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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 characterize the secretion of corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) into the hypophysial-portal circulation of the conscious sheep. In addition, we examined the temporal relationship between the secretion of these two hypothalamic peptides and the secretion of three pro-opiomelanocortin peptides--adrenocorticotropic hormone (ACTH), ir-beta-endorphin, and ir-alpha-melanocyte-stimulating hormone--and cortisol and determined the effects of an audiovisual emotional stimulus and insulin-induced hypoglycemia on the entire hypothalamic-pituitary-adrenal axis. In the basal state, the secretion of CRF, AVP, the three pro-opiomelanocortin peptides, and cortisol was pulsatile in nature, and three CRF and AVP pulse patterns were observed: a concordant increase in CRF and AVP, an isolated rise in CRF, and an isolated increase in AVP. In 4 of the 5 animals, a 3-min audiovisual stress (barking dog) rapidly increased the plasma levels of all the measured substances, although the magnitude and duration of the effect differed markedly between the animals. Insulin-induced hypoglycemia markedly increased AVP and, to a lesser extent, CRF concentrations in portal plasma and thereby altered the CRF:AVP molar ratio. Although pituitary-adrenal activation was closely correlated with the increased hypothalamic activity, a strict 1:1 concordance between CRF/AVP secretion and ACTH secretion was not seen. The anesthetic ketamine selectively increased portal AVP concentrations to levels which exceeded those attained during hypoglycemia and rapidly activated the pituitary-adrenal axis. We conclude the following: (1) CRF and AVP are secreted by the hypothalamus in a pulsatile fashion; (2) ACTH secretion can be stimulated by increases in either CRF or AVP; (3) the absence of a strict 1:1 concordance between hypothalamic CRF/AVP release and pituitary ACTH secretion during stress may be partly due to the release of additional hypothalamic ACTH secretagogues; (4) the ability of both audiovisual stimuli and insulin-induced hypoglycemia to augment CRF and AVP secretion indicates that the paraventricular hypothalamus may be activated by a variety of neural inputs, and (5) the marked alteration of the CRF:AVP molar ratio during stress suggests that AVP may be an important ACTH secretagogue in vivo in the sheep.
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PMID:Studies of the secretion of corticotropin-releasing factor and arginine vasopressin into the hypophysial-portal circulation of the conscious sheep. I. Effect of an audiovisual stimulus and insulin-induced hypoglycemia. 254 60

To investigate possible abnormalities of the hypothalamic-pituitary axis in patients with chronic renal failure on dialysis, we have examined the effects of insulin-induced hypoglycemia on the adrenal steroid responses. In normal subjects, plasma aldosterone and cortisol concentrations increase significantly in response to hypoglycemia, with good correlation. In the patients with end-stage renal disease (ESRD) however, insulin-induced hypoglycemia fails to elicit significant increases in the plasma cortisol and aldosterone levels. To test the adrenal responsiveness to adrenocorticotropin (ACTH), we administered ACTH to both groups. Plasma cortisol and aldosterone responses are similar in both groups suggesting that the adrenal responsiveness to ACTH is not impaired. We also investigated the responsiveness of the renin-angiotensin-aldosterone system in response to volume contraction by hemofiltration in patients with ESRD. Neither plasma renin activity nor plasma aldosterone concentration change significantly following such contrived volume contraction. These results reveal several endocrinologic abnormalities in the patients with ESRD on chronic hemodialysis.
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PMID:Aldosterone response to insulin-induced hypoglycemia in hemodialysis patients. 254 16

These experiments were designed to test whether the pattern of change in plasma corticosteroid or the total corticosteroid dose is important in determining the degree of inhibition of adrenocorticotropic hormone (ACTH) responses to stress by corticosteroid intermediate-delayed feedback. Five conscious dogs were studied. The ACTH response to induced hypoglycemia was measured after no prior corticosteroid feedback signal or after a corticosteroid feedback signal produced by infusion, two bolus injections, or three bolus injections of cortisol and corticosterone. The total corticosteroid dose (45 micrograms/kg) and the total interval of steroid treatment (60-30 min before hypoglycemia) were the same in all three cases of corticosteroid treatment. Changes in plasma glucose concentration during induced hypoglycemia were not altered by corticosteroid treatment. The plasma ACTH response to hypoglycemia was inhibited by all three patterns of treatment with corticosteroids. The inhibition of ACTH response was not significantly altered among the patterns of treatment with corticosteroids. The data suggest that the integrated (total) or the mean change in plasma corticosteroid concentration over time determines the degree of inhibition of stimulated ACTH in this time domain.
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PMID:Control of canine ACTH by corticosteroids: an integral feedback effect of steroids. 254 11

