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)

Thyrotropin-releasing hormone (TRH) immunoreactivity was localized in the rat anterior pituitary with rabbit anti-TRH sera and the unlabeled antibody peroxidase-antiperoxidase complex (PAP) technique. Stain was present in secretory granules of cells possessing morphological characteristics of thyrotropes, gonadotropes and lactotropes. Antibody absorption studies with anti-TRH sera absorbed with TRH, 3 diastereoisomeric analogues of TRH, gonadotropin-releasing hormone (GnRH), bovine serum albumin, thyrotropin, prolactin, adrenocorticotropin, luteinizing hormone, follicle stimulating hormone were performed to determine the specificity of the staining reaction. Only absorption with TRH resulted in a significant reduction in staining intensity. In vitro experiments were then begun with hemipituitaries to ascertain if intrapituitary TRH might originate by sequestration of exogenous, plasma membrane bound TRH or by de novo synthesis. The results suggest that anterior pituitary TRH is of endogenous origin.
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PMID:Endogenous thyrotropin-releasing hormone in the anterior pituitary: sites of activity as identified by immunocytochemical staining. 8 70

The effects of bombesin and other unrelated oligopeptides on hormonal changes induced by stress were studied in conscious adult male rats. Restraint in the cold for 1 h increased plasma corticosterone and PRL levels and decreased GH values but had no effect on LH levels. Bombesin (5 microgram), given intracerebroventricularly (ivt) before stress, inhibited the PRL rise without affecting corticosterone, GH, or LH response. A complete blockade of PRL rise was observed with doses of bombesin ranging from 5 microgram to 100 ng ivt, regardless of the duration (15, 30, 45, or 60 min) or the nature (cold exposure or restraint at room temperature) of the stressor agents. Bombesin was 10(3) more potent as a PRL inhibitor when given ivt than when given iv, and its ivt effect was not reversed by naloxone (1 or 10 mg/kg). Among other unrelated peptides tested (beta-endorphin, neurotensin, substance P, and TRH; 5 microgram ivt), only neurotensin decreased plasma PRL levels in rats subjected to restraint in the cold for 1 h. These results show that in conscious male rats, centrally administered bombesin has a very potent and long acting inhibitory effect on PRL release induced by acute stress. Since a bombesin-like peptide has been found in rat brain, its physiological role in PRL regulation remains to be elucidated.
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PMID:Effects of neuropeptides on adenohypophyseal hormone response to acute stress in male rats. 10 88

The adenylate cyclase responses of the human GH or ACTH producing pituitary adenomas and ectopic ACTH producing tumors to TRH, LH-RH, biogenic amines, peptides hormones, PGE1 and rat median eminence extract (MEE) have been examined. Out of 4 GH producing pituitary adenomas obtained from patients with active acromegaly at hypophysectomy two were stimulated by TRH, two by LH-RH, three by norepinephrine, one by dopamine, four by PGE1 and none by serotonin. Glucagon stimulated the adenylate cyclase in one of three and MEE in both of two tested. The positive responses of paradoxical GH release after TRH and/or LH-RH before surgery in these patients coincidentally related to the response of adenylate cyclase of each pituitary adenoma. There seems, however, to be no consistent correlation between the adenylate cyclase responses to biogenic amines and the GH release after L-Dopa or 5-hydroxytroptophan tested. The adenylate cyclase of a pituitary adenoma from case of Cushing's disease was stimulated by LH-RH, norepinephrine glucagon and MEE but not by TRH. Plasma levels of ACTH, beta-MSH and cortisol increased after LH-RH but not after TRH in this patient before hypophysectomy. The adenylate cyclase of two ectopic ACTH producing tumors (gastric carcinoid and malignant thymoma) was activated by TRH, LH-RH, norepinephrine, epinephrine, serotonin, PGE1 and MEE. These results indicate the presence of multiple hormone receptors in GH or ACTH producing pituitary adenomas and ectopic ACTH producing tumors, and suggest that the paradoxical GH or ACTH release after TRH and/or LH-RH injection in acromegaly and Cushing's syndrome might be caused by an alteration of the cellular membrane receptors of the pituitary adenomas.
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PMID:Adenylate cyclase of GH and ACTH producing tumors of human: activation by non-specific hormones and other bioactive substances. 19 Feb 56

