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)

Studies were undertaken to investigate the effects of synthetic 1-24 adrenocorticotropin (ACTH), bovine alpha melanocyte-stimulating hormone (alpha-MSH), and ovine beta lipotropin (beta-LPH) on plasma calcium and phosphate in rabbits. Equimolar concentrations of these hormones were infused intravenously in intact and thyroidectomized animals. In addition, ACTH was similarly administered to adrenalectomized rabbits. ACTH, alpha-MSH, and beta-LPH all lowered plasma calcium and raised plasma phosphate. These changes were not prevented by prior thyroidectomy. ACTH was equally effective in inducing hypocalcemia and hyperphosphatemia in the absence of the adrenal glands, while adrenalectomy alone raised plasma calcium. From these findings we have concluded that 1) ACTH, alpha-MSH, and betaLPH affect phosphate as well as calcium metabolism; 2) these hormones do not act by releasing calcitonin; and 3) ACTH exerts its hypocalcemic-hyperphosphatemic effect, at least in part, independently of its trophic action on the adrenal glands.
Endocrinology 1975 Dec
PMID:Effect of ACTH, alpha-MSH, and beta-Lipotropin on calcium and phosphorus metabolism in the rabbit. 17 30

Simultaneous measurements of both beta-melanocyte stimulating hormone (beta-MSH) and adrenocorticotropic hormone (ACTH) in extracted plasma were performed by specific radioimmunoassays. During insulin-induced hypoglycemia, there was a marked increase of plasma ACTH levels and a slight but significant increase of plasma beta-MSH levels. Lysine-vasopressin on the other hand, caused a significant rise of plasma ACTH levels without corresponding response of plasma beta-MSH. Following glucagon administration, neither hormone rose significantly. However, metyrapone infusion caused a significant increase of both ACTH and beta-MSH levels, and frequent blood sampling revealed that both hormones were secreted episodically, and that peaks generally coincided with each other. These data suggest that the secretion of these two hormones can occur together in most instances, and that the same mechanism is involved in the secretion of both hormones under the negative feedback control.
J Clin Endocrinol Metab 1975 Dec
PMID:Plasma levels of beta-MSH and ACTH during acute stresses and metyrapone administration in man. 17 35

A sensitive and specific radioimmunoassay for alpha-melanocyte-stimulating hormone (alpha-MSH) was developed. Extracts of the neurointermediate lobe of the rat produced displacement curves which were parallel to those obtained with synthetic alpha-MSH. The mean immunoreactive alpha-MSH concentration in neurointermediate lobes from normal adult rats was 2768 +/- 200 (S.E.M.) ng/lobe. This accounted for approximately 78% of the MSH activity of the neurointermediate lobe as measured by bioassay. Much lower levels of immunoreactive alpha-MSH were found in the anterior lobe of the rat. Extracts of rat serum and plasma also contained immunoreactive alpha-MSH and the mean level was found to be 237 +/- 20 pg/ml. This was slightly lower than the level measured in rat plasma by bioassay. Increased levels of alpha-MSH were found in plasma of rats 1 and 3 h after a single injection of trifluoperazine and after 1-5 min of ether anaesthesia. These changes were reflected by decreases in the alpha-MSH content of the neurointermediate lobe.
J Endocrinol 1975 Dec
PMID:Development of a radioimmunoassay for alpha-melanocyte-stimulating hormone in the rat. 17 84

