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

Normal subjects were studied to test the feasibility of a combined anterior pituitary function test using iv administration of four hypothalamic releasing hormones: ovine corticotropin-releasing hormone, human GH-releasing hormone, GnRH, and TRH. Initially, nine normal men were studied with various combinations of these four hormones to exclude the possibility that they might inhibit or synergize with each other in releasing the individual anterior pituitary hormones. When given in combination, the releasing hormones were administered as sequential 20-sec iv infusions in the following order and doses: ovine corticotropin-releasing hormone, 1 microgram/kg; GnRH, 100 micrograms; human GH-releasing hormone, 1 microgram/kg; and TRH, 200 micrograms. Plasma or serum samples were assayed for ACTH, cortisol, GH, PRL, FSH, LH, and TSH at multiple times for 120 min after injection. Compared to individual administration, combined administration of these four hypothalamic releasing hormones caused no apparent inhibition or synergism with respect to the individual hormone responses of these normal subjects. Side-effects of the combined test were the same as those observed with individual hormone administration. No unusual or dangerous side-effects were observed. Having confirmed the efficacy of combined administration of the four releasing hormones, we administered the combination to five additional normal men and 12 normal women. Anterior pituitary hormone and cortisol responses were the same in men and women, except for a lower LH and a greater PRL response in women. There was a rapid increase in all hormones, with peak levels usually reached by 60 min. Adequate assessment of individual hormone responses can be achieved by assaying a basal and only 2 (or 3 in the case of ACTH and GH) postinfusion samples. A rapid, safe, and useful test of combined anterior pituitary function appears to be feasible using these four hypothalamic releasing hormones.
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PMID:Rapid sequential intravenous administration of four hypothalamic releasing hormones as a combined anterior pituitary function test in normal subjects. 298 3

Within the past year, three similar peptides with specific growth hormone (GH) releasing effects have been extracted from human tissue, identified, and synthesized. Human pancreatic tumor GH releasing factor (I-40)-OH (hpGRF-40) was the sole hpGRF isolated from the pancreatic tumor of a patient in Charlottesville and was the predominant peptide isolated from the pancreatic tumor of a patient in Lyon. The Lyon tumor also contained hpGRF(1-37)-OH and hpGRF(1-44)-NH2. Both immunological and biochemical data suggest that hpGRF-40 and hpGRF-44 are present in the human hypothalamus and may be the human GH releasing hormone(s) (GHRH). In cultures of rat pituitary cells, hpGRF stimulates GH but affects neither basal and dopamine-inhibited prolactin release nor basal and gonadotropin releasing hormone (GnRH)-stimulated luteinizing hormone (LH) release. hpGRF stimulates cyclic AMP production within seconds, an effect which is blocked by somatostatin. In contrast, while hpGRF stimulates phosphatidylinositol turnover in the pituitary, the effect is not inhibited by somatostatin. In the human, hpGRF-40 (1 microgram/kg) given intravenously (i.v.) stimulates GH release within 5 minutes. hpGRF-40 does not elevate serum prolactin levels, thyrotropin (TSH), LH, or corticotropin (measured indirectly through plasma cortisol), or blood glucose or plasma concentrations of insulin, glucagon, pancreatic polypeptide, cholecystokinin, gastrin, gastric inhibitory peptide, motilin, or somatostatin. When graded doses of hpGRF (0.1-10 micrograms/kg) are given i.v., no differences are noted in the maximal levels of serum GH achieved.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Human pancreatic tumor GH-releasing factor. 298 23

A comparison was made with the data of 62 cases of pituitary adenoma, evaluated pre- and postoperatively, including as well the results of immunohistochemical hormone examination (also for calcitonin). Prolactin was found in 18 of the 21 adenomas carrying the preoperative diagnosis of prolactinoma, whereas cells containing other hormones (growth hormone, LH, FSH, TSH, ACTH, beta-endorphin), were only occasionally present. The growth hormone was strongly positive in the adenoma tissue in 16 of the 17 cases of acromegaly. 5 of these adenomas were accompanied by a marked hyperprolactinemia and also contained many prolactin cells. 6 of the 19 adenomas diagnosed as being 'inactive' contained hormone-positive cells, but only a very small number of cells. ACTH was found in 3 of the 4 pituitary adenomas of patients with Cushing's disease. 2 of these were also positive for beta-endorphin. The tissue of 1 gonadotrophic adenoma (with elevated FSH in serum) gave positive results with an anti-LH antiserum. Calcitonin was not found in any adenoma. The preoperative serum prolactin levels did not quantitatively correlate with the percentage of prolactin-positive cells.
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PMID:Immunohistochemical examination of pituitary adenomas. Comparison to clinical and endocrinological findings. 298 43

