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)

Immunoreactive beta-endorphin (ir-beta EP) and immunoreactive N-acetyl-endorphin (ir-NacEP) have been demonstrated in the rat thyroid by specific RIA and characterized by reverse phase HPLC. In addition, pituitary and thyroid ir-beta EP and ir-NacEP levels have been determined after manipulation of the pituitary-thyroid axis by chronic (21 days) treatment with 1) propylthiouracil (PTU), 2) L-T4, 3) L-T3, or 4) T3 plus PTU. No difference in anterior pituitary or neurointermediate lobe ir-beta EP was seen between controls and treated groups (n = 8/group). In contrast, levels of ir-NacEP were markedly lower (P less than 0.01) in both hypo- and hyperthyroid groups than in controls, in both anterior pituitary and neurointermediate lobe. In the thyroid, levels of both ir-beta EP and ir-NacEP were profoundly depressed (P less than 0.01) in all treated groups, with no change in calcitonin levels, suggesting that the thyroid effect of PTU and T3/T4 may be specific for the synthesis, processing, and/or release of pro-opiomelanocortin derived peptides. The findings in this study suggest 1) that acetylation of pituitary and thyroid beta EP is similarly sensitive to PTU and thyroid hormone administration and 2) that in the thyroid, but not in the pituitary, both PTU and thyroid hormones markedly lower levels of pro-opiomelanocortin-derived peptides.
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PMID:Beta-endorphin and its congeners in rat pituitary and thyroid: effects of propylthiouracil and thyroid hormone administration. 294 90

Thyrotropin-releasing hormone (TRH) stimulates alpha-melanocyte-stimulating hormone (alpha-MSH) secretion in amphibia as well as thyrotropin-stimulating hormone (TSH) and prolactin secretions in mammals. Since thyroid hormones regulate the stimulatory effect of TRH on TSH and prolactin, the possible role of thyroxine (T4) in the control of alpha-MSH secretion in amphibia, has been investigated. Neurointermediate lobes of Rana ridibunda were perifused in amphibian culture medium for 7 hr and the amounts of alpha-MSH released into the effluent perfusate were measured by radioimmunoassay. In vivo treatment with T4 (0.5 mg/kg twice a day for 9 days) did not modify the in vitro response of the neurointermediate lobes to TRH (10(-9) to 10(-7) M). In addition, prolonged infusion of T4 in vitro did not alter spontaneous and TRH-induced alpha-MSH release. In spite of the inhibitory effect of T4 on TRH-induced TSH and prolactin secretions in mammals, the present data show that, in frogs, thyroid hormone does not modulate the stimulation of alpha-MSH secretion induced by TSH.
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PMID:In vitro study of frog (Rana ridibunda Pallas) neurointermediate lobe secretion by use of a simplified perifusion system. II. Lack of action of thyroxine on TRH-induced alpha-MSH secretion. 641 78

Cold intolerance and secondary amenorrhea developed in a patient who had meningoencephalitis 4 yr prior to study. A clinical diagnosis of hypothalamic hypothyroidism was made on the basis of low serum thyroxine and triiodothyronine levels, and low plasma thyrotropin concentrations, which were responsive to thyrotropin-releasing hormone (TRH). The secretion of the remaining pituitary hormones (growth hormone, prolactin, adrenocorticotropin and gonadotropins) was intact. Not only was thyroid function normalized by oral administration of TRH, but also menses resumed after adequate replacement therapy with thyroid hormone. These results imply that hypothyroidism in this patient was due to isolated dysfunction of hypothalamic TRH release.
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PMID:Hypothalamic hypothyroidism due to isolated thyrotropin-releasing hormone (TRH) deficiency. 643 93

We studied the hormonal millieu and possibility of altered thyroid function in 25 patients in a surgical intensive care unit (ICU) who had severe life-threatening illnesses. Sixteen patients had septic complications and nine patients had multiple-system injuries. On admission to the ICU, serial measurements were begun of thyroxine (T4), triiodothyronine (T3), T4-binding globulin, thyrotropin (thyroid-stimulating hormone [TSH]), corticotropin (adrenocorticotropic hormone [ACTH]), cortisol, prolactin, human growth hormone, catecholamine, insulin and glucose, lactate, retinol-binding protein, prealbumin, and transferrin levels. All patients initially had low normal levels of T4 (4.5 +/- 2 micrograms/dL) and T3 (55 +/- 26 ng/dL), with normal TSH levels (2.3 +/- 2.3 microU/mL) (the "low T3 syndrome"). The 11 surviving patients had their levels increase to normal before leaving the ICU (T4, 7.0 +/- 2.1 micrograms/dL; T3, 110 +/- 48 ng/dL; and TSH, no change). The 14 patients who died showed further decreases before death (T4, 2.6 +/- 2.1 micrograms/dL; T3, 30.6 +/- 23.5 ng/dL; and TSH, 0.9 +/- 0.7 microU/mL). The corticotropin, cortisol, prolactin, and growth hormone levels were normal throughout the study. Catecholamine levels were high initially and decreased in surviving patients. Epinephrine levels increased greatly in nonsurvivors before death, and the norepinephrine-epinephrine ratio decreased from 5.7:1 to 2:1. After protirelin (thyroid-releasing hormone [TRH]) stimulation, the TSH level increased either minimally or not at all in six patients who eventually died. This indicates hypothalamic-pituitary dysregulation or suppression, and altered release and/or peripheral metabolism of T4. Whether this represents a deficiency of thyroid hormone for cell and organ function remains to be established.
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PMID:Altered hormonal activity in severely ill patients after injury or sepsis. 647 95

