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)

Cyclic AMP and cyclic GMP phosphodiesterase activities (3',5'-cyclic AMP 5'-nucleotidohydrolase, EC 3.1.4.17) were investigated in the human thyroid gland from patients with hyperthyroidism. Low substrate concentration (0.4 muM) was used. About 60% of the cyclic-AMP and 80% of the cyclic-GMP hydrolytic activities in the homogenate were obtained in the soluble fraction (105 000 X g supernatant). The thyroid gland contains two forms of cyclic-AMP phosphodiesterase, one with a Km of 1.3-10(-5) M and the second with a Km of 2-10(-6) M. Cyclic-AMP and cyclic-GMP phosphodiesterase were purified by gel filtration on a Sepharose-6B column. Cyclic-AMP phosphodiesterase activities were found in a broad area corresponding to molecular weights ranging from approx. 200 000 to 250 000 and cyclic-GMP phosphodiesterase activity was found in a single area corresponding to a molecular weight of 260 000. Cyclis-AMP phosphodiesterase activities were stimulated by the protein activator which was found in human thyroid and this stimulation was dependent on Ca2+. Stimulation of cyclic-AMP phosphodiesterase by the activator was not significant even in the presence of enough Ca2+. The effect of D,L-triiodothyronine, D,L-thyroxine, L-diiodotyrosine, L-monoiodotyrosine, L-thyronine, L-diiodothyronine, thyrotropin, hydrocortisone, adrenocorticotropin, cyclic-AMP and cyclic-GMP on the phosphodiesterase activities was studied. Cyclic-AMP, cyclic-GMP, D,L-triiosothyronine, D,L-thyroxine, adrenocorticotropin and hydrocortisone where found to inhibit the phophodiesterase. Triiodothyronine and thyroxine inhibited cyclic-AMP phosphodiesterase more effectively than cyclic-GMP phosphodiesterase. Thyroxine was a more potent inhibitor than triiodothyronine. The concentration of cyclic AMP producing a 50% inhibition of cyclic-GMP phosphodiesterase activity was 5-10(-5) M, while the concentration of cyclic GMP producing a 50% inhibition of cyclic-AMP phosphodiesterase was 3-10(-3) M. Both cyclic-AMP and cyclic-GMP phosphodiesterase activities in the homogenate of hyperthyroidism, thyroid carcinoma and adenoma were higher than in normal thyroid tissue, when assayed with a low concentration of the substrate (0.4 muM). When a higher concentration (1 mM) of cyclic nucleotides was used as the substrate, cyclic-AMP hydrolytic activity in adenoma tissue was similar to that of normal tissue, while the other activities were higher than normal.
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PMID:Human thyroid cyclic nucleotide phosphodiesterase. Its characterization and the effect of several hormones on the activity. 18 33

To elucidate whether insulin-induced hypoglycemia enhances the release of beta-endorphin in man, plasma extracts obtained from healthy subjects and patients with Graves' disease before and 45 min after insulin injection were subjected to gel chromatography, and the fractions obtained were measured by RIA for beta-endorphin. In four healthy subjects, basal plasma beta-endorphin levels were less than 3 to 3.1 pg/ml, and the levels rose substantially to 47.5 +/- 12.4 pg/ml (mean +/- SE) 45 min after insulin injection. Basal plasma beta-endorphin levels in three hyperthyroid patinets (less than 3 to 3.8 pg/ml) did not seem to be different from those in healthy subjects; however, the rise after insulin injection tended to be higher in cases of hyperthyroidism, with a peak value of 68.5 +/- 9.7 pg/ml. Plasma beta-lipotropin and ACTH levels also rose in parallel with beta-endorphin in response to insulin-induced hypoglycemia in both healthy subjects and hyperthyroid patients. It would thus appear that beta-endorphin, like ACTH or beta-lipotropin, is released in human subjects by hypoglycemic stress.
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PMID:Substantial rise of plasma beta-endorphin levels after insulin-induced hypoglycemia in human subjects. 22 18

Using in situ hybridization histochemistry, we have investigated the effect of thyroid hormone on the expression of several peptide mRNAs in the hypothalamic paraventricular nucleus (PVN) of adult male rats. Hypothyroidism was induced by surgical ablation of the thyroid gland. The animals (control sham-operated, thyroidectomized, thyroidectomized+T4 replaced rats) were studied 28 and 50 days after surgery. Sections of the PVN were hybridized using synthetic oligonucleotide probes complementary to mRNA for thyrotropin-releasing hormone (TRH), corticotropin-releasing hormone (CRH), galanin (GAL), enkephalin (ENK), neurotensin (NT), vasoactive intestinal polypeptide (VIP) and vasopressin (VP). GAL mRNA was also analyzed in the anterior paraventricular, arcuate, and dorsomedial nuclei of the hypothalamus. At the PVN level, a feedback effect of thyroid hormone on TRH synthesis was demonstrated by the TRH mRNA increase in hypothyroidism and by its decrease in hyperthyroidism. Hypothyroidism caused a dramatic decrease in GAL mRNA in parvo- and magnocellular PVN neurons both 28 and 50 days after thyroid ablation, whereas no effect was seen in VP mRNA, the main peptide hormone coexisting with GAL. The T4 replacement prevented the GAL mRNA impairment. Hypothyroidism did not influence GAL mRNA in the anterior PVN, perifornical area or in the arcuate nucleus, whereas a decrease in GAL mRNA was observed in the dorsomedial nucleus. VIP mRNA, which is undetectable in the PVN of normal animals, was present in several PVN neurons after thyroidectomy. CRH mRNA was decreased after thyroidectomy, whereas the T4 restitution caused an upregulation. The levels of ENK or NT mRNA were not significantly affected by the thyroid status. The present results show that, in addition to TRH mRNA, other hypothalamic peptide mRNAs are affected by thyroid hormone levels.
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PMID:Response of hypothalamic peptide mRNAs to thyroidectomy. 128 6