Thyrotropin-releasing hormone (TRH) has been reported to stimulate the release of melanocyte-stimulating hormone (MSH) from the pars intermedia (PI) of Rana esculenta. To test its effect on the rat PI, acutely dispersed rat PI cells, as well as whole nervosa-intermedias (NI), were incubated with synthetic TRH, from 10(--10)--10(--4)M. TRH did not alter the release of either MSH or adrenocorticotropic hormone (ACTH).
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PMID:Thyrotropin-releasing hormone does not alter the release of melanocyte-stimulating hormone or adrenocorticotropic hormone from the rat pars intermedia. 20 81

A 43 year old man with diabetes insipidus who showed panhypopituitarism and marked hypergammaglobulinemia due to histiocytosis X is reported. His low basal plasma adrenocorticotropin (ACTH) and growth hormone (GH) failed to respond to insulin-induced hypoglycemia. His basal serum thyroid hormone level was below normal and normal basal plasma thyrotropin (TSH) showed a delayed response with normal peak value to TSH-releasing hormone (TRH). Normal basal plasma pituitary gonadotropin also showed a delayed response with normal peak value to luteinizing hormone-releasing hormone (LH-RH). Suppression of plasma prolactin (PRL) by levodopa (l-dopa) was impaired and elevation of basal plasma PRL was noted at the second admission. These results, combined with diabetes insipidus, suggested that the panhypopituitarism in these patients was hypothalamic in origin. The polyclonal hypergammaglobulinemia was characterized by elevated serum IgG and IgE levels which returned to normal after corticosteroid treatment with concomitant clinical improvement. Elevated serum IgE levels, tissue and peripheral eosinophilia, and the effectiveness of corticosteroid therapy support the hypothesis that some allergic mechanism may be involved in the pathogenesis of this disease.
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PMID:A case of histiocytosis X associated with panhypopituitarism and hyperimmunoglobulinemia G and E. 22 67

Four patients with idiopathic pituitary dwarfism were shown to have growth hormone (GH), adrenocorticotropin (ACTH), and luteinizing hormone (LH) deficiencies. Basal levels of thyrotropin (TSH) were within normal range in three patients and slightly elevated in one. Exaggerated and delayed responses were obtained after TSH-releasing hormone (TRH) stimulation. Serum thyroxine (T4) values were low (2.3 +/- 0.4 mug/100 ml), while triiodothyronine (T3) levels were in the normal range (1.22 +/- 0.25 ng/ml), both rising substantially after exogenous TSH and consecutive TRH administration. Their hypothyroid state was, therefore, probably due to TRH deficiency. To examine the dose of L-T4 necessary to produce inhibition of the TSH response to TRH, 50 mug/m2/day of L-T4 was administered to these patients. At the end of 4 weeks of replacement, serum T4 rose to 5.2 +/- 0.5 mug/100 ml, whereas T3 was unchanged from the previous levels, after which TSH responses to TRH were completely suppressed in all patients. As a control group, six patients with primary hypothyroidism received gradually increasing doses of L-T4 for 4-week periods, and TSH response to TRH was tested at the end of each dosage of L-T4, until complete inhibition of TSH release was obtained. The primary hypothyroid patients required approximately 150 mug/m2/day of L-T4 for suppression of TSH response to TRH. At this dosage, serum T4 and T3 levels were 8.5 +/- 0.9 mug/100 ml and 2.34 +/- 0.5 ng/ml respectively, which were significantly higher than those levels in the pituitary dwarfs (P less than 0.001 for T4 and P less than 0.01 for T3). These observations indicate that the set point of TSH release in feedback inhibition by throxine is low in idiopathic hypopituitarism with TRH deficiency, and TRH seems to control the pituitary sensitivity to feedback regulation of thyroid hormones.
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PMID:Low setting of feedback regulation of TSH secretion by thyroxine in pituitary dwarfism with TSH-releasing hormone deficiency. 81 7

