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)

66 pituitary tumors detected at autopsy were investigated for the presence of corticotropin, beta-lipotrophin, growth hormone, prolactin, thyrotropin and gonadotropins by immunocytochemistry. 56 tumors contained hormone-producing cells; 45 were found to contain 2 or more hormones. This finding confirms and extends previous morphologic and clinical observations. The majority of pituitary tumors are mixed and they probably arise from impaired regulation at the hypothalamic and/or pituitary level.
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PMID:Multihormonal pituitary adenomas. 21 78

A 5-year-old girl had hypoglycemia and was of short stature. Studies of pituitary function demonstrated combined growth hormone and adrenocorticotropic hormone (ACTH) deficiency. She was shown to have ketotic hypoglycemia. In contrast to patients previously reported with hypopituitarism and ketotic hypoglycemia, she had no deficiency of gluconeogenic substrate. Serum levels of alanine and other gluconeogenic amino acids were normal during fasting and hypoglycemia. These studies suggest that inadequate gluconeogenic precursors are not the cause of her ketotic hypoglycemia. Ketotic hypoglycemia in association with hypopituitarism may be secondary to multiple biochemical defects.
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PMID:Ketotic hypoglycemia and hypopituitarism. 22 May 86

An animal model using dexamethosone-suppressed, castrated dogs was developed to test the hypothesis that a pituitary hormone other than ACTH modulates adrenal androgen (AA) secretion. Plasma samples were obtained every 15 min during infusions of saline, synthetic alpha 1-24 corticotropin, porcine 1-39 corticotropin (ACTH), or bovine pituitary gland extract (PE) in a wide range of doses. Androstenedione (A), dehydroepiandrosterone (DHA), and cortisol (F) were quantified by radioimmunoassay. When the ratio of AA levels was related to those of F, in order to correct for ACTH content in the PE, the slopes of the dose-response curves for corticotropin and PE were different at the 0.01 level. For A the dose-response slope for the PE was 0.18 +/- 0.5 SE, whereas that of ACTH was 0.02 +/- 0.01. For the DHA response the slopes were 0.17 +/- 0.04 for the PE and 0.04 +/- 0.03 for ACTH. Related studies showed no increase in AA levels in response to luteinizing hormone-releasing hormone, bovine growth hormone (GH), bovine prolactin, ovine thyroid-stimulating hormone (TSH), or synthetic aqueous arginine vasopressin (AVP). We conclude that a pituitary factor other than ACTH, prolactin, GH, luteinizing hormone, follicle-stimulating hormone, TSH, or AVP may be responsible for the observed increase in AA concentrations.
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PMID:Evidence for existence of cortical androgen-stimulating hormone. 22 Aug 83

The localization of various neuropeptides is described in the gut and in the hypothalamus in the rat. Evidence is given for the presence of material resembling corticotropin-like intermediate peptide in arcuate and periarcuate neurons, projecting to various hypothalamic nuclei, limbic areas and the thalamus. beta-Endorphin and glucagon decrease dopamine turnover in the median eminence, while secretin increases dopamine turnover and vasoactive intestinal polypeptide (VIP) has no effect. beta-Endorphin, VIP, secretin, and glucagon all produce discrete changes in norepinephrine turnover in various hypothalamic nuclei. Mainly increases of norepinephrine turnover were observed. These catecholamine turnover changes appear to cause changes in the secretion of prolactin and growth hormone. The results therefore indicate that gut hormones and opioid peptides may act directly on the hypothalamus on specific types of receptors to participate in the control of hypothalamic functions such as control of hormone secretion from the anterior pituitary and of food intake. It seems possible that gastrointestinal peptides released from the gastrointestinal tract into the circulation under certain circumstances could reach the hypothalamus and modulate its activity via the above-mentioned mechanisms. It may therefore be speculated that disturbances in gastrointestinal functions could lead to pathological changes in food intake via modulation of hypothalamic activity.
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PMID:Localization and possible function of peptidergic neurons and their interactions with central catecholamine neurons, and the central actions of gut hormones. 22 24

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

Two micrograms of beta-endorphin (beta-lipotropin61-91) injected intraventricularly in rats that had been treated with antiserum against somatostatin led to a 6- and 10-fold stimulation of the concentration of plasma growth hormone (somatotropin) measured 10 and 20 min after injection of the peptide, whereas 400 mug of methionine-enkephalin led to a 4- to 6-fold increase of levels of plasma growth hormone at 10 min with a rapid return to basal levels at later time intervals. At doses of 5 and 25 mug, beta-endorphin led to a 20- to 30-fold stimulation of levels of plasma growth hormone, the maximal effect being measured between 20 and 30 min after injection. These data suggest the possible role of the endogenous opiate-like peptides in the control of growth hormone secretion.
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PMID:Beta-endorphin: stimulation of growth hormone release in vivo. 26 87