Various drugs and hormones influence the light microscopic and especially the electron microscopic structure of the anterior pituitary and its tumors. Many structural effects are known only from animal experiments since specimens from human pituitaries are mostly not available. The structure of growth hormone (GH) cells is relatively stable. A massive GH cell hyperplasia is known only in rare cases with growth hormone releasing factor (GRF) excess from tumors. Prolactin cells can be stimulated by drugs, neurotransmitters, and hormones which decrease the dopamine inhibition. Adrenocorticotropic hormone (ACTH) cells are stimulated by stress, some hormones, loss of adrenals, and drugs which activate the alpha 1- and beta-receptors or inhibit the alpha 2-receptors. They are suppressed and changed into Crooke's cells by treatment with glucocorticoids. Thyroid-stimulating hormone (TSH) cells increase in number and size in states for overstimulation especially by thyrotropin releasing hormone (TRH). A decrease results from hyperthyroidism and possibly from somatostatin, L-dopa, and dopamine. Gonadotroph cells transform into castration cells in strongly hyperactive states (gonadectomy, antiandrogens, gonadotropin releasing hormone [Gn-RH]agonists, aminoglutethimide). Special types of pituitary adenomas can be treated with drugs which suppress hormone production and proliferation. Dopamine agonists and somatostatin reduce the tumor size of varying proportions of GH secreting adenomas in acromegaly. Ultrastructurally, a decrease of cytoplasmic and nuclear volume and an increase of lysosomes are found. Bromocriptine and other dopamine agonists are established in the treatment of prolactin secreting adenomas. They induce a shrinkage in many cases. Ultrastructurally, a reduction of cellular and nuclear size, an increase in number of secretory granules and of lysosomes, and a reduction of rough endoplasmic reticulum can be demonstrated.
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PMID:Effect of drugs on pituitary ultrastructure. 154 57

Among 436 patients with hypertension unrelated to any renal lesion, renovascular damage, pheochromocytoma, Cushing's syndrome or hyperthyroidism, 15 patients had low plasma renin activity (PRA) and elevated plasma aldosterone concentrations in the upright position and resultant high aldosterone/PRA ratios: 8 with aldosterone-producing adenoma (APA; group 1) and 7 with idiopathic hyperaldosteronism (IHA; group 2). Thirty-nine patients had suppressed PRA in the presence of normal plasma aldosterone levels and moderately elevated aldosterone/PRA ratios (group 3). Thirty of them had elevated plasma 11-deoxycorticosterone (DOC) and 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) concentrations (group 3a) and 9 of them had normal levels of those mineralocorticoids (group 3b). The rest of them (382 patients) had low aldosterone/PRA ratios (group 4). Adrenal scintigraphy with dexamethasone pretreatment revealed [13I]-cholesterol accumulation not only in patients with APA (unilateral) or IHA (bilateral), but also in patients of group 3a (bilateral). In patients in groups 3a and 3b adrenal size (especially thickness), as measured by computed tomography (CT scan), was enlarged, as in patients with IHA (group 2), and was significantly greater than in patients of group 4 (p less than 0.001). Spironolactone reduced blood pressure in all tested patients of group 3a, and the removal of adrenal tumor or hyperplastic tissue normalized blood pressure in patients of groups 1, 2 and 3a. Excised adrenal glands exhibited cortical hyperplasia with or without nodular hyperplasia in patients of group 3a. Good agreement was found between the actual size of the excised tissue and the measurement obtained by CT scan. Since beta-endorphin and beta-lipotropin were depressed in patients of group 3a, it is suggested that an unknown pituitary substance stimulates the adrenal cortex to release too large amounts of DOC and 18-OH-DOC and inappropriate secretion of aldosterone.
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PMID:Inappropriate elevation of the aldosterone/plasma renin activity ratio in hypertensive patients with increases of 11-deoxycorticosterone and 18-hydroxy-11-deoxycorticosterone: a subtype of essential hypertension? 207 Mar 75

