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)

Patterning of plasma ACTH, beta-EP/beta-LPH and cortisol in response to ovine CRF (1 microgram/kg b.w.t. injected i.v.), was studied in three normal subjects and in five patients with Cushing's disease, two of whom had undergone total bilateral adrenalectomy. CRF caused in all subjects a prompt and concurrent rise of plasma hormone levels. The hormonal response was of the same magnitude in normal controls and in the three untreated Cushing's patients, but was much greater in the two adrenalectomized subjects. No changes were noted, after CRF, in plasma levels of GH, PRL, TSH, LH and FSH. These findings indicate that CRF specifically promotes the pituitary release of ACTH and ACTH-related peptides both in normal subjects and patients with Cushing's disease. In view of the likely CRF hypersecretion of the adrenalectomized patients, their ACTH and beta-EP/beta-LPH hyperresponsiveness to exogenous CRF would denote that the peptide does not down regulate its own pituitary receptors.
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PMID:Effect of CRF on the release of anterior pituitary hormones in normal subjects and patients with Cushing's disease. 632 64

Implantation of the PRL, ACTH, beta-endorphin (beta-EP), and beta-lipotropin (beta-LPH)-secreting transplantable rat pituitary tumor 7315a resulted in a suppression of the PRL and the ACTH content of the anterior pituitary gland and also of the beta-EP/beta-LPH content of the neurointermediate (NI) lobe. Treatment with bromocriptine further diminished the anterior lobe PRL content, whereas haloperidol partially inhibited this tumor-mediated diminution. The administration of these drugs did not influence the suppressed ACTH content of the anterior pituitary lobe. The diminished beta-EP/beta-LPH content of the NI lobe of tumor-bearing rats became completely normal after treatment with haloperidol, whereas bromocriptine administration further diminished the NI lobe beta-EP/beta-LPH content. There was a close correlation between the anterior pituitary lobe PRL content and the beta-EP/beta-LPH content of the NI lobe in all four groups of rats taken together (including nontumor-bearing controls, control tumor rats, and tumor rats treated with bromocriptine or haloperidol; P less than 0.01). Implantation of the pure PRL-secreting pituitary tumor 7315b resulted in hyperprolactinemia and a suppression of the PRL content of the anterior lobe and the beta-EP/beta-LPH content of the NI lobe, without affecting the ACTH content of the anterior pituitary lobe. There was a negative correlation between the level of the circulating PRL concentration and the beta-EP/beta-LPH content of the NI lobe. These results suggest a possible relationship between the synthesis of PRL by the anterior pituitary lactotroph and of the hormones of the NI lobe. The level of the circulating PRL concentration may play, directly or indirectly, a role in the regulation of both systems.
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PMID:Hyperprolactinemia exerts a negative effect on the beta-endorphin content of the rat neurointermediate pituitary lobe. 632 44

The purpose of this study was to investigate whether TRH could be an important PRL-releasing factor during suckling in the rat. Plasma PRL, TSH, beta-endorphin-like immunoreactivity, and GH responses in serial blood samples from unanesthetized suckled rats were determined. The resulting hormonal profile was compared with that obtained when TRH (500 ng/kg BW, iv) was injected at the onset of suckling. Suckling evoked a rise in plasma levels of PRL, beta-endorphin-like immunoreactivity, and GH, but not in TSH. In contrast, exogenous TRH caused a 9-fold increase in plasma TSH levels during suckling without further increasing the PRL response. Since plasma PRL responses are reportedly enhanced by previous suckling, we also determined plasma PRL and TSH levels when TRH (25 ng/rat, iv) was given 30 min after a brief suckling episode. TRH caused a 2.5-fold increase in plasma TSH, but did not significantly increase plasma PRL levels. Since suckling increases plasma PRL without increasing plasma TSH, and TRH increases TSH but not PRL levels, we conclude that TRH is not a major PRL-releasing factor during suckling.
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PMID:Evidence that thyrotropin-releasing hormone is not a major prolactin-releasing factor during suckling in the rat. 632 54

Human GRF-(1-44)-NH2 (GRF-44) was administered iv in graded doses of 0.01-10 micrograms/kg to 35 normal young adult men and 38 women. GRF-44 stimulated the release of GH in a dose-dependent fashion, although the individual responses varied widely. The ED50 values for this effect were 0.4 micrograms/kg in men and 0.2 micrograms/kg in women in the midfollicular phase of the menstrual cycle. Maximal responses in men and women were not significantly different, and a dose of 1 micrograms/kg was sufficient to produce a maximal response. There was, likewise, no difference between responses of women tested in the midfollicular and midluteal phases of the cycle. There were no changes in PRL, LH, FSH, TSH, ACTH, beta-endorphin, or cortisol at doses up to 1 microgram/kg; at 10 micrograms/kg, PRL increased by an average of 7.6 ng/ml in the women. Side effects occurred in approximately 20% of both men and women at 1 microgram/kg and in nearly all subjects given 10 micrograms/kg; these consisted primarily of flushing and a sense of warmth. Thus, a dose of 1 microgram/kg GRF-44 is safe and effective, and would appear to be a reasonable choice for use in studying GH responses in normal subjects of other ages and in patients with disorders of GH secretion.
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PMID:Dose-response relationships for the effects of growth hormone-releasing factor-(1-44)-NH2 in young adult men and women. 633 Jan 51

