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)

Subcutaneous administration of ACTH 1-24 to mice increased the incorporation of [3H]lysine into brain and liver proteins, an effect which resembled that due to footshock. Corticosterone administration did not mimic these effects. ACTH 4-10 increased the [3H]lysine incorporation into brain or liver. These results are consistent with ACTH mediating the effects of footshock. However, dexamethasone decreased the brain responses to both footshock and ACTH, but while the liver response to ACTH was blocked, the footshock response was only diminished. This suggests a neural component in the response of the liver and possibly the brain. Intraventricular administration of ACTH 1-24 or ACTH 4-10 (D-phe), but not ACTH 4-10, increased [3H]lysine incorporation into brain protein. These neurochemical responses parallelled a distinctive pattern of behavior characterized by stretching, yawning and excessive grooming. Treatment for 3 days with long-acting preparations of ACTH 4-10, ACTH 4-10 (D-phe) or ACTH 1-24 increased the conversion of [3H]tyrosine into dopamine but not norepinephrine, alpha-MSH, beta-MSH or LVP had no such effect. Similar treatment with ACTH 4-10 or ACTH 1-24 increased striatal tyrosine hydroxylase activity measured in vitro, but did not significantly alter the enzyme activity from other brain regions. We conclude that ACTH peptides can stimulate protein and dopamine metabolism in mouse brain and that LVP has no such effects.
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PMID:Neurochemical responses of mice to ACTH and lysine vasopressin. 1 13

A specific radioimmunoassay is described which allows the simultaneous determination of serum corticosterone and deoxycortisol. The method involves extraction with dichloromethane, purification by paper chromatography in a modified Bush-system and quantitation by radioimmunoassay. The normal serum concentration of both steroids were found to be dependent on sex and menstrual cycle. Mean concentrations (+/- S.D.) in males, females (follicular phase) and females (luteal phase) were 4210 +/- 2170 ng/1,2410 + 1480 ng/1 and 4390 +/- 2320 ng/1 for corticosterone and 499 +/- 273 ng/1, 207 +/- 152 ng/1 and 335 +/- 182 ng/1 for deoxycortisol. After adrenal stimulation by corticotropin itself or by insulin induced hypoglycemia, the serum concentrations of corticosterone became significantly higher than those of deoxycortisol. After oral administration of dexamethasone serum concentrations of both steroids were suppressed to levels below the limit of the normal range. One hour after oral metyrapone administration at midnight, serum corticosterone decreased, while serum deoxycortisol increased by a factor of about five. After eight hours serum concentrations of both steroids were increased considerably. Corticosterone attained levels slightly higher than the normal range and deoxycortisol rose to levels which were higher than the normal mean concentrations by a factor of about 500.
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PMID:Simultaneous radioimmunoassay for corticosterone and deoxycortisol in human serum: sex differences in the mean serum concentrations. 19 62

To define the role of calcium during corticotropin-induced steroidogenesis, adrenal sections were incubated under conditions of varying degrees of calcium depletion. Corticosterone production, [14C]leucine incorporation into protein, and tissue cyclic AMP levels were measured concomitantly. Omitting calcium from the incubation media inhibited all three processes to variable extents, thus limiting conclusions regarding which process is most dependent on calcium. While calcium was required during the early phase of corticotropin action, it was not required during later phases: rapid induction of calcium deficiency did not diminish the heightened rate of steroidogenesis previously induced by corticotropin in the presence of calcium. Thus, while calcium is required for induction of steroidogenesis factor(s), the operation of the latter is not dependent upon calcium in the extracellular fluid.
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PMID:Localization of the metabolic processes affected by calcium during corticotropin action. 19 12

Studies have been made with the mouse pituitary tumor cell line AtT-20 in culture to determine whether or not the suppression of pituitary corticotropin messenger RNA activity observed upon the administration of glucocorticoids to adrenalectomized rats is due to a direct action of these steroid hormones on the pituitary. The levels of corticotropin messenger RNA activity in AtT-20 cells treated with various steroid hormones were measured with the use of the cell-free protein-synthesizing system derived from wheat germ. The addition of dexamethasone to culture medium reduced the level of corticotropin messenger RNA activity to 30-40% of that in untreated cells. Corticosterone and cortisol exhibited a suppressive effect to a lesser extent. In contrast, nonglucocorticoids such as testosterone and 17beta-estradiol were essentially ineffective. These results indicate that at least part of the glucocorticoid action is exerted directly on the pituitary to suppress corticotropin messenger RNA activity.
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PMID:Effects of steroid hormones on the level of corticotropin messenger RNA activity in cultured mouse-pituitary-tumor cells. 20 19