To study the possible involvement of hypothalamic corticotropin-releasing factor (CRF) in the stimulation of adrenocorticotropic hormone (ACTH) release caused by insulin-induced hypoglycemia (IIH), we measured CRF secretion in hypophysial portal blood (HPB) in rats anesthetized with sodium thiopental after injection of insulin. Before treatment, systemic ACTH levels (952 +/- SE 143 pg/ml; n = 12) were well above normal values, probably reflecting the anesthetic and surgical stress consecutive to the preparation for portal blood collection. Insulin injection induced a significant increase of ACTH release within 15 min (1,588 +/- 168 vs. 741 +/- 144 pg/ml; n = 6, in vehicle-injected rats) which lasted for at least 1 h. CRF levels in HPB were 857 +/- SE 168 pg/ml (n = 13) during the first-hour pretreatment collection. Vehicle injection did not modify CRF secretion (759 +/- 142 pg/ml; n = 6). Insulin injection provoked a significant increase in CRF release (1,449 +/- 257 pg/ml; n = 7). These data suggest that an increased hypothalamic CRF secretion is responsible for the stimulation of pituitary ACTH release following IIH. The possible involvement of central neuromediators in the IIH-induced CRF production is discussed.
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PMID:Corticotropin-releasing factor secretion increases in rat hypophysial portal blood during insulin-induced hypoglycemia. 254 41

Eleven patients with major depression and 12 control subjects were administered corticotropin-releasing hormone (CRH), aqueous arginine vasopressin (AVP), and insulin hypoglycaemia (IH) to test for differences in hypothalamic-pituitary-adrenal (HPA) axis function. Patients with major depression demonstrated lower ACTH responses to CRH when compared with controls, and a trend toward such after administration of AVP. Despite lower ACTH responses in patients with depression, there were no differences in cortisol responses to these stimuli. In the CRH and AVP tests, there was no correlation between the basal cortisol and ACTH responses in either controls or patients, but in the IH test there was a negative correlation between these responses for both groups. The ACTH responses to CRH and AVP were positively correlated in controls and patients. Cortisol responses to all three provocative stimuli were positively correlated in both subject groups. These findings are consistent with the hypothesis that hypothalamic or supra-hypothalamic overactivity may be involved in the development of HPA-axis abnormalities in patients with depression.
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PMID:Consistent reduction of ACTH responses to stimulation with CRH, vasopressin and hypoglycaemia in patients with major depression. 255 71

Altogether 28 patients with adrenocortical tumors (corticosteromas and corticoandrosteromas) were examined using a radioimmunoassay to determine the concentration of corticotropin, cortisol, blood cyclic nucleotides, the circadian rhythm and time course of corticotropin and cortisol levels against a background of insulin hypoglycemia. In patients with Itsenko-Cushing's syndrome the basel level of cortisol was notably raised, that of corticotropin was sharply decreased. The circadian rhythm of the levels of corticotropin and cortisol was disturbed, a response of the hypophyseal-adrenal system to a stressor was suppressed. The concentration of blood cyclic nucleotides was increased, and these changes were dependent on the nature of adrenal pathology.
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PMID:[The function of the hypothalamo-hypophyseal-adrenal system in Itsenko-Cushing syndrome]. 256 Jan 86

