4-en-3-one: a major product of the steroid pathway in Y-1 cells) produced by ACTH but does not inhibit conversion of cholesterol to pregnenolone by mitochondrial and purified enzyme preparations from Y-1 cells and bovine adrenal, respectively. Cytochalasin does not inhibit the conversion of pregnenolone to 20alpha-dihydroprogesterone but was shown to inhibit increased transport of [3H]cholesterol to mitochondria resulting from the action of ACTH. These findings indicate that cytochalasin acts after cholesterol has entered the cells and before it is subjected to side-chain cleavage in mitochondria. In view of the known action of cytochalasin on microfilaments, it is proposed that these organelles are necessary for the transport of cholesterol to the mitochondrial cleavage enzyme and that at least one effect of ACTH (and cyclic AMP) is exerted upon this transport process. The specificity of the effects of cytochalasin is considered in relation to this conclusion.
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PMID:Response of adrenal tumor cells to adrenocorticotropin: site of inhibition by cytochalasin B. 19 28

Using antibodies against synthetic corticotropic hormones (1-24 ACTH and 17-39 ACTH), and melanotropic hormones (alpha-MSH and beta-MSH), it is possible to identify corticotropic and melanotropic cells in the adenohypophysis of three species of monkeys : Erythrocebus patas, Cercopithecus aethiops and Papio hamadryas. The corticotropic cells are numerous in the anterior lobe in both the adult and infant male and female monkeys of these three species. The intermediate lobe reacts with antibodies against ACTH and also with antibodies against the two MSH. In the anterior lobe, the corticotropic cells react also with anti-beta MSH antibody but not with the anti-alpha MSH antibody.
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PMID:[Demonstration by immunofluorescence of adenohyphysis corticotropin and melanotropin cells in Erythrocebus patas, Cercopithecus aethiops and Papio hamadryas]. 19 18

The in vitro corticotropic releasing effects of vasopressin (VP) and hypothalamic median eminence (HME) extract were compared as a function of their concentration and preincubation and incubation times. Whereas HME extract augmented the ACTH secretion from non-preincubated adenohypophyses, VP released corticotropin from the pituitaries only after a 2 h preincubation period. The disappearance of endogenous VP during the preincubation time rendered the gland responsive. The maximal stimulation of ACTH secretion by VP was markedly less than that induced by HME extract. The results suggest the presence of VP receptor sites in the anterior pituitary (AP) which are probably different from the receptor sites of the hypothalamic corticotropin releasing factor (CRF).
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PMID:Comparative in vitro studies on corticotropin releasing activity of vasopressin and hypothalamic median eminence extract. 19 42

Double-antibody immunoprecipitation procedures with antisera to endorphins and to corticotropin (ACTH) were used to study the biosynthesis of these peptides in a mouse pituitary tumor cell line. Cultures were incubated with a (3)H-labeled amino acid, and aliquots of culture medium were immunoprecipitated. Sodium dodecyl sulfate/polyacrylamide gel electrophoresis of [(3)H]phenylalanine-labeled immunoprecipitates prepared with endorphin antisera resolved three forms of endorphin with apparent molecular weights of 31,000, 11,700, and 3500; immunoprecipitates prepared with the ACTH antiserum contained four forms of ACTH with apparent molecular weights of 31,000, 23,000, 13,000 and <4500. Sequential immunoprecipitation of culture medium with the ACTH antiserum and then with the endorphin antiserum (or the reverse order) indicated that both antisera precipitated the same 31,000 dalton molecule. Purified pools of the different forms of ACTH and endorphin were prepared by immunoprecipitation and gel filtration. The tryptic peptides found in [(3)H]phenylalanine- or [(3)H]tryptophan-labeled 31,000 dalton ACTH were identical to the tryptic peptides found in digests of 31,000 dalton endorphin labeled with the same amino acid. A tryptic peptide similar to the lipotropin tryptic peptide [betaLPH(61-69)] that contains the opiate-active methionine-enkephalin sequence could be identified in 31,000 dalton ACTH and in all the different forms of endorphin. Most of the peptide cleaved from 31,000 dalton ACTH when it is converted to 23,000 dalton ACTH could be precipitated by endorphin antisera; this 11,700 dalton endorphin molecule is similar to the pituitary hormone betaLPH in size and structure. The 3500 dalton endorphin is similar to beta-endorphin in size and structure. The culture medium from the AtT-20 mouse pituitary tumor cells contained approximately equimolar amounts of ACTH-related peptides and endorphin-related peptides.
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PMID:Common precursor to corticotropins and endorphins. 19 29

