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 histological and ultrastructural study has demonstrated that cutaneous pigmentation in primary biliary cirrhosis (PBC) is due to the presence of increased amounts of melanin, widely dispersed throughout both epidermis and dermis. No deposits of stainable iron were observed. Compared with skin from matched sites from control patients with alcoholic cirrhosis and no pigmentation, the melanocyte: keratinocyte ratio was not significantly higher in PBC. However, in PBC, melanosomes persisted to unusually high levels in the epidermis and were packaged in larger membrane-bound clusters than was the case in the controls. Whether excess melanin results from increased melanogenesis or defective melanin degradation remains unclear, although there is some evidence favouring the latter mechanism. No hormonal (beta-MSH and ACTH) or chemical (bile salt irritation) stimuli to increase melanogenesis were demonstrated.
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PMID:Melanin pigmentation of the skin in primary biliary cirrhosis. 627 1

ACTH and lipotropins (beta- and gamma-LPH) are synthesized from a common precursor by the pituitary corticotropic cell. We have measured LPH plasma levels under physiological and pathological conditions and we have compared them with ACTH plasma levels in the same circumstances. Spontaneous variations (nycthemeral rhythm) in LPH, ACTH and cortisol plasma levels were parallel, while responses to Dexamethasone freination test and stress (Insulin induced hypoglycemia) or more specific stimulation (Metopirone, lysine-vasopressin) were parallel and superimposable. LPH levels were always higher than ACTH levels in two pathological circumstances: chronic renal failure and Cushing's syndromes with ectopic ACTH producing tumors. The determination of both ACTH and LPH levels assists the diagnosis of corticotropic insufficiency and etiologic investigation of Cushing's syndrome, after hypercorticolism had been established. Although unable to confirm the presence of corticotropic adenoma in patients with Cushing's disease, or the predict effectiveness of pituitary surgery, these determination bring good arguments for treated Cushing's diseases follow up.
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PMID:[ACTH, beta-endorphin and lipotropins: physiopathological studies in man (author's transl)]. 628 91

Human fetal adrenal (HFA) tissue was maintained in organ culture to evaluate the biosynthesis of prostaglandins and hormonal regulation of prostaglandin formation by this tissue. The HFA tissue secreted substantial amounts of prostaglandin E(2), prostaglandin F(2alpha), 13,14-dihydro-15-ketoprostaglandin F(2alpha), 6-ketoprostaglandin F(1alpha), and thromboxane B(2); secretion of prostaglandin D(2) could not be demonstrated. Prostaglandin biosynthesis in HFA tissue was inhibited in a time-dependent manner by corticotropin (ACTH; 0.4 muM); by the fourth day of culture, the extent of inhibition of biosynthesis of each prostaglandin was 60-90%. Progesterone (1 muM), cortisol (1 muM), and dexamethasone (1 muM) inhibited prostaglandin biosynthesis whereas estradiol (1 muM) did not. Of the compounds tested for inhibitory activity, dexamethasone was the most potent. An inhibitor of 11beta-hydroxylase activity (metyrapone; 0.1 mM) effectively eliminated the inhibition of prostaglandin biosynthesis caused by corticotropin and progesterone. Metyrapone treatment alone caused a 3-fold increase in prostaglandin biosynthesis by fetal adrenal tissues. Similar stimulatory effects resulted from treatment with inhibitors of (i) 3beta-hydroxysteroid dehydrogenase (cyanoketone; 15 muM), (ii) steroid 17alpha-hydroxylase (SU 10603; 19 muM), and (iii) cholesterol side-chain cleavage (aminoglutethimide; 1 mM). Inhibition of prostaglandin biosynthesis by dexamethasone in the presence or absence of metyrapone was concentration dependent and 50% inhibition could be demonstrated at 1 nM. A competitive inhibitor of the binding of glucocorticosteroids to cytoplasmic receptors (cortisol 21-mesylate; 1 muM) significantly reduced the inhibition of prostaglandin biosynthesis effected by dexamethasone (10 nM). These findings suggest that prostaglandin biosynthesis in the HFA gland is regulated by endogenously synthesized glucocorticosteroids, the actions of which are mediated by a glucocorticosteroid receptor. Such glucocorticosteroids induce the synthesis of a substance that inhibits prostaglandin biosynthesis.
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PMID:Prostaglandin biosynthesis in the human fetal adrenal gland: regulation by glucocorticosteroids. 629 39