To validate the adequacy of saliva as a biological specimen for the study of glucocorticoid adrenal function, the concentrations of salivary cortisol (SC) and serum total cortisol (TC) were measured by radioimmunoassay (RIA) in several groups of individuals in baseline state and during stimulation tests. The study of diurnal variations of SC in the reference population (n = 29) showed a nyctohemeral rhythm similar to that of TC, with maximal concentrations at 08.00-09.00 h (18 +/- 9 nmol/L) and 61% and 80% decreases at 15.30 and 23.00 h, respectively. After the administration of 1 mg of dexamethasone, SC was reduced in a 95% of its baseline value (n = 18). In all patients with Cushing's syndrome (n = 8) SC was increased whereas TC was normal in 3. All patients with adrenal failure (n = 11) had subnormal SC levels, while TC was normal in 4. The SC response to stimulation with intravenous synthetic adrenocorticotropin (Nuvacthen) (with and without previous suppression with 1 mg dexamethasone), insulin hypoglycemia and glucagon were qualitatively similar to those of TC, although more marked in proportion. These results, together with the practical advantages of saliva as a biological sample (easy obtention of specimen, absence of stress during its collection, and stability of cortisol in it), indicate that SC represents a more reliable measurement than TC as a useful clinical test to detect glucocorticoid dysfunction.
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PMID:[Usefulness of the determination of saliva cortisol in the study of adrenal gland glucocorticoid function]. 260 98

As is obvious from the previous discussions, obesity is associated with a wide variety of changes in endocrine parameters (Table 1). Some of these changes, such as the reduction in SHBG without change in serum free testosterone levels, reflect merely laboratory abnormalities that may influence interpretation of diagnostic tests but have no important physiologic relevance. Other abnormalities have major clinical impact, such as hyperestrogenemia-endometrial carcinoma and hyperlipidemia-coronary artery disease. In some cases, endocrine changes in obesity are beneficial--that is, hyperestrogenemia leading to lower incidence of osteoporosis. In other cases, such as the profound suppression of growth hormone output in obesity, the physiologic relevance is unknown. Several endocrine changes in obesity, such as the impaired response of many hormones (growth hormone, prolactin, vasopressin, corticotropin) to insulin-induced hypoglycemia and elevated endorphin levels, suggest hypothalamic dysfunction. Furthermore, the failure of all of these abnormalities to be normalized after weight reduction raises the possibility of an underlying disorder leading to both endocrine dysfunction and obesity, rather than the endocrine dysfunction being simply a consequence of the obesity. Successful elucidation of the pathogenesis of obesity, which might then lead to much needed specific treatment modalities, may be advanced if we can solve some of these puzzles.
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PMID:Endocrine aspects of obesity. 264 1

A 7-year-old spayed female Cocker Spaniel was hospitalized with a history of chronic vomiting, anorexia, and weight loss. Laboratory abnormalities included leukocytosis, metabolic alkalosis, hypoglycemia, hypoproteinemia, and hyperinsulinemia. Gastroscopy and ultrasonography revealed multiple gastric masses and a possible pancreatic mass, respectively. Examination of tissues obtained at necropsy showed a pancreatic adenocarcinoma with hepatic metastasis, gastric hypertrophy, and multiple duodenal ulcers. Immunocytochemical staining of the neoplasia was positive for pancreatic polypeptide (PP) and insulin and negative for gastrin, calcitonin, adrenocorticotropic hormone (ACTH), serotonin, L-enkephalin, chromagranin, glucagon, and somatostatin. Subsequent serum gastrin and PP assays showed a fasting hypergastrinemia with a normal response of gastrin to provocative testing and extremely increased PP values. The high PP values may have resulted in the vomiting and gastrointestinal ulceration. A PP-secreting tumor has not previously been reported in the dog.
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PMID:Pancreatic polypeptide and insulin-secreting tumor in a dog with duodenal ulcers and hypertrophic gastritis. 267 25

In 24 patients with a functioning kidney transplant, hypoglycemia-induced somatotropin (STH), adreno-corticotropin and cortisol secretion was studied. In a further 24 transplanted patients, secretion of lutropin, follitropin and testosterone after the intravenous administration of luliberin was assessed. Data obtained in this paper suggest the presence of abnormal function of the pituitary-adrenal and pituitary-gonadal axis and abnormal STH secretion in patients with a functioning transplant. Type and duration of immunosuppressive therapy seem to influence the intensity of the above-mentioned endocrine abnormalities.
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PMID:Influence of type of immunosuppressive therapy on secretion of somatotropin and function of the pituitary-adrenal and pituitary-gonadal axis in patients with a kidney transplant. 207 24


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