We have obtained direct evidence that shows the cellular formation and subsequent release of a potent inhibitor (feedback regulator) of adenylate cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] by adipocytes, upon stimulation with epinephrine. The appearance of such a feedback regulator in adipocytes preceded its release into the medium. During a 30 min incubation, intracellular regulator levels rose rapidly and reached 39-61 units/g of adipocyte at 10 min. Release of inhibitor into the medium increased slowly and was 11-16 units/g of adipocyte at 10 min. Upon continued incubation, the cells at 30 min contained 30-41 units/g of ingibitor, slightly less than the content at 30 min; meanwhile, the medium content rose more than 3-fold. The inhibitor from both locations appeared to have the same characteristics, judging from the purification procedures and the biological activities on hormone-stimulated adenylate cyclase. Adenylate cyclase was inhibited by the feedback regulator in vitro when either epinephrine, corticotropin (ACTH), or glucagon was used as activator. The site of action of this inhibitor is therefore most likely beyond the specific hormone receptors. A new in vitro action of insulin has been found. Insulin, 50-500 microunits/ml, inhibited the formation and release of this factor from isolated rat or hamster adipocytes by 29-81% after these cells were stimulated by hormones that raise intracellular adenosine 3':5'-cyclic monophosphate. This factor enhaced the effect of insulin in lowering the adenosine 3':5'-cyclic monophosphate levels in fresh rat adipocytes. A reduced formation of such a factor may modify the metabolic events in adipocytes, and some as yet unexplained effects of insulin could therefore be linked to the metabolic effects of this factor.
Proc Natl Acad Sci U S A 1975 Dec
PMID:Cellular levels of feedback regulator of adenylate cyclase and the effect of epinephrine and insulin. 17 73

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.
Cancer 1976 Dec
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.
Dtsch Med Wochenschr 1976 Dec 03
PMID:[Nasal application of a synthetic alpha1-18 corticotropin: an effective form of ACTH treatment (author's transl)]. 18 98

Polyadenylate-containing RNA prepared from the membrane fraction of bovine anterior pituitary gland was shown to direct the synthesis of a large translation product related to corticotropin (adrenocorticotropic hormone) in a cell-free system derived from wheat germ. This product was identified by immunoprecipitation with specific antibody against corticotropin, followed by electrophoretic analysis of the dissociated immunoprecipitate on sodium dodecyl sulfate-polyacrylamide gel. Further evidence for the identity of the translation product was provided by the presence of a common peptide in the chymotryptic digest of [35S]methionine-labeled cell-free product and in that of authentic corticotropin. The molecular weight of the translation product was estimated to be approximately 35,000, based on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. These results indicate that corticotropin messenger RNA directs the cell-free synthesis of a product that contains the amino acid sequence of corticotropin but is much larger than this hormone.
Proc Natl Acad Sci U S A 1976 Dec
PMID:A large product of cell-free translation of messenger RNA coding for corticotropin. 18 32

The transfer of lipoprotein-bound cholesterol into adrenal cells was examined. Adrenal glands from unstimulated or corticotropin stimulated hypophysectomized rats were incubated with high density lipoprotein (HDL) or low density lipoprotein LDL containing radiolabeled cholesterol. The rate of transfer of labeled cholesterol from HDL into the glands was two to three times greater than from LDL. Corticotropin stimulation increased the transfer of cholesterol from HDL but not LDL. The effects of corticotropin were not dependent on subsequent cholesterol utilization for steroidogenesis. The process of cholesterol transfer from HDL was linear with time over 2 hr at 37 degrees and greatly reduced at 4 degrees. In addition, the transfer process became saturated above an HDL cholesterol concentration of 900 mug/ml. About 25% of the labeled adrenal cholesterol arising from HDL was recovered within the mitochondria. The labeled cholesterol within isolated mitochondria could undergo mitochondrial conversion to pregnenolone. Finally, the delipidated HDL apolipoproteins, apoA-I and apoA-II, when added to incubations containing less than saturating concentrations of HDL, stimulated transfer of labeled cholesterol from HDL to adrenal cells. These studies suggest that rat adrenal tissue possesses an HDL specific hormonally-responsive mechanism for accumulating extracellular cholesterol and that apoA-I and apoA-II have a significant function in the uptake process.
Proc Natl Acad Sci U S A 1976 Dec
PMID:Adrenal cholesterol uptake from plasma lipoproteins: regulation by corticotropin. 18 33

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.
Virchows Arch B Cell Pathol 1976 Dec 02
PMID:The immunolocalization of ACTH and alpha MSH in human and rat pituitaries. 18 28

Corticotropin 1-24 and [Gly1]corticotropin1-18 amide increased the fluorescence of 1-anilinonaphthalene-8-sulfonate which bound to the bovine adrenocortical membranes. The two ACTH fragments interacted with the protein of the membranes and membranes and increased the net positive charge of the membranes.
Experientia 1976 Dec 15
PMID:Fluorometric study of interaction between ACTH fragments and bovine adrenocortical membranes. 19 Dec 82


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