Using a specific anti-rat transferrin (Tf) antiserum, Tf-like immunoreactivity (Tf-lir) was detected by immunostaining in intact rat pituitaries and in reaggregated pituitary cells cultured in serum-free medium. Tf-lir cells were present in the anterior pituitary (AP), and in the intermediate (IL) and neural lobes (NL). In the AP, Tf-lir cells were oval or polygonal. An unusual topographical distribution was found. Tf-lir cells mainly occurred as dense clusters in the lateral wings. In the central part of the AP, Tf-lir was found in flattened perisinusoidal cells. Double immunostaining for Tf and the different pituitary hormones showed that Tf-lir co-localized with some gonadotrophs and somatotrophs (7% and 3% of Tf-lir cells, respectively, in typical sections). No co-localization was seen with PRL, ACTH, TSH, or alpha-MSH. The distribution of Tf-lir cells and their cell shape completely differed from that of S-100-positive cells in the AP. In the IL, clusters of large stellate Tf-lir cells were found. Again, their distribution completely differed from S-100-positive cells. In the NL, diffuse staining was found. Double immunostaining of paraffin-embedded sections of reaggregate cell cultures of the AP did not reveal any co-localization of Tf-lir with ACTH, alpha-MSH, LH, FSH, TSH, GH, or PRL. In aggregates consisting of NL + IL cells, Tf-lir was located in clusters: no co-localization with ACTH or alpha-MSH could be demonstrated. Reaggregate cell cultures of AP and NL + IL secreted Tf-lir as measured by radioimmunoassay, at least during 21 days of culture. After metabolic labeling with [35S]-methionine and immunoprecipitation of [35S]-methionine-labeled material present in the culture medium of both AP and NL + IL aggregates with anti-Tf antiserum, a 35S-labeled substance was found, which on SDS-PAGE showed an apparent M(r) of approximately 78 KD, corresponding to the M(r) of rat Tf. The present data show that a specific population of cells of rat anterior pituitary is capable of synthesizing, storing, and secreting transferrin or a substance closely related to it. Cells different from melanotrophs and S-100 cells in the IL, as well as pituicytes in the NL, also appear to produce this material. We suggest that transferrin or a transferrin-like substance may have a local role in the transport of iron or other metals or may play a role as growth factor in the three lobes of the pituitary gland.
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PMID:Production of transferrin-like immunoreactivity by rat anterior pituitary and intermediate lobe. 760 20

The authors studied 15 patients at risk for central adrenocortical insufficiency to evaluate the role of naloxone in establishing the integrity of the hypothalamic-pituitary-adrenal axis. Each patient was admitted to the General Clinical Research Center for 2 days. Naloxone, 125 micrograms/kg body weight, was administered intravenously, and plasma adrenocorticotropic hormone (ACTH) and cortisol concentrations were measured at -15, 0, 30, 45, 60, 90, and 120 minutes. Metyrapone, 30 mg/kg body weight, was administered orally at 11 PM on the second day of hospitalization. Plasma ACTH, cortisol, and 11-deoxycortisol concentrations were measured at 8 AM pre- and postmetyrapone. The results of the metyrapone test were used to distinguish patients who had central adrenal insufficiency from those who were normal. In 11 patients who had a normal metyrapone test, the plasma ACTH level increased from 6 +/- 1 pmol/L at baseline to 11 +/- 2 pmol/L 30 minutes after naloxone administration. The plasma cortisol increased from 191 +/- 21 nmol/L at baseline to 379 +/- 47 nmol/L 45 minutes after naloxone administration. In four patients with central adrenal insufficiency, the plasma ACTH and cortisol concentrations did not increase after naloxone administration. Reliance solely on the individual ACTH and cortisol responses to naloxone would have permitted a correct decision regarding glucocorticoid replacement therapy in 14 (93%) of 15 patients. Naloxone stimulation testing may have a role in the clinical evaluation of patients with suspected central adrenocortical insufficiency.
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PMID:Naloxone-induced activation of the hypothalamic-pituitary-adrenal axis in suspected central adrenal insufficiency. 807 33

We hypothesized that augmented responses of glucoregulatory hormones in iron deficiency would enhance liver and muscle glycogenolysis, leading to increased gluconeogenic precursor (lactate) supply and upregulation of hepatic gluconeogenesis. Female weanling rats were randomly placed on either a mildly iron-deficient (-Fe; 15 mg Fe/kg diet) or an iron-sufficient (+Fe; 50 mg Fe/kg diet) diet for 4 wk and studied at rest and during exhaustive treadmill running. Hemoglobin was 9.0 +/- 0.2 and 13.1 +/- 0.3 g/dl in -Fe and +Fe, respectively, after 3.5 wk of dietary iron deficiency. Arterial plasma epinephrine (Epi), norepinephrine (NE), adrenocorticotropic hormone (ACTH), corticosterone, insulin, and glucagon levels were similar at rest in both groups, as were liver, gastrocnemius, and superficial and deep vastus medialis glycogen levels. Liver and kidney phosphoenolpyruvate carboxykinase (PEPCK) activities were similar in both groups. Maximum O2 consumption was decreased (22%) in -Fe. Respiratory exchange ratio (CO2 production/O2 consumption) was unaffected at rest but increased at maximum O2 consumption in -Fe. Time to exhaustion during a standardized running test (13.4 m/min, 0% grade) was decreased 45% in -Fe (63 +/- 5 vs. 116 +/- 10 min). During exercise, euglycemia was maintained in both groups, but blood lactate was elevated in -Fe. The mean net glycogen utilization during exercise was increased in liver (43%), soleus (33%), and superficial vastus medialis (106%) and decreased in the gastrocnemius (36%) in -Fe. Liver and kidney PEPCK activities were increased similarly at exhaustion in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Augmented glucoregulatory hormone concentrations during exhausting exercise in mildly iron-deficient rats. 823 58

