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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma and adrenal cholesterol disposition have been examined to gain further insight into the mechanisms by which 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) treatment decreases the diurnal peak in plasma corticosterone concentrations. TCDD induces an increase in plasma cholesterol concentration that is nearly complete on Day 2, at least 2 days before the most pronounced increase in adrenal cholesterol concentration (Days 4-6). This adrenal increase involves both free cholesterol and cholesterol esters, in contrast to the response to dietary hypercholesterolemia where only cholesterol esters increase. Although adrenocorticotropin (ACTH) does not increase adrenal mitochondrial cholesterol in normal rats (cholesterol turnover is faster than cholesterol uptake), this response changes between Days 6 and 9 after TCDD treatment such that ACTH then stimulates accumulation of mitochondrial cholesterol. This additional cholesterol is fully available to cytochrome P-450SCC, as judged both by active cholesterol metabolism in isolated mitochondria and by increased cholesterol-P-450SCC complex formation. The accompanying in vivo suppression of the peak plasma corticosterone concentration suggests a TCDD-induced inhibition of cholesterol side-chain cleavage (SCC). Consistent with this hypothesis, similar effects on adrenal mitochondrial cholesterol were produced by in vivo administration of the cholesterol side-chain cleavage inhibitor, aminoglutethimide, to ACTH-stimulated rats. Although the putative TCDD-induced inhibitory factor is apparently readily lost from mitochondria during preparation, inhibition may be retained in isolated cells. TCDD, therefore, affects adrenal cholesterol regulation by at least two mechanisms. Adrenal cholesterol content increases in part as a consequence of elevated plasma cholesterol, and cholesterol side-chain cleavage becomes partially inhibited in vivo.
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PMID:Hypercholesterolemia and the regulation of adrenal steroidogenesis in 2,3,7,8-tetrachlorodibenzo-p-dioxin-treated rats. 376 17

Adrenal rest tumors of the testes may occur in conditions associated with increased circulating adrenocorticotropic hormone (ACTH), including congenital adrenal hyperplasia (CAH) and Addison disease. Sonographically, these tumors appear as multiple round, hypoechoic nodules near the testicular hilus and are usually bilateral. They may undergo extensive fibrosis and become hyperechoic with acoustic shadowing. In the absence of excess ACTH or characteristic ultrasound findings, biopsy is recommended to exclude malignancy. Because malignant degeneration is very rare, close clinical and sonographic follow-up without biopsy is generally sufficient. Serial sonograms are useful to document stability or regression of tumor size during glucocorticoid replacement therapy.
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PMID:Intratesticular adrenal rests diagnosed by ultrasound. 388 14

Adrenal and/or thyroid gland function tests were evaluated in horses at various times during short-term therapy with phenylbutazone, stanozolol, and boldenone undecylenate. There were no significant treatment or time effects on mean basal plasma cortisol concentrations in horses during treatment with the following: phenylbutazone, given twice daily (4 to 5 mg/kg, IV) for 5 days; stanozolol, given twice weekly (0.55 mg/kg, IM) for 12 days; boldenone undecylenate, given twice weekly (1.1 mg/kg, IM) for 12 days; or nothing. There was no significant effect of phenylbutazone treatment on the changes in plasma cortisol concentration during the combined dexamethasone-suppression adrenocorticotropic hormone (ACTH)-stimulation test. Plasma cortisol concentration was significantly decreased from base line at 3 hours after dexamethasone administration and was significantly increased from base line at 2 hours after ACTH in all horses (P less than 0.05). Likewise, the stimulation of basal plasma cortisol concentrations at 2 hours after administration of ACTH (P less than 0.05) was not affected by treatment with stanozolol or boldenone undecylenate. There were no significant treatment effects on mean basal plasma concentrations of thyroxine (T4) or triiodothyronine (T3) among horses during the following treatments: stanozolol, given twice weekly (0.55 mg/kg, IM) for 12 days; boldenone undecylenate, given twice weekly (1.1 mg/kg, IM) for 12 days; or nothing. There was a significant time effect on overall mean basal plasma T4 and T3 concentrations (P less than 0.05): plasma T4 was lower on day 8 than on days 1, 10, and 12; plasma T3 was higher on day 8 than on days 4 and 12.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of phenylbutazone and anabolic steroids on adrenal and thyroid gland function tests in healthy horses. 399 2