A 32-year-old woman had seizures and coma due to severe hypoglycemia (26 mg/dL) in the 32nd week of an otherwise uncomplicated pregnancy. She responded dramatically to the administration of cortisol. Initial endocrine evaluation disclosed prolactin (PRL), corticotropin, and thyrotropin (TSH) deficiencies. The patient recovered completely with cortisol and thyroid hormone therapy and was delivered of a healthy male child at term. Endocrine reevaluations one week and six months postpartum disclosed luteinizing hormone, follicle-stimulating hormone, growth hormone, PRL, corticotropin, and probable TSH deficiencies. The cause of this panhypopituitarism has not been determined. This case suggests that the appropriate initial treatment for spontaneous symptomatic hypoglycemia in pregnancy, while awaiting further endocrine evaluation, is the administration of cortisol.
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PMID:Spontaneous hypoglycemic seizures in pregnancy. A manifestation of panhypopituitarism. 669 58

These studies investigated the effect of aging on thyroid hormone regulation of beta-endorphin in rat corpus striatum and hypothalamus. In both brain areas, basal levels of beta-endorphin declined with age. In addition, age modified the response of beta-endorphin to thyroid hormone status. Hypothyroid rats aged 6 months (mature) exhibited a 67% mean decline in the level of beta-endorphin in the corpus striatum. Hypothyroid rats aged 20-24 months (senescent) exhibited no change in the level of beta-endorphin in the corpus striatum. Hypothyroid rats aged 6 months had a 28% mean decline in the level of hypothalamic beta-endorphin. There was no change in hypothalamic beta-endorphin content in hypothyroid senescent rats. Hyperthyroidism resulted in elevations of beta-endorphin in both the corpus striatum and hypothalamus in senescent, but not mature rats. Changes in beta-endorphin seen with age are at least in part thyroid hormone dependent. In addition, age is capable of modifying the response of brain tissue to thyroid hormone.
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PMID:Interaction of age and thyroid hormone status on beta-endorphin content in rat corpus striatum and hypothalamus. 720

Effects of opioid peptide antisera treatment on the secretion of thyrotropin (TSH) and thyrotropin-releasing hormone (TRH) in rats were studied. Anti-beta-endorphin antiserum, anti-methionine-enkephalin antiserum, or antidynorphin antiserum was injected intraperitoneally and the rats were serially decapitated. TRH levels in the hypothalamus along with plasma TRH, TSH and thyroid hormone levels were measured by individual radioimmunoassay. TRH contents in the hypothalamus decreased significantly after opioid peptide antisera treatment, while its plasma levels tended to decrease, but not significantly. Plasma TSH levels increased significantly after opioid peptide antisera injection. Plasma TRH and TSH level responses to cold as well as plasma TSH level response to TRH were enhanced with treatment of antisera to these peptides. Plasma 3,3',5-triiodothyronine levels increased significantly after treatment of antisera to these peptides. From these findings it is concluded that the treatment of opioid peptide antisera stimulates TRH and TSH secretion in rats.
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PMID:Effects of immunoneutralization of endogenous opioid peptides on the hypothalamic-pituitary-thyroid axis in rats. 840 44

Embryonic chickens (Day 18 of incubation) and 8-day-old posthatch chicks were subjected to an acute glucocorticoid challenge by a single iv injection of corticosterone (B), dexamethasone, or porcine adrenocorticotropin. Plasma samples were analyzed for changes in T4, T3, rT3, alpha-subunit, LH, GH, and B levels; iodothyronine deiodinase activity was measured in liver, kidney, and hypothalamus at several time points after injection. The effects of the different treatments were broadly similar within one age group, but differed clearly between pre- and post-hatch animals. In 18-day-old embryos glucocorticoids increased plasma T3 and decreased plasma T4, rT3, and the calculated TSH index, within hours after injection. These changes were accompanied by an immediate (1-4-24 hr after injection) decrease in hepatic inner ring deiodinating type III enzyme (IRD-III) activity and a delayed (24-48 hr after injection) increase in hepatic outer ring deiodinating type I enzyme (ORD-1) activity. Glucocorticoid challenge in 8-day-old chicks similarly decreased plasma T4 and the TSH index but tended to also lower plasma T3. Hepatic ORD-I activity decreased within 1 hr after injection, while the already very low hepatic IRD-III activity was for the most part unaffected. Acute increases in glucocorticoids lower thyroidal T4 secretion in both pre- and posthatch chickens but have clearly different effects on peripheral thyroid hormone deiodination and hence on circulating T3 at both developmental stages.
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PMID:Plasma thyroid hormone levels and iodothyronine deiodinase activity following an acute glucocorticoid challenge in embryonic compared with posthatch chickens. 893 Jun 11