Thyrotropin-releasing hormone (TRH) is a potent stimulator of melanotropin (alpha-MSH) release from pituitary melanotrophs in pig, frog, and fish. Concurrently, it has recently been shown that injection of TRH induces skin darkening in the lizard Anolis carolinensis (Licht and Denver, 1988). In the present study, we have thus investigated in vitro the possible effect of TRH on alpha-MSH release from the lizard (Lacerta vivipara) neurointermediate lobe, by means of the perifusion technique. Using our radioimmunoassay procedure, we found that serial dilutions of L. vivipara NIL extracts and synthetic alpha-MSH gave parallel binding curves. Administration of graded doses of TRH (10(-8)-10(-6) M) did not cause any modification of alpha-MSH release. In contrast, infusion of a depolarizing concentration of K+ induced a robust stimulation of alpha-MSH secretion. These results indicate that, in the lizard L. vivipara, the neuropeptide TRH does not stimulate pituitary melanotrophs.
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PMID:Lack of effect of TRH on alpha-MSH release from the neurointermediate lobe of the lizard Lacerta vivipara. 139 12

Thyrotropin-releasing hormone (TRH), ovine corticotropin-releasing hormone (oCRH) (both 268 nM), and mammalian gonadotropin-releasing hormone (mGnRH) (268 and 2680 nM) stimulated the secretion of bioactive thyrotropin (TSH) by Rana esculenta pituitaries (pars distalis) in vitro. Preincubation of the pituitaries with 50 ng/ml (64 nM) thyroxine (T4) for 6 hr suppressed the TRH- and oCRH-induced (268 nM) secretion of bioactive TSH, but did not affect the response of the pituitaries to 268 nM mGnRH. Triiodothyronine (T3) (64 nM) reduced both the TRH- and mGnRH-stimulated release of bioactive TSH; the response of TSH to TRH even decreased toward basal levels while a significant TSH response to mGnRH remained. In a separate experiment, pituitaries were preincubated for 6 hr with different equimolar doses of T3 and T4 (6.4, 32, and 64 nM); neither treatment affected the mGnRH-stimulated secretion of bioactive TSH. On the other hand, T4 suppressed the TSH response to TRH in a dose-dependent manner. The inhibitory effects of thyroid hormones on the TRH-induced release of bioactive TSH was present for at least 4 hr after their removal from the incubation medium. These results suggest that thyroid hormones exert a negative feedback control on the secretion of bioactive TSH in adult frogs by a direct action on the pars distalis. There may also be differences in thyroid hormone sensitivities of the TSH responses to mGnRH and TRH.
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PMID:Thyroid hormone feedback regulation of the secretion of bioactive thyrotropin in the frog. 149 May 87

Using high-performance liquid chromatography (HPLC) in combination with radioimmunoassay, three forms of alpha-MSH (des-acetyl, mono-acetyl and di-acetyl alpha-MSH) were separated and identified in tilapia neurointermediate lobes and plasma, and in medium from lobes superfused in vitro. The presence of acetylated forms in lobe extracts indicated that the peptides are acetylated intracellularly. Di-acetyl alpha-MSH was, especially in comparison with monoacetyl alpha-MSH, relatively more abundant in lobe extracts than in plasma. This suggests that the three forms of alpha-MSH are not released according to their relative intracellular abundances. The possibility of regulation of this differential release by dopamine and TRH was investigated, using a microsuperfusion system. Dopamine was a potent inhibitor of alpha-MSH release, but did not modulate the relative abundance of the different forms of alpha-MSH released from the MSH cells. TRH was a potent stimulator of alpha-MSH release. It enhanced in vitro the release of di-acetyl alpha-MSH more than the release of mono-acetyl alpha-MSH. Thus tilapia may be able to modulate not only the quantitative but also the qualitative signal from the MSH cells. This might enhance the flexibility of the animals to respond to environmental challenges.
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PMID:Regulation of differential release of alpha-melanocyte-stimulating hormone forms from the pituitary of a teleost fish, Oreochromis mossambicus. 164 62

Several of the non-sex hormones have been found to be useful in the treatment of seizures. These hormones have an effect on seizures, and seizures have an effect on these hormones. Adrenocorticotropic hormone (ACTH) and corticosteroid drugs have been found to be useful in the treatment of infantile spasms and other seizure disorders. Unfortunately, there is no clear consensus regarding superiority of ACTH versus prednisone in regard to efficacy and long-term benefits, dosage, or duration of treatment. There is also considerable debate regarding reasons why ACTH and prednisone are useful in infantile spasms, their mechanism of action, and their long-term effects on brain development. Thyrotropin-releasing hormone also has been used in the treatment of infantile spasms and other seizure types in children, with modest success. As with ACTH and prednisone, the mechanisms of action remain unclear.
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PMID:Effect of non-sex hormones on neuronal excitability, seizures, and the electroencephalogram. 165 81


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