The pharmacokinetics and the hormonal, analgesic, and behavioral effects of several doses of human beta-endorphin were evaluated after intravenous administration to three patients and intracerebroventricular administration to one patient with pain caused by cancer. These effects were compared to the hormonal effects of intravenously administered morphine sulfate in two patients and an enkephalin analog in two baboons. The mean terminal half-life after intravenous administration of 5 or 10 mg of human beta-endorphin to three patients was 37 min; the mean volume of distribution was 178 ml/kg, and the metabolic clearance rate was 3.2 (ml/min)/kg. The half-life of beta-endorphin in cerebrospinal fluid after intracerebroventricular administration was 93 min, and the volume of distribution was 0.74 ml/kg. A rapid rise in plasma prolactin followed both intravenous and intracerebroventricular beta-endorphin. Intravenous administration did not affect plasma growth hormone, but intracerebroventricular administration suppressed plasma growth hormone. No significant change in plasma growth hormone was noted after intravenous administration of morphine to humans, but plasma growth hormone decreased in one baboon after administration of the enkephalin analog. beta-Endorphin-stimulated release of prolactin occurred at doses lower than those required to produce analgesic and other behavioral effects. When both hormonal and analgesic effects were observed (after 7.5 mg were given intracerebroventricularly), the onset of the hormonal response slightly preceded the analgesic and behavioral responses. These studies suggest that the hormonal effects of beta-endorphin are species dependent and are similar to those of morphine. Hormonal and analgesic effects of beta-endorphin appear to result from the activation of opiate receptors that differ in their locations and characteristics.
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PMID:beta-Endorphin: analgesic and hormonal effects in humans. 29 54

Alpha-melanotropin stimulated the spontaneous secretion of human growth hormone in vivo and in vitro. This novel extrapigmentary action of alpha-MSH is also demonstrated in preparations of isolated pituitary tissue and cell cultures. It is concluded that alpha-MSH meets some of the criteria of a genuine growth hormone releasing hormone.
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PMID:[Stimulation of growth hormone secretion: a novel extrapigmentary action of alpha-melanotropin]. 35 64

Serial sections from epoxy resin-embedded rat anterior pituitaries were sequentially immunostained for endorphin, [Met]enkephalin, and growth hormone, respectively. We found that [Met]enkephalin immunoreactivity was confined to the growth hormone producing cells. Corticotropin/endorphin cells in the anterior pituitary from both normal and adrenalectomized rats did not contain any [Met]enkephalin immunoreactivity. When anterior pituitary cells were maintained in monolayer culture for 10 days, [Met]enkephalin immunoreactivity was still located in the growth hormone-producing cells although the staining was weaker than in the somatotrophs in pituitary tissue fixed immediately after death of the animals. This suggested that somatotrophs synthesize [Met]enkephalin. However, this cannot be proved conclusively until biosynthesis experiments have been performed. The following conclusions were drawn from these findings. (i) Anterior pituitary [Met]enkephalin is not an extraction artifact derived from beta-endorphin with which it shares the NH2-terminal pentapeptide sequence. (ii) In the anterior pituitary, beta-endorphin is not the precursor to [Met]enkephalin. [Met]Enkephalin in somatotrophs may be of brain origin and in the somatotrophs may be bound to intracellllar receptors as has been shown for luteotropin releasing hormone in gonadotropic cells.
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PMID:Pituitary somatotrophs contain [Met]enkephalin-like immunoreactivity. 36 11

Using a highly specific antibody we found Met-enkephalin-like immunoreactivity in large granules of numerous distinct cells that are embedded in a layer of secretory terminals inside the octopus vena cava. Application of antibodies against fragments of the mammalian pro-opiocortin precursor -- alpha-MSH, ACTH, beta-endorphin and 16k-fragment -- and against growth hormone did not produce immunostaining in the octopus enkephalin cells. The vena cava neuropil may represent a favourable system for the examination of the physiological role of the opioid peptide enkephalin.
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PMID:Met-enkephaline-like immunoreactivity in a cephalopod neurohemal organ. 39 32


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