Previous work with chickens (Gallus gallus domesticus) suggests a relationship between depressed thyroid hormone status and enhanced adrenal steroidogenic function. In addition, in hypophysectomized chickens, replacement of the thyroid hormone, 3,5,3'-triiodothyronine (T3), maintains chicken adrenal steroidogenic cell sensitivity to adrenocorticotropin (ACTH) but decreases steroidogenic capacity further than that due to hypophysectomy alone. The present in vivo and in vitro studies were conducted to determine the influence of thyroid status and T3 per se on avian adrenal steroidogenic function. Chicks (1 day old) were thyroidectomized using combined surgical and chemical (6-propyl-2-thiouracil) treatments and were administered a replacement dose of T3 (0, 1.5, 4.5, 15, and 45 microg/kg body wt/day) for 5 weeks. Whereas thyroidectomy (TX) decreased adrenal weight (-20%), it increased relative adrenal weight (mg/100 g body weight) (+171%), trunk plasma corticosterone (+880%), and aldosterone (+124%). In addition, TX increased basal, maximal ACTH-induced, maximal 8-bromo-cyclic AMP-induced, and maximal 25-hydroxycholesterol-supported corticosterone production (+520, +93, +124, and +195%, respectively) and aldosterone production (+578, +288, +280, and +275%, respectively) by isolated adrenal steroidogenic cells. T3, in a dose-dependent manner, reversed the effects of TX on these in vivo and in vitro parameters of adrenal steroidogenic function. Restoration of most of these parameters to those in the sham-treated control was attained with 4.5-15 microg/kg body wt/day. Although some of the effects of TX and T3 replacement on adrenal steroidogenic function may have been mediated through changes in circulating levels of ACTH, other data suggest a direct effect on adrenal steroidogenic cell function. Adrenal steroidogenic cells from sham-treated and TX birds were preincubated (0, 4, and 12 hr) with various concentrations of T3 (0, 0.3, 3, and 30 nM), washed, and then incubated for an additional 2 hr in medium containing the same respective concentrations of T3, with or without a maximal steroidogenic concentration of ACTH (100 nM). T3 had no acute effects on TX-dependent enhancement of adrenal steroidogenic cell function (2-hr incubation). However, with preincubation (4 and 12 hr), T3 inhibited basal and maximal ACTH-induced corticosterone production in a dose-dependent manner. This concentration-dependent, direct effect of T3 was not observed with cells from sham-treated birds. In addition, the ostensibly inactive thyroid hormone metabolite, 3,3',5'-triiodothyronine [reverse T3; 30 nM], was without effect. Taken collectively, these studies indicate that T3 is a direct negative modulator of avian adrenal steroidogenic function.
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PMID:The thyroid hormone, 3,5,3'-triiodothyronine, is a negative modulator of domestic fowl (Gallus gallus domesticus) adrenal steroidogenic function. 924 33

The pituitary gland plays a key role in the regulation of growth, differentiation and function of all cells in the body, including immunocytes. Immune reactions are generated through the proliferation of antigen-specific lymphocyte clones. Growth hormone and prolactin are required for the development of mature lymphocytes and for the maintenance of immunocompetence. These hormones enable lymphocytes to respond to antigen, which is delivered as an adherence signal in the context of major histocompatibility surface molecules of antigen-presenting cells. Numerous other adhesion molecules play a role in the regulation of lymphocyte activation. The activation process is completed by cytokine signalling, after which lymphocyte proliferation, differentiation and functional maturation take place. Interleukins, hormones and growth factors may all function as cytokines. Many lymphocytes exist in the body in a quiescent state, with minimal metabolic activities. These cells are maintained by competence hormones and insulin-like growth factor 1, which are present in the systemic and local environment. Apparently, some steroid hormones, opioid peptides and catecholamines are capable of modulating delivery of the signal from the lymphocyte membrane receptor to the nucleus. Steroid and thyroid hormones control nuclear transcription factors as their receptors, and thus are powerful regulators of lymphocyte signalling at the nuclear level. The bioactive forms of thyroid hormone and of several steroid hormones are generated locally by immunocytes. These important hormonal immunoregulators function both at systemic and local levels. Glucocorticoids are major regulators of cytokine production, and alpha-melanocyte-stimulating hormone functions as a powerful cytokine antagonist. The hormones secreted or regulated by the pituitary gland therefore regulate every level of immune activity, including the competence of lymphocytes to respond to immune/inflammatory stimuli, signal transduction, gene activation, the production and activity of cytokines and other immune effector functions.
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PMID:Pituitary hormones and immune function. 940 45


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