The endocrine function of the hypophysial pars tuberalis is currently unknown. Recent immunocytochemical and electron microscopic studies have shown the presence of gonadotropin-producing cells in this tissue in intact rats. Because the pars tuberalis is not destroyed by hypophysectomy, the objective of the present study was to determine whether this gland is activated to produce pituitary hormones following hypophysectomy. Hormone-producing cells were identified by the unlabeled antibody peroxidase-antiperoxidase method of immunocytochemistry using primary antisera generated against the following hormones: LH, FSH, TSH, GH, PRL, ACTH, and beta-endorphin. In intact control rats, the only cell types detected in the pars tuberalis were gonadotropes and thyrotropes. Most gonadotropes contained both LH and FSH. The TSH cells were a separate cell population, and constituted the majority of pars tuberalis parenchymal cells. As early as 1 week after hypophysectomy, a hyperplastic and hypertrophic response was noted in the gonadotropes, and both cell types showed cytological features characteristic of enhanced hormonal synthesis and secretion. These responses increased with time post hypophysectomy. Secretory cell types not present in the pars tuberalis before hypophysectomy, i.e. somatotropes, mammotropes, opiocorticotrophes, were not activated or induced to differentiate after hypophysectomy. Based on these immunocytochemical observations, the hypophysectomized rat cannot be viewed as an animal totally devoid of anterior pituitary hormones. It has the capacity, or at least the potential, for secretion of LH, FSH, and TSH.
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PMID:Hormone production in the hypophysial pars tuberalis of intact and hypophysectomized rats. 640 Dec 46

The hypophysiotropic activities of a synthetic human pancreatic growth hormone releasing factor (hpGRF) with 40 residues was examined in vitro using rat pituitary halves. At concentrations from 10(-10) M to 10(-7) M the peptide stimulated GH release in a dose-dependent manner with the ED50 being 1.2 x 10(-9) M. The concentration of 10(-10) M hpGRF is comparable to the basal hypophyseal portal blood levels of other known hypothalamic hypophysiotropic hormones. However, GH release was enhanced three-fold by concentration as low as 10(-12) M, though no dose-response relationship was observed up to 10(-10) M. Thus, this peptide not only stimulates the release of GH in a dose-dependent manner, but at lower concentrations also maintains elevated GH levels. The release of ACTH, beta-endorphin, LH, and FSH was not affected by hpGRF at any of the concentrations tested. At hpGRF concentrations less than 10(-7) M, the release of TSH and PRL were unaffected. However, at 10(-6) M, TSH release was enhanced about 2.5 fold and prolactin release was elevated slightly.
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PMID:In vitro pituitary hormone releasing activity of 40 residue human pancreatic tumor growth hormone releasing factor. 640 22

Serum LH, FSH, TSH, PRL, GH and cortisol levels were measured in 10 patients with a craniopharyngioma both before and after a combined insulin-induced hypoglycaemia, GnRH and TRH test. In pre-operative studies, only two patients did not show hormonal abnormalities, while eight patients had deficiencies of one or more hormones. The most frequent abnormality was GH deficiency (six cases), followed by gonadotropin (four cases), cortisol (four cases), and TSH (one case), whereas four patients showed high serum PRL values. In post-surgical studies, a significant improvement of pituitary function was observed in two cases, whereas an impairment of previously normal corticotropin reserve was recorded in another case. The data obtained suggest that endocrine abnormalities in patients with craniopharyngiomas are irreversible in most cases.
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PMID:Evaluation of anterior pituitary function in adult patients with craniopharyngiomas. 643 39