(Log dose)-response curves have been determined for lipolysis and for the conversion of glucose-(14)C to (14)CO(2) by adipose tissue from rats in the presence of epinephrine, corticotropin, and thyrotropin. The stimulatory effect of epinephrine on lipolysis was greater than that of corticotropin or thyrotropin. Lipolysis induced by epinephrine was inhibited by propranolol but only slightly by phenoxybenzamine, whereas lipolysis induced by corticotropin was inhibited by phenoxybenzamine to a much greater extent than by propranolol. Neither blocking drug had a pronounced effect on the response to thyrotropin. Epinephrine stimulated the oxidation of glucose-(14)C to CO(2) more than did either thyrotropin or corticotropin. Moreover, epinephrine stimulated the conversion of glucose-(14)C to CO(2) and fatty acids even when lipolysis was not increased. These studies indicate that epinephrine can affect glucose utilization independently of its effect on lipolysis.
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PMID:Effects of epinephrine, corticotropin, and thyrotropin on lipolysis and glucose oxidation in rat adipose tissue. 429 37

In the ovariectomized rat, the adrenal gland secretes progesterone. Adrenocorticotropin treatment elevates concentrations of this steroid in plasma, and inhibitors of adrenocorticotropin or progesterone biosynthesis lower the concentration. Adrenocorticotropin controls progesterone secretion by the adrenal but not by the ovary. Adrenal progesterone and its mode of control may have important influences on reproductive processes.
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PMID:Endocrine control of adrenal progesterone secretion in the ovariectomized rat. 430 58

Epinephrine stimulated lipolysis and the uptake of oxygen by subcutaneous adipose cells of man. When glucose-(14)C was present in the medium, its utilization was not increased by epinephrine, although lipolysis was accelerated. Insulin did not reduce the production of fatty acids that had been stimulated by epinephrine. The combination of human growth hormone and cortisol stimulated the production of fatty acids by isolated human adipose cells to a lesser extent than epinephrine. When human growth hormone or cortisol was used singly, or when bovine growth hormone was added in combination with cortisol, no effect on fatty acid production was observed. Furthermore, an acetone-dried preparation of human pituitary glands, which was shown to stimulate lipolysis in rat adipose cells, had no effect on fatty acid formation in human adipose cells. This suggested that the human pituitary gland contained no more potent lipolytic agents than growth hormone and was supported by the lack of response of human adipose cells to purified corticotropin.
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PMID:Studies on lipolysis in human adipose cells. 602 Dec 10

In primary 2-day cultured bovine adrenocortical cells, adrenaline stimulated the steroidogenesis, while the effect of adrenaline did not appear in the freshly isolated cells. Thus the primary 2-day cultured cells were used to study the effect of adrenaline on steroidogenesis. Adrenaline showed the steroidogenesis-stimulating effect at concentrations higher than 10(-9) M, and the maximum effect was obtained between 10(-6) M and 10(-5) M in the primary 2-day cultured cells. The maximum effect of adrenaline was 50-70% of that of adrenocorticotropic hormone (ACTH). Noradrenaline, isoproterenol and phenylephrine also stimulated the steroidogenesis. However, the order of the potency was isoproterenol much greater than adrenaline = noradrenaline much much greater than phenylephrine. Propranolol and alprenolol inhibited the effect of adrenaline, but phenoxybenzamine and phentolamine did not inhibit the effect. Moreover, adrenaline stimulated the cyclic AMP production dose-dependently at concentrations higher than 10(-8) M. These results suggest that there are steroidogenesis-linked adrenergic receptors in primary 2-day cultured bovine adrenocortical cell membrane and that the steroidogenesis-stimulating effect of adrenaline occurs through the beta-adrenergic receptor.
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PMID:Effect of adrenaline on steroidogenesis in primary cultured bovine adrenocortical cells. 609 1