Experiments were designed to evaluate the role of activators of protein kinase C, such as 1,2-diacylglycerol and phorbol esters, on the release of all the anterior pituitary (AP) hormones in vitro. Dispersed rat AP cells were incubated in the presence of 1,2-didecanoylglycerol (DiC10), a synthetic diacylglycerol, or phorbol 12,13-dibutyrate (PDBu), a tumor-promoting phorbol ester, at different concentrations and for varying periods of time. ACTH and beta-endorphin (beta-End) secretion were enhanced by DiC10 in a concentration-dependent manner, with a minimal effective concentration of 5 microM. PDBu at 5 nM produced a significant release of both ACTH and beta-End. The effect of DiC10 and PDBu was time dependent, with maximal responses occurring at 15-30 min for DiC10 and 30-60 min for PDBu. Release of GH was also enhanced significantly by DiC10 and PDBu, with minimal effective concentrations of 1 microM and 1 nM, respectively. Maximal release of GH was already attained within 15 min with DiC10 or 60 min with PDBu. In additional experiments, the effects of DiC10 and PDBu on secretion of LH, FSH, PRL, and TSH were evaluated. The results indicate that 5-25 microM DiC10 produced a concentration-dependent release of each of those hormones, and that 5 microM was the minimal effective concentration in every case. Nearly maximal stimulation was achieved within 15 min for each hormone. PDBu (50 nM) significantly enhanced LH, FSH, PRL, and TSH release within 30 min. Although qualitatively all hormones were similarly stimulated, both with respect to time and concentration, some quantitative differences were observed. ACTH and beta-End release were enhanced 100% by DiC10 and 300% by PDBu, whereas the increase in other hormones was of a lesser magnitude. The present study indicates that two specific stimulators of protein kinase C, diacylglycerol and phorbol ester, can enhance secretion of all AP hormones in a concentration- and time-dependent manner. This suggests that formation of endogenous 1,2-diacylglycerol may represent a physiological intracellular messenger in the events leading to AP peptide hormone release.
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PMID:1,2-Didecanoylglycerol and phorbol 12,13-dibutyrate enhance anterior pituitary hormone secretion in vitro. 299 14

A new TRH analogue containing a C-terminal thioamide group was synthesized. This peptide was shown to have receptor-binding affinity, and TSH- as well as alpha-MSH-releasing activities very similar to native TRH.
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PMID:TRH analogue with C-terminal thioamide group. Synthesis, receptor binding, TSH-releasing activity and alpha-MSH-releasing activity. 300 Aug 15

L-pyroglutamyl-L-histidyl-L-proline thioamide--([Prot3]TRH), a new TRH analogue, has been previously found to have the same binding affinity to adenopituitary receptors as well as TSH and alpha-MSH releasing activities as native TRH. In this paper we report also the same time course of TSH response after i.p. injection of this compound (10 micrograms kg-1) to rats. Binding affinity to specific receptors in rat amygdala, cortex (frontal lobes), hypothalamus, striatum (order according to decreasing affinity) of both peptides was also similar. In contrast to TRH, however, [Prot3]TRH in doses 0.5 and 5 mg kg-1 i.p. did not affect sleeping time and breathing frequency in the rats during barbiturate anaesthesia. Surprisingly, human plasma degraded the new analogue much faster (T1/2 8.5 min) than native TRH (T1/2 30 min). [Prot3]TRH was also degraded faster in plasma of adult rats. Plasma of 6-day-old rat pups failed to degrade both peptides. It was concluded that the substitution of proline amide, for proline thioamide group in TRH molecule did not change binding affinity to receptors in the central nervous system, but decreased biological effectiveness in CNS and substantially decreased the resistance to degradation in human and rat plasma.
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PMID:TRH analogue with C-terminal thioamide group: rapid degradation by plasma and its biological effects. 300 50