Carcinoid of the thymus rarely occurs during childhood. The authors identified eight cases in patients younger than 17 years of age. All were associated with Cushing syndrome. Adrenocorticotropic hormone (ACTH) produced by the tumor may be released intermittently, delaying the findings of Cushing syndrome. The authors describe a case of ectopic ACTH production in a teenaged boy who had longstanding hyperpigmentation, increased ACTH levels, and normal cortisol levels. Magnetic resonance imaging of the pituitary had normal findings. Subsequently, severe Cushing syndrome developed. Computed tomography (CT) scans of the chest showed a mediastinal mass that proved to be a thymic carcinoid. The lesion was inoperable. Radiation and chemotherapy were of limited benefit. Metyrapone was used to control hypercortisolism. The patient died with extensive metastases 6 years after initial presentation. CT scans of the chest should be performed in an attempt to localize ectopic ACTH-producing tumors. Surgical excision of the lesion is the treatment of choice. Control of hypercortisolism is essential.
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PMID:Adrenocorticotropic hormone--producing thymic carcinoid in a teenager. 838 Jan 12

Recent studies performed with depressed patients and normal subjects suggest that corticosteroids may alter dopaminergic activity. We measured the time course of the interaction between corticosteroid and plasma homovanillic acid (HVA) levels in 10 young healthy subjects after the administration of 2 mg of dexamethasone in session 1 and after the administration of 4.5 g of metyrapone in session 2. Plasma levels of adrenocorticotropic hormone (ACTH), 11-desoxycortisol, cortisol, HVA, and prolactin (PRL) were measured at 08:00, 09:00, 12:00, 15:00, and 16:00 h on a baseline day and during both drug-administration sessions. Dexamethasone administration resulted in a significant decrease in plasma levels of ACTH, 11-desoxycortisol, and cortisol at all time points and to a significant decrease in PRL secretion in the early morning. Plasma HVA levels were unchanged after dexamethasone administration. Metyrapone administration resulted in a significant decrease in cortisol levels and a significant increase in ACTH and 11-desoxycortisol levels. Plasma HVA levels were significantly increased in the early morning, while PRL levels were unaltered. These results are discussed in relation to the neurochemical and behavioral changes associated with steroid administration and interpreted with regard to a possible association between HVA and PRL in the effects of corticosteroids on dopaminergic activity.
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PMID:Time course of the corticosteroid-dopaminergic interaction during metyrapone and dexamethasone administration. 853 9

Excess secretion of cortisol in depressed patients has been documented by a number of investigators, which is presumed secondary to increased corticotropin (ACTH) and ACTH-releasing hormone (CRH) secretion. To unmask the proposed increased central (CRH) drive, we administered metyrapone in the AM to 13 depressed and 13 age- and sex-matched normal control subjects. Metyrapone administration resulted in a prompt decrease in plasma cortisol and in an increase in 11-deoxycortisol, the inactive precursor, in all subjects. Both depressed patients and normal control subjects demonstrated clear increases in ACTH and beta-lipotropin/beta-endorphin production. There were no significant differences between patients and controls in any hormonal measures following metyrapone administration. These data suggest that: 1) in the absence of negative feedback (cortisol blockade), mildly to moderately depressed outpatients do not manifest increased central drive in the morning; and 2) the secretory capacity of the corticotropes do not differ between such depressed patients and controls.
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PMID:Normal pituitary response to metyrapone in the morning in depressed patients: implications for circadian regulation of corticotropin-releasing hormone secretion. 917 5

Transferrin (Tf), a major transport protein for iron in the blood and an essential growth factor in some tissues, acts via specific transferrin receptor (TfR). We studied the cellular distribution of Tf and TfR gene expression in 50 human nontumorous autopsy pituitaries and 42 surgically removed pituitary adenomas. Tf and TfR mRNA accumulation was correlated with Ki-67 proliferation marker. In nontumorous pituitaries without iron deposits Tf immunoreactivity was localized in some growth hormone, prolactin, adrenocorticotropin, thyrotropin, and luteinizing hormone cells. Most adenohypophysial cells were immunopositive for TfR. In pituitaries with iron deposits, Tf and TfR were localized only in iron-free cells. Tf mRNA and protein were present in 27 and 32 adenomas, respectively; Ki-67 labeling index of tumors positive for Tf mRNA was significantly higher than in those without transcript (0.94% versus 0.51%; P < 0.025). A positive linear correlation between tumor growth fraction and Tf mRNA signal intensity was evident (r = 0.32; P = 0.04). TfR mRNA and encoded protein were demonstrated in 26 and 31 adenomas, respectively; Ki-67 immunoreactivities were not correlated with the presence of TfR transcripts and signal intensities. These data suggest that Tf may act as a growth-promoting factor for pituitary tumors.
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PMID:Transferrin and transferrin receptor in human hypophysis and pituitary adenomas. 946 67


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