Characteristics of the alpha-adrenergic stimulation of ACTH, beta-endorphin + beta-LPH and alpha-MSH release were studied in rat anterior pituitary cells in primary culture. Parallel changes of ACTH, beta-endorphin + beta-LPH and alpha-MSh release were found under all stimulatory and inhibitory conditions by natural and synthetic catecholamine agonists and antagonists. (-)Epinephrine and (-)norepinephrine lead to a 8--10-fold stimulation of peptide release at ED50 values of 20 and 90 nM, respectively. The stereoselectivity of the alpha-adrenergic stimulatory action on peptide release is indicated by a 100-fold higher activity of (-)- than (+)norepinephrine while (-)epinephrine is 10 times more potent than the corresponding (+) stereoisomer. The involvement of a typical alpha-adrenergic mechanism in the control of release of ACTH, beta-endorphin and related peptides in rat anterior pituitary gland is indicated by the following order of potency of a series of catecholaminergic agents (ED50 values): (-)epinephrine (20 nM) greater than (-)norepinephrine (90 nm) greater than phenylephrine (400 nM) greater than isoproterenol (6000 nM). The stimulatory effect of (-)epinephrine or phenylephrine is completely reversed by low concentrations of the alpha-adrenergic antagonist phentolamine while the beta-adrenergic antagonist propranolol has no effect up to 10 muM. Beside providing an easily accessible pure population of post-synaptic alpha-adrenergic receptors having potential applications as a model for other less accessible alpha-adrenergic brain systems, the present data suggest the possibility of the direct involvement of a catecholamine in the physiological control of ACTH secretion in the rat anterior pituitary gland.
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PMID:Parallel stimulation of ACTH, beta-LPH + beta-endorphin and alpha-MSH release by alpha-adrenergic agents in rat anterior pituitary cells in culture. 611

The effects of adrenocorticotropic hormone (ACTH) administration to guinea pigs on the activities of adrenal microsomal monooxygenases were studied. ACTH treatment decreased the rates of adrenal benzphetamine (BZ) demethylation and benzo[a]pyrene (BP) hydroxylation but had no effect on the same reactions in hepatic microsomes. Adrenal microsomal steroid hydroxylation reactions were unaffected (21-hydroxylation) or stimulated (17 alpha-hydroxylation) by ACTH. Although ACTH treatment decreased adrenal BP hydroxylase activity, the relative quantity of the various BP metabolites, as determined by HPLC, did not change. Adrenal microsomal cytochrome P-450 concentrations were decreased by ACTH but proportionately less than the decreases in adrenal xenobiotic metabolism. The maximal type I spectral changes produced by xenobiotics in adrenal microsomes were decreased in size by ACTH treatment, but steroid-induced difference spectra were unaffected. The results indicate that ACTH selectively decreases the rates of adrenal xenobiotic metabolism, perhaps by producing a selective decline in the concentration(s) of those cytochromes P-450 involved in the metabolism of foreign compounds.
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PMID:Differential effects of adrenocorticotropic hormone on adrenal microsomal xenobiotic and steroid metabolism in guinea pigs. 612 29

Adrenal glands from early, mid, and late fetuses of rabbit, guinea pig, and rat, and from newborn animals of each species, were incubated for 1-4 h with and without 0.1 nM-1 microM ACTH, alpha- or beta-melanocyte-stimulating hormone (alpha MSH or beta MSH). The effects of the peptides were measured on production of glucocorticoids, and on incorporation of labeled thymidine or leucine into DNA or protein, respectively. The findings were similar in all three species. ACTH stimulated synthesis of glucocorticoids throughout fetal life. Potency increased progressively, as reflected by declining minimal effective dose and rising maximal response. In early and mid fetus alpha MSH and beta MSH caused a modest glucocorticoid steroidogenic effect. ACTH and alpha MSH stimulated DNA and protein synthesis in the early and mid fetal gland. alpha MSH was more potent than ACTH in these respects, minimal effective dose being generally 10 times less and maximal response 25-200% greater. The effects diminished or disappeared in the late fetal and newborn gland. These data indicate that alpha- and beta MSH possess steroidogenic or growth-promoting properties, or both, for the fetal adrenal gland.
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PMID:Effects of melanotropic peptides on fetal adrenal gland. 624 34


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