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)

The adenylate cyclase system present in a preparation enriched in plasma membranes derived from bovine adrenal cortex was investigated in considerable detail. This system is stimulated by adrenocorticotropic hormone (ACTH), by biologically active analogs of this hormone, and by fluoride ion. The preparation contains sodium-potassium- and magnesium-dependent ATPases that are markedly inhibited by 50 mM sodium fluoride. Incorporation of a pyruvate phosphokinase ATP generating system into the adenylate cyclase assay medium provided constant substrate levels. In the presence of the ATP generating system, the rate of cyclic AMP formation (basal, fluoride, and ACTH-activated) was proportional to enzyme concentration and was linear with time. Proportionality with respect to enzyme concentration as concerned the hormone-activated adenylate cyclase was achieved only when the ratio of hormone to enzyme protein was kept constant. The temperature optimum of the adenylate cyclase, basal or activated, was approximately 30 degrees. Michaelis-Menten kinetics were observed when the ratio of Mg2+ to ATP was approximately 6:1. Both calcium and ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid completely inhibited the adenylate cyclase system at concentrations of 5 and 0.5 mM, respectively. GTP was inhibitory at concentrations of 10-2 M but had little effect at lower concentrations. Freezing in liquid nitrogen and storage at -60 degrees exerted little effect on the fluoride-stimulated enzyme but lowered hormone stimulated activity. Preincubation in the presence of ACTH afforded a high degree of stabilization of the enzyme system while preincubation with a biologically inactive analog afforded no protection.
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PMID:Adenylate cyclase system of bovine adrenal plasma membranes. 16 47

Glucagon activated adenylate cyclase in a homogenate of a pheochromocytoma over the concentration range 1 times 10 minus 8M to 1 times 10 minus 6M. Several other hormones including adrenocorticotropin, thyrotropin, parathyroid hormone and histamine were without effect. The tumor glucagon receptor was characterized and found to be similar in several ways to the glucagon receptor previously reported in normal tissue such as liver and heart. One, the receptor specifically bound 125-I-glucagon. Two, solubilization of the pheochromocytoma abolished glucagon-activation of the adenylate cyclase. Three, glucagon-responsiveness of the adenylate cyclase was partially restored by the addition of phosphatidylserine to the incubations. One major difference was observed between the glucagon receptor in tumor tissue and that in liver and heart, namely, a marked lability in 125-I-glucagon binding and adenylate cyclase activity. Within four days, despite storage in liquid nitrogen, 75% of the binding activity and all of the adenylate cyclase activity in the solubilized preparation were lost. The factor(s) responsible for this lability remains unidentified.
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PMID:Characterization of the glucagon receptor in a pheochromocytoma. 16 16

In idiopathic or generalized epilepsy, serum glucose and cholesterol concentrations tend to be low, especially just before the seizure. Glucose tolerance curves are abnormal and variable. The electrolyte balance is disturbed, and epileptics tend to go readily into alkalosis. Serum [Na+] is usually unaffected, but [K+] is normal to low between attacks and increases during and after the seizure. Serum [Cl-] is usually high just before the seizure. Epileptics are generally mildly hypocalcemic, especially in the period before the seizure. Serum urea and nonprotein nitrogen values are low between paroxysms but increase after the seizure. Serum protein concentration is usually normal. Stress, which releases epinephrine and corticotropin, results in high serum citrate concentration, which probably contributes to decreased serum [Ca2+] just before a seizure. In the healthy individual, any increase in serum citrate is accompanied by increasing [Ca2+]. In the rabbit, convulsions can be induced with corticotropin, a result of increased serum citrate concentration coupled with a decrease in [Ca2+]. The net result is severe hypo-ionic-calcemia. A similar phenomenon has been reported in a few humans. Administration of insulin causes serum citrate concentrations to decrease. Apparently, the dynamic system that controls glucose and lipid metabolism, and thus electrolyte balance, through the hormones epinephrine, corticotropin, insulin, glucagon, calcitonin, and parathormone, is abnormal in the epileptic.
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PMID:Clinical biochemistry of epilepsy. I. Nature of the disease and a review of the chemical findings in epilepsy. 22 Nov 36

The simultaneous purification and concentration of synthetic human beta-endorphin from plasma is described, which when used together with an appropriate isocratic high-performance liquid chromatographic-electrochemical detection (HPLC-ED) system allows the determination of elevated physiological levels of beta-endorphin. Purification of plasma was gained by flash-freezing in liquid nitrogen, acidifying with 100 microliters of trifluoroacetic acid (10%, v/v) per ml of plasma, thawing at 4 degrees C and centrifuging to remove any precipitate. Solid-phase extraction with silica sorbent was utilised, which allowed further isolation of the analyte, a method of concentration and a procedure whereby beta-endorphin could be transferred to the HPLC mobile phase. Silica sorbent demonstrated greater selectivity than C18 for synthetic human beta-endorphin and, in addition, provided improved recovery of this analyte when utilising elution volumes of 500 microliters or less. Proteolytic degradation and heparin-induced high-affinity binding in plasma were shown not to effect the recovery of beta-endorphin if blood was rapidly chilled and plasma quickly obtained, frozen and acidified. Validation of this purification/concentration method using [125I]beta-endorphin demonstrated a recovery of 85.6% which was not jeopardised when concentrating the sample twenty-fold. This provided an increase in the sensitivity of detection, when used in conjunction with HPLC-ED, from 5 ng/ml to 250 pg/ml.
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PMID:Measurement of beta-endorphin in human plasma by high-performance liquid chromatography with electrochemical detection: validation of a method employing the simultaneous purification and concentration of beta-endorphin. 138 50