The prostaglandin (PG) synthesis inhibitor, indomethacin, has been found to enhance adrenocorticotropin (ACTH) secretion upon injection directly into the anterior pituitary at a dose that is ineffective intravenously. Such stimulation was observed in combination with, and in the absence of, stimulation by a corticotropin-releasing factor (CRF) preparation. It was reversed to varying degrees by replacing certain PGs exogenously. It suggested that endogenous PGs in the anterior pituitary participate in the modulation of the sensitivity of this gland to the hypothalamic neurohormone, CRF.
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PMID:Stimulation of ACTH secretion by indomethacin and reversal by exogenous prostaglandins. 19 69

To examine hindbrain pathways mediating release of adrenocorticotropin (ACTH) in response to hemodynamic changes we tested, in 19 cats (chloralose/urethan), 70 neurons in ACTH-active areas of the medulla for their response to volume pulsation (+/- 1 ml, 1 Hz, 60 s) of the right atrium (RA) or to hemorrhage (3 ml/kg per 30 s), and to electrical stimulation in ACTH-active areas of the dorsal rostral pons (DRP). The activity of 16 neurons was increased (P less than 0.05) by RA. Of these, 6 were driven antidromically from the locus subcoeruleus (LSC), and were located in the lateral solitary nucleus and in posteromedial nucleus intercalatus (NI). The activity of 11 neurons was decreased by RA. Of these, 5 were driven antidromically from LSC and lateral ventral tegmental nucleus and were located in anterolateral NI. No rostral projections were found to more medial sites in DRP. Responses to the first trial of RA were rapid, but slowed and attenuated with repeated trials. Responses to hemorrhage were rapid and in the opposite direction, but did not attenuate. The results suggest that pathways displaying rate sensitivity project from the right atrium via B-receptors to the DRP.
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PMID:Neurons in medullary areas controlling ACTH: atrial input and rostral projections. 19 72

Rat adrenal glomerulosa and fasciculata-reticularis cell sensitivity to comparable molar doses of angiotensin II (AII) (2.4 X 10(-12) to 2.4 X 10(-4) M) and ACTH (alpha-1-24-adrenocorticotropin) (3.5 X 10(-13) to 3.5 X 10(-8) M) as well as small increments in potassium (K+) (3.7 to 13 meq/liter) was investigated. Glomerulose cells responded to physiological levels of AII (2.4 X 10(-10) M) and alpha-1-24-ACTH (3.5 X 10(-12) M), whereas an increment of as little 0.3 meq/liter in medium K+ also significantly increased aldosterone production. Of the three stimuli, alpha-1-24-ACTH caused the greatest aldosterone rise (11 times control). Fasciculata-reticularis cells responded only to alpha-1-24-ACTH. Whereas the threshold sensitivity was no lower than with glomerulosa cells, the maximum response was significantly greater (63 times control). These findings are consistent with findings documented in vivo in man, suggesting that the control of aldosterone secretion is similar in these two species.
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PMID:Rat adrenal cell sensitivity to angiotensin II, alpha-1-24-ACTH, and potassium: a comparative study. 20 Jan 47

The relationships among exogenous adrenocorticotropin (ACTH), plasma corticosteroids, and circulating leukocytes were studied in 7 lactating cows. Blood samples were obtained from jugular cannulas at -2, -1, and 0 hours before ACTH was injected (base line) and 0.25, 0.50, 1, 2, 3, 6, and 24 hours after injection. Plasma corticosteroids were increased progressively by injecting doses of ACTH between 1 and 200 IU. Plasma corticosteroids reached peak concentrations between 15 and 30 minutes and returned to base line within 1 to 3 hours after 1, 5, and 10 IU doses of ACTH were injected, but required as long as 6 hours after injection of 100 and 200 IU. Base line counts of circulating leukocytes averaged 7.3 X 10(3) cells/mm3 and remained unchanged after injecting 0 and 1 IU of ACTH (P less than 0.05). Significant dose-dependent increases in circulating leukocytes were detected within 2 hours after administering 5, 10, and 100 IU of ACTH. Responses to 100 and 200 IU were similar. The average concentration of leukocytes increased up to 6 hours after ACTH administration and returned to base line values within 12 to 24 hours in cows injected with 5 and 10 IU, but not until 48 hours in cows injected with 100 and 200 IU of ACTH. In contrast to the delayed and sustained responses observed for leukocytes, corticosteroid responses were rapid and transient. Moreover, the administration of 200 IU of ACTH was considered to increase circulating corticosteroids and leukocytes beyond that found in dairy cattle exposed to stress associated with overmilking, acute coliform mastitis, or parturition.
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PMID:Response of plasma corticosteroids and circulating leukocytes in cattle following intravenous injection of different doses of adrenocorticotropin. 20 Jan 55


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