The acute in vitro action of adrenocorticotropin (ACTH) and corticosterone alone and in combination were determined in the Cloudman S-91 melanoma grown in vivo. Hormone-treated melanoma dice (5-240 min) were analyzed for tyrosinase activity (EC 1.14.18.1), cyclic AMP (cAMP) and cyclic GMP (cGMP). ACTH elevated cAMP levels in the S-91 melanoma. However, these increases in cAMP were not accompanied by increased tyrosinase activity. Corticosterone depressed cAMP levels while stimulating tyrosinase activity. ACTH plus corticosterone produced an early cAMP peak followed by depression. ACTH plus corticosterone stimulated tyrosine activity coincident with the early cAMP peak followed by a drop in tyrosinase activity which was subsequently elevated. cGMP levels were not altered by any hormone treatment. The results indicate that cAMP is not the sole modulator of tyrosinase activity and suggest the interaction of ACTH, corticosterone and cAMP in the regulation of melanoma tyrosinase activity.
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PMID:Glucocorticoid modulation of adrenocorticotropin-induced melanogenesis in the Cloudman S-91 melanoma in vitro. 20 85

The acute in vitro action of adrenocorticotropin (ACTH) and corticosterone alone and in combination were determined in the Harding-Passey (HP) melanoma grown in vivo. Hormone treated melanoma dice (5--240 min) were analyzed for tyrosinase activity, cyclic AMP (cAMP) and cyclic GMP (cGMP). ACTH elevated cAMP and cGMP levels 20- and 13-fold, respectively, in the HP melanoma. However, these large increases in cyclic nucleotide levels were accompanied by only a 49% increase in tyrosinase activity. Corticosterone elicited a similar response. ACTH plus corticosterone produced an early cAMP and cGMP peak followed by depression. ACTH plus corticosterone stimulated tyrosinase activity coincident with the early cyclic nucleotide peak followed by a drop in tyrosinase activity which was subsequently elevated. The results indicate that neither cAMP nor cGMP are the sole modulators of tyrosinase activity and suggest the interaction of ACTH, corticosterone and cyclic nucleotides in the regulation of melanoma tyrosinase activity.
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PMID:Interaction of ACTH, corticosterone and cyclic nucleotides in Harding-Passey melanoma melanogenesis. 21 Jul 23

The bibliography concerning the interaction of the thymus with other endocrines is summarized. The thymus, the lymph nodes and the spleen of Sprague-Dawley rats were extracted with the method of Bezssonoff and Comsa and the extracts fractionated with the method of Bernardi and Comsa. The animals were (1) normal, (2) adrenalectomized, (3) adrenalectomized and substituted with one or several corticosteroids, (4) adrenalectomized and thymectomized, (5) thyroidectomized, (6) thyroidectomized and substituted with thyroxine, (7 and 8) castrated (males or females), (9 and 10) castrates substituted with sexual hormones, (11) castrated and adrenalectomized, (12) castrated and thyroidectomized, (13) castrated, adrenalectomized and thyroidectomized, (14) hypophysectomized, and (15) hypophysectomized and substituted with one hypophyseal hormone. In the Bernardi-Comsa preparations hormone was determined by UV-spectrophotometry. Adrenalectomy resulted in a significant decrease of the hormone content of the thymus (which was still more attenuated by cortisol) and its increase in the lymph nodes and the spleen. Corticosterone and desoxycorticosterone increased the hormone content in all three tissues, whilst aldosterone increased it in the thymus and decreased it in the lymph nodes and the spleen. Thyroidectomy resulted in a significant decrease of the hormone in the thymus and its quasi-disappearance from the lymph nodes and the spleen. This was prevented by thyroxine therapy. Castration resulted in an increase of the hormone content in all three tissues. This was prevented by sexual hormone therapy. Hypophysectomy resulted in decrease of the hormone content in all three tissues. This was prevented by injections with growth hormone, corticotropin and thyrotrophin. These results were compared with those of histological examinations of thymus, lymph nodes and spleen in the corresponding experimental groups. The consistency was found satisfactory.
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PMID:Hormonal influences on the secretion of the thymus. 57 3