Ten normal young men (22-28 yr of age), within 10% of their ideal body weight, were given the four releasing hormones (TRH, 200 micrograms; GnRH, 100 micrograms; ovine corticotropin-releasing hormone, 50 micrograms; GH-releasing hormone, 80 micrograms) iv on separate days and then in combination on the same day. Plasma TSH, PRL, FSH, LH, cortisol, ACTH, and GH were measured by RIA in samples collected from 20 min before to 120 min after injection. There were no significant differences in responses to the separate and combined tests for FSH, LH, cortisol, ACTH, and GH. The plasma TSH (0.001 less than P less than 0.01) and PRL (P less than 0.001) responses were significantly higher after the combined test. The tolerance was identical to that of TRH alone. In eight patients studied after pituitary surgery, combined administration provided results comparable to those obtained after separate administration of TRH, GnRH, and insulin.
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PMID:Pituitary stimulation by combined administration of four hypothalamic releasing hormones in normal men and patients. 300 59

Twenty-two subjects (11 patients with major endogenous depression and 11 controls) received an intravenous test dose of 100 micrograms human corticotropin-releasing hormone (h-CRH). Corticotropin (ACTH), but not cortisol, responses were blunted in depressives. Basal cortisol secretion was higher in depressives than in controls and was negatively correlated to the corticotropin response following h-CRH. This finding indicates the integrity of the glucocorticoid-dependent negative feedback regulation in depression and supports the view that hypercortisolism in depression is primarily due to a suprapituitary disturbance. Comparison of ACTH responses after h-CRH with thyrotropin (TSH) output following thyrotropin-releasing hormone (TRH) revealed a positive correlation (r = 0.65, p less than 0.001). The concordance between ACTH and TSH responses after specific challenges suggests that regulation of both systems is at least in part under a common control.
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PMID:Human corticotropin-releasing hormone in depression--correlation with thyrotropin secretion following thyrotropin-releasing hormone. 301 Nov 29

We used a double-blind crossover design to study the effects of alpha 2 adrenoreceptor blockade with yohimbine on levels of anterior pituitary hormones. A dose of yohimbine was used which raised plasma norepinephrine from 379 +/- 74 (S.E.) to 730 +/- 143 pg/ml and mean arterial pressure from 83 +/- 4 to 92 +/- 5 torr (p less than 0.025). This dose (125 micrograms/kg, then 1 microgram/kg/min) also altered mood when compared to saline infusion. In spite of these changes, when prolactin, cortisol, ACTH, beta-endorphin, TSH and growth hormone were measured after 45 minutes of yohimbine infusion, no changes from baseline were noted. These data suggest that in normal man, at rest, alpha 2 adrenoreceptors in the hypothalamus, adenohypophysis or other brain areas do not tonically modulate release of these hormones into the blood.
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PMID:Influence of yohimbine on release of anterior pituitary hormones. 301 39

Opiates stimulate the growth hormone and prolactin responses to stimuli in non-obese humans. Obese patients, however, show lowered growth hormone and prolactin responses and raised beta-endorphin levels. We therefore investigated the effect of the opiate antagonist naloxone on the stimulated growth hormone and prolactin secretions in a controlled double-blind study in obese patients. All patients received 200 micrograms TRH and 0.5 g/kg b.w. arginine together with 2 mg of naloxone or placebo i.v. in a randomized sequence. The TRH- and arginine-induced increases in prolactin and growth hormone were significantly greater after administration of naloxone (p less than 0.05). Naloxone also produced a significant increase in ACTH, cortisol and beta-endorphin when compared with placebo. TSH, triiodothyronine, thyroxine, insulin, glucagon and blood glucose showed no significant differences between both days of the trial. The effect of naloxone on growth hormone and prolactin secretions in obese humans can thus be regarded as a partial normalization. We therefore conclude that the hypothalamic regulatory disturbance of growth hormone and prolactin secretions in the obese could be caused by raised opiate levels.
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PMID:Naloxone increases the response of growth hormone and prolactin to stimuli in obese humans. 303 2


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