The effect of tumor necrosis factor (TNF) on the hypothalamic-adrenal stress response was determined by infusion of TNF, 0, 2 x 10(5), and 4 x 10(5) U/kg per 24 hours, in parenterally fed male Wistar rats. Following infusions over 1 to 6 days, adrenal weight was increased with increasing dosage of TNF. Tumor necrosis factor at a dosage of 4 x 10(5) U/kg per 24 hours increased the plasma corticotropin level over the same period. In a further series of experiments the metabolic effects of TNF were compared with the effects of corticosterone, the predominant glucocorticoid in the rat. In comparison with controls, rats given corticosterone (75 mg subcutaneously) or TNF (2 x 10(5) U/kg per 24 hours) demonstrated decreased nitrogen balance and diminished carcass nitrogen content over a 6-day period. Tumor necrosis factor alone, however, induced a significant increase in liver nitrogen content and diminished jejunal mucosa DNA and protein levels in comparison with the control and corticosterone groups. Finally, adrenalectomized animals receiving basal corticosterone replacement were infused with TNF. Urinary nitrogen loss was significantly diminished in these animals compared with sham adrenalectomized controls, indicating that an intact adrenal stress response is necessary for the increased nitrogen loss following TNF infusion. Tumor necrosis factor may exert an important regulatory influence on the interorgan substrate flux that occurs during critical illness. The effects of TNF on skeletal muscle proteolysis can be simulated by adrenal glucocorticoid administration. The effects of this cytokine on visceral organs appear to be unique to TNF and cannot be reproduced by the administration of glucocorticoids alone.
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PMID:Are the catabolic effects of tumor necrosis factor mediated by glucocorticoids? 215 19

Plasma levels of the N-terminal peptide of proopiomelanocortin (NPP) were measured in rainbow trout, Salmo gairdneri, following treatment of handling stress with or without administration of dexamethasone, adaptation to white and black background, and maintenance on a constant light/dark cycle. Effects of exogenously administered NPP on plasma constituents were also examined to provide insight into the biological significance of NPP. Thirty minutes of handling stress in shallow water had no effect on plasma levels of NPP during and after the stress period, whereas significant increases in plasma cortisol and glucose were observed. Intraperitoneal administration of dexamethasone blocked the stress-induced elevation of plasma levels of cortisol and caused a depression of plasma NPP. No difference was observed in plasma levels of NPP between trout adapted to a white background and those adapted to a black background. No diurnal changes in NPP were observed under an artificial light/dark cycle (14L/10D light cycle, 0500-1900 hr light) in May and September. Thus, plasma levels of NPP were considerably constant under various physiological conditions, and no synchronism was observed between plasma NPP and cortisol, although NPP modifies the corticotropin-induced release of cortisol from the interrenal. Plasma constituents such as cortisol, total protein, albumin, plasma amino nitrogen, glucose, free fatty acid, ketone body, sodium, potassium, calcium, and magnesium were not altered by intraperitoneal injections of NPP (1 or 10 micrograms) once daily for 6 days (total of six injections) or once every other day for 28 days (14 injections). High concentrations of NPP were found in the plasma 24 hr after cessation of the serial injections of NPP (10 micrograms), suggesting slow metabolic clearance of the peptide.
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PMID:Plasma profiles of the N-terminal peptide of proopiomelanocortin in the rainbow trout with reference to stress. 229 28

The effect of hypoxic hypoxia (HH) and carbon monoxide hypoxia (COH) on adrenal medullary (MQ) and cortical (CQ) blood flow (radiolabeled microsphere technique) was studied in pentobarbital sodium-anesthetized, mechanically ventilated dogs. Animals were exposed to 60 min of hypoxia (arterial O2 content 8 vol%) induced by adding either nitrogen (HH, n = 6) or carbon monoxide (COH, n = 6) to the inspired gas. Whole adrenal Q and CQ increased by 70 and 50%, respectively, with HH but were unchanged during COH. MQ, however, increased threefold during both HH and COH. HH and COH both increased arterial levels of epinephrine, corticosteroids, and adrenocorticotropic hormone (ACTH). To determine whether the increase in CQ during HH was because of HH-induced increases in mean arterial blood pressure (MAP, approximately 20 mmHg), an additional group of animals (n = 6) was exposed to HH but had MAP maintained at control levels using a pressurized-bottle system. MAP control did not alter the CQ response to HH. We conclude that MQ appears to be associated with medullary secretory activity during hypoxia and that HH and COH stimulate adrenal medullary secretion equally. In contrast, CQ increases only with HH, despite similar increases in ACTH and corticosteroid levels during HH and COH, suggesting that an alternative mechanism is responsible for increased cortical blood flow during HH.
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PMID:Regional adrenal blood flow during hypoxia in anesthetized, ventilated dogs. 253 47