Human adrenal glands produce considerable amounts of the C-19 steroids dehydroepiandrosterone (DHEA) and androstenedione. To investigate the capability of rodent adrenals to produce these steroids, cell suspensions of mouse and rat adrenal glands were incubated in the absence and presence of adrenocorticotropic hormone (ACTH). Corticosterone levels in the incubation medium increased dramatically in the presence of ACTH, but no significant amounts of 17-hydroxyprogesterone or androstenedione could be detected. This indicates that the adrenals of rat and mouse lack the enzyme 17 alpha-hydroxylase. Absence of plasma cortisol in the presence of high levels of corticosterone confirmed these data. Plasma levels of androstenedione were significantly decreased in castrated male rats as compared to levels observed in intact males, showing the contribution of the testes to the plasma content of androstenedione. Very low levels of androstenedione were observed in female, male and castrated male mice. Plasma concentrations of DHEA were not detectable in intact and castrated male mice and rats. It is concluded that rat and mouse lack the enzyme necessary to synthesize adrenal C-19 steroids and that the adrenals in these animals, therefore, do not contribute to plasma levels of androstenedione and DHEA.
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PMID:Adrenal glands of mouse and rat do not synthesize androgens. 131 93

To investigate the possible involvement of pituitary hormones in the regulation of steroidogenesis during reptilian sexual differentiation, we tested the ability of gonadotropin (ovine FSH), adrenocorticotropin (porcine ACTH), and growth hormone (bovine GH) to stimulate in vitro steroidogenesis in embryonic adrenal-kidney-gonad complexes (AKGs) of a turtle, Trachemys scripta, during and after the temperature-sensitive period for sex determination (TSP). Radioimmunoassays were used to measure progesterone, testosterone, estradiol, and corticosterone in incubation media; additionally, immunoreactive ACTH was measured in plasma. Presumptive male and female AKGs were stimulated by both FSH and ACTH at each stage investigated. Secretion of progesterone and corticosterone was usually far greater than that of testosterone or estradiol in both basal and hormone-stimulated incubations. In general, AKGs from presumptive males secreted more progesterone and corticosterone than AKGs from presumptive females. Progesterone and estradiol secretions were stimulated by both FSH and ACTH, but testosterone secretion was stimulated only by ACTH. Corticosterone secretion was strongly stimulated by ACTH. GH failed to significantly stimulate steroid secretion. Plasma ACTH levels were significantly higher in males than in females, and both sexes had significantly higher plasma levels of ACTH after the TSP compared to during the TSP. Our data demonstrate that during the temperature-sensitive period AKGs are responsive to both gonadotropin and ACTH, and that there are significant sex differences in steroidogenesis, sensitivity to gonadotropin and ACTH, and plasma ACTH levels.
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PMID:Stimulation of in vitro steroidogenesis by pituitary hormones in a turtle (Trachemys scripta) within the temperature-sensitive period for sex determination. 133 78

Intracerebroventricularly (icv) administered corticotropin-releasing hormone (CRH) produces a dose-dependent increase in heart rate in association with behavioral activation. The present study was designed to investigate whether these CRH-induced responses are dependent on adrenal function. The effects of adrenalectomy (ADX) and subsequent corticosterone replacement were studied. Administration icv of 300 ng of CRH failed to produce behavioral activation and tachycardia in ADX rats. Corticosterone replacement restored the CRH-induced behavioral response to preoperative levels, whereas the CRH-induced tachycardia was partially restored. This latter result may be related to the fact that the baseline heart rate of ADX animals appeared to be significantly higher than that of corticosterone-treated ADX animals. It is concluded that circulating adrenal corticosterone in ADX rats is involved in the expression of the behavioral and cardiac effect of central CRH.
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PMID:Behavioral and cardiac responses after intracerebroventricular corticotropin-releasing hormone (CRH) administration: role of adrenal cortical hormones. 139 56


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