Despite its occurrence in most vertebrate species, the function of the hypophysial pars tuberalis (PT) remains obscure. Recent immunocytochemical studies have demonstrated the presence of hormone-containing cells in the few species studied. In the present study the secretory cell composition of the PT was characterized in a variety of mammals using immunocytochemistry. Species studies were the mouse, rat, guinea pig, rabbit, sheep, rhesus monkey, baboon, and human. Antisera were chosen on the basis of their ability to identify a distinct cell population in the pars distalis. A total of 21 antisera were used to identify GH, PRL, ACTH, beta-endorphin, LH, FSH, and TSH. Gonadotropes were identified in the PT of all eight species and were the predominant immunoreactive cell type in the human, baboon, rhesus monkey, sheep, guinea pig, rabbit, and mouse. Thyrotropes were detected in all species except the sheep. They were the predominant cell type in the rat but were less common than gonadotropes in other species. No other secretory cell types were found, with the exception of occasional somatotropes and mammotropes in some human specimens, and small clusters of opiocorticotropes in the guinea pig. Thus the general pattern in the mammalian PT is the presence of gonadotropes and thyrotropes and the absence of other pituitary cell types. In the human, baboon, and rat, all PT parenchymal cells can be identified immunocytochemically. However, in the rhesus monkey, sheep, guinea pig, rabbit, and mouse, the majority of PT cells do not react with any antisera, and thus their function is unknown. Follicles are common in the PT of most mammalian species, however, the luminal contents do not react with antisera to adenohypophysial hormones.
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PMID:The mammalian hypophysial pars tuberalis: a comparative immunocytochemical study. 651 Jun 90

In the sea turtle Caretta caretta the dorsal wall of the pituitary anlage and the apex of the hypophyseal angle are derived from stomodeal epithelium adherent to the neural epithelium of the diencephalon; a substantial part of the ventral wall of the anlage is derived from epithelium of mixed origin (stomodeum and foregut). Distribution of immunoreactive cells in the embryonic gland suggests that pituitary peptide hormones (adrenocorticotropin, ACTH; melanotropin, MSH; prolactin, PRL; growth hormone, GH) are synthesized in cells from the dorsal wall, while cells producing glycoprotein hormones (luteinizing hormone, LH; thyrotropin, TSH) trace their lineage to ventral and ventrolateral areas of the anlage that include some endoderm. Mesenchymal movements mold the epithelial anlage in two steps, delineating first the posterior and subsequently the anterior area of the gland. During the former process the lateral lobes are defined, and material immunoreactive with antiserum to ACTH appears in epithelial cells of presumptive pars distalis (PD) and pars intermedia (PI). Delineation of the anterior end of the pituitary gland occurs as the hypophyseal stalk forms, approximately one-fourth through ontogenesis. Shortly thereafter, immunoreactions demonstrate synthetic activity of distinctively distributed cells containing ACTH, PRL, GH, LH and TSH. In Caretta the lateral lobes of the pituitary anlage give rise to a distinct layer of tissue around the PD (pars tuberalis interna, PTint) and a thick layer on the floor of the hypothalamus (juxtaneural pars tuberalis, juxPT). In the pituitaries of late embryos, juxPT tissue proximal to the PD contains many cells immunoreactive with LH antiserum; whereas cells in distal areas of the juxPT do not react with any antisera tested. LH-cells also occur in large numbers in the PTint and in the posterior PD where tissues of the partes tuberalis and distalis are continuous. Cells reactive with antiserum to TSH are found in small numbers in the PTint, and in larger numbers along with the LH-cells in the posterior PD. PRL-cells occur in the anterior PD, GH-cells in the posterior. ACTH-cells are found primarily in the anterior two-thirds of the PD.
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PMID:Ontogeny and immunocytochemical differentiation of the pituitary gland in a sea turtle, Caretta caretta. 688 41

A variety of neuropeptides, such as TRH, somatostatin, VIP, Substance P, neurotensin, CCK, gastrin, and opioid peptides, alter secretion of GH and PRL from the pituitary. These actions differ according to the route of administration or with experimental conditions, especially anesthesia. Among these peptides, the most consistent results have been obtained with opioid peptides, which stimulate GH and PRL release. Both beta-endorphin and enkephalins are capable of stimulating GH and PRL release in anesthetized and unanesthetized, freely moving rats. The effect is blocked by naloxone, an opiate receptor antagonist. GH secretion induced by opioid peptides seems to be mediated by an alpha-adrenergic mechanism, since treatment with DDC and fusaric acid, which are dopamine-beta-hydroxylase inhibitors, reserpine, and phenoxybenzamine which is an alpha-adrenergic blocking agent, blunted GH secretion. However, pimozide, a dopamine receptor antagonist, and propranolol, a beta-adrenergic blocking agent, were without effect. On the other hand, basal PRL secretion was augmented by pimozide, suggesting the possible involvement of dopamine. It is also possible that serotonin is involved in the GH and PRL release induced by opioid peptides. The physiological significance of opioid peptides in regulating GH and PRL secretion is still unclear. Contradictory results (12,25) have been obtained concerning the effect of naloxone on basal or stimulated GH and PRL secretion in rats, monkeys and humans when tested by the continuous blood sampling method, which rules out the erroneous evaluation of results caused by episodicity of plasma hormone levels. Further studies should clarify the physiological role of opioid peptides in regulating pituitary function.
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PMID:Effect of CNS peptides on hypothalamic regulation of pituitary secretion. 701 Sep 47


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