Metabolic defects in obese (fa/fa) Zucker rats have previously been shown to be reversed by adrenalectomy; however, hypercorticosteronemia has not been demonstrated. We now report that the total daily excretion of corticosterone and urea nitrogen are significantly greater (P less than 0.01) in obese Zucker rats than in age-matched lean Zucker rats. This excessive excretion of corticosterone is not of autonomous adrenal origin, since dexamethasone treatment (20 micrograms/kg X day) for 2 days induced a proportionate reduction in corticosterone excretion (approximately 50%) in both obese and lean Zucker rats. Corticosterone excretion was further suppressed to levels not different from those in lean rats after 2 days of dexamethasone (40 micrograms/kg X day). Both the peak and total pituitary beta-endorphin secretion in response to an iv bolus of corticotropin-releasing factor (CRF) were diminished in obese Zuckers. The response to CRF in obese Zucker rats was dampened and superimposable on that of dexamethasone-treated lean Zucker rats, suggesting the existence of chronic hypercorticosteronemia as a component of this genetic obesity. These observations provide evidence for a compensatory alteration of the pituitary-adrenal axis. We suggest that corticosterone turnover may be increased in obese Zucker rats.
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PMID:Hypercorticosteronuria and diminished pituitary responsiveness to corticotropin-releasing factor in obese Zucker rats. 293 45

Several new problems in obesitology were pointed out in this book and commented with respect to experiments and experiences of our working group. The problem of the low triiodothyronine (T3) syndrome was treated in chapter 2. The decrease of serum T3 and increase of serum reverse T3 in obese subjects was induced by several factors, namely by fasting. A resistance to administered thyroxine and triiodothyronine was observed in these patients. This energy saving mechanism is at variance with slimming regimens. The prevention and treatment of this awkward complication was discussed. The next chapter (3) is concerned with the hormonal and metabolic effects of diet and motor activity in the course of slimming regimens. The different effects of diet and motor activity on epinephrine and norepinephrine in obese subjects were similar to those obtained by other investigators in nonobese humans. A great importance was attributed to an increased plasma level of cortisol in obese and nonobese subjects in the course of different forms of motor activity and related to a different intensity of exercise. Parallel to several of these experiments, beta-endorphin, thyroid hormones and glucagon were also estimated. It was suggested that motor activity for exercising subjects should not lead to an enhanced secretion of cortisol in view of the health deteriorating effects of increased cortisolemia and in view of an already stimulated secretion of this hormone in obese subjects on basal conditions. Vice versa, a decreased cortisolemia should be obtained in obese subjects treated with an appropriate motor activity and diet. It has been shown that diet without motor activity reduced the level of plasma androgens but in cooperation with motor activity, the level of androgens remained unaltered in the course of the reducing regimen. The conservation of a normal or even higher level of androgens is probably prerequisite for a positive nitrogen balance observed in the course of a combined slimming regimen, while diet without motor activity led in the studied conditions to a negative nitrogen balance. Chapter 4 was devoted to the role of motor activity in slimming regimens. In view of the metabolic effects of motor activity and the clinical late effects of obesity (osteoarthritis of the knees, hips and spine, arterial hypertension, overload of the cardiovascular system, diabetes mellitus etc.), a selection of motor activities was proposed. According to our long experience, we do not recommend jogging, running, jumping and all sports leading to collisions of players.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:New trends in obesitology. 307 25

The amine precursor uptake and decarboxylase (APUD) cells and neuroepithelial bodies (NEBs) in airways of adult rats have been studied by immunocytochemical methods for the presence of adrenocorticotropic hormone (ACTH), growth hormone (hGH), calcitonin, and bombesin in control animals and following exposure to nitrosodiethylamine and nitrogen dioxide (NO2). Calcitonin-like immunoreactivity (CLIR) is present in APUD cells of the trachea and bronchioles and in NEBs in the lung. Rats treated with nitrosodiethylamine and NO2 exhibit increased numbers of argyrophilic cells but no increase in cells containing specific intracytoplasmic CLIR. The presence of ACTH, hGH, and bombesin in respiratory tract APUD cells was not observed. These studies indicate that APUD cells in the trachea and bronchioles of adult rats harbor endocrine cells with immunohistochemical characteristics similar to C cells of the thyroid, and that these cell do not appear to be altered in number when rats are treated with agents known to produce an increase in APUD cells.
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PMID:Immunocytochemical studies of APUD cells in airways: effects of nitrosodiethylamine and nitrogen dioxide. 612 41


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