Based on clinical findings of diminished nocturnal serum melatonin levels in affective illness, we hypothesized that alterations in the pituitary-adrenal or thyroid axes of the rat might alter the nocturnal rise of melatonin content of the pineal gland in that species. Two experiments were conducted to investigate these issues. In the first, rats were injected for nine days with adrenocorticotropic hormone (ACTH) or corticosterone, timed to accentuate and prolong the normal circadian corticosterone rise. Although both these treatments produced significant elevations of serum corticosterone, there was no difference in pineal melatonin content during the day or night from that measured in control rats. In the second experiment, hypothyroidism was induced in rats by thyroid-parathyroidectomy, and hyperthyroidism was produced by injection of triiodothyronine (T3) for nine days. Despite clear evidence of metabolic and endocrine effects of these thyroid manipulations, pineal melatonin content was not altered during the day or night. The nocturnal increase of melatonin may have been phase-advanced in the hypothyroid group, although the experiment was not designed to detect such a shift. There thus is no evidence from this study in the rat to suggest that diminished nocturnal melatonin production in affective illness might be due to associated alterations in the pituitary-adrenal or thyroid systems.
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PMID:Pituitary-adrenal and thyroid effects on melatonin content of the rat pineal gland. 254 23

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

Neonatal rats were daily injected with 100 microg/kg T4 and killed at 4, 8 or 15 days. Circulating corticosterone and corticosteroid binding globulin concentrations increased in 8- and 15-day-old rats after T4 treatment. Plasma adrenocorticotropic hormone (ACTH) concentrations, pituitary ACTH content and pro-opiomelanocortin mRNA expression were unaffected in T4-treated rats. T4 treatment induced an increase in corticotropin-releasing factor (CRF) mRNA expression in the whole population of CRF synthesizing cells of the paraventricular nucleus (PVN) that became significant at day 8 and disappeared at day 15. Double labelling in situ hybridization revealed that CRF gene expression in the CRF+/arginine vasopressin (AVP)+ subpopulation was increased at days 4 and 8 and decreased at day 15. CRF immunoreactivity in the zona externa of the median eminence increased with age but was not affected by the experimental hyperthyroidism. The degree of CRF and AVP colocalization, the concentration of AVP mRNA in the parvo and magnocellular cell bodies of the PVN and the density of immunoreactive AVP in the zona interna or zona externa of the median eminence did not change after T4 treatment. Our data demonstrate that experimental hyperthyroidism accelerates the maturation of hypothalamic CRF gene expression, including in particular in the CRF+/AVP+ subpopulation, during the stress hyporesponsive period. These observations suggest that the physiological peak of plasma thyroxine that occurs between days 8-12 may participate in the maturation of hypothalamic CRF cells.
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PMID:Thyroxine modulates corticotropin-releasing factor but not arginine vasopressin gene expression in the hypothalamic paraventricular nucleus of the developing Rat. 1092 90

Pituitary tumors, depending on their respective cell type, manifest various endocrinopathies. Prolactinomas may present as hypogonadism and galactorrhea and can be diagnosed by measuring morning prolactin levels. Gonadotropinomas rarely cause gonadal hyperstimulation, and dynamic thyrotropin-releasing hormone stimulation testing is often required to elicit a diagnostic gonadotropin and/or subunit secretory response. Acromegaly is a multisystemic debilitating disease for which early diagnosis and treatment are crucial. Diagnostic criteria include a lack of plasma growth hormone suppression during the oral glucose tolerance test and elevation of age- and sex-matched insulin growth factor-1 levels. Patients harboring corticotropin-secreting adenomas characheristically present with signs and symptoms of hypercortisolism. Inferior petrosal sinus sampling for corticotropin may be required for microadenoma localization. Thyrotropinomas produce inappropriate thyrotropin (TSH) secretion and hyperthyroidism. The new third-generation TSH assay has improved the rate of detection of these lesions at an earlier stage.
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PMID:Pituitary tumor endocrinopathies and their endocrine evaluation. 1269 Sep 78

Tumors vary in how they affect pregnancy depending upon the hormone secreted. Some hormone oversecretion syndromes must be controlled to allow pregnancy to proceed without undue maternal and fetal morbidity (Cushing's disease and hyperthyroidism) whereas treatment during pregnancy for other tumors is not necessary. Surveillance for tumor growth during pregnancy is necessary primarily for prolactinomas. A literature search was conducted to identify the effects of pregnancy on pre-existing pituitary tumors and the effects on the outcome of pregnancy due to hormone oversecretion by pituitary tumors. Results show that hyperprolactinemia and Cushing's disease may interfere with fertility and usually need to be controlled to allow for conception. Cushing's syndrome, acromegaly and hyperthyroidism secondary to hypersecretion of thyroid-stimulating hormone (TSH) may increase maternal morbidity (gestational diabetes, hypertension) and fetal morbidity and mortality. Intervention is warranted to remove a tumor that secretes adrenocorticotropic hormone (ACTH) during pregnancy to reduce the risk of fetal loss and to control hyperthyroidism. In contrast, surgery or medical therapy for adenomas that secrete growth hormone (GH) and for clinically nonfunctioning adenomas is not indicated during pregnancy. Pregnancy may cause an increase in the size of tumors that secrete prolactin (PRL), especially macroadenomas, so close surveillance is indicated and re-institution of bromocriptine therapy may be necessary to treat such an increase in tumor size. An increase in the size of other types of tumors during pregnancy is very rare.
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PMID:Pituitary tumors and pregnancy. 1291 26


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