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)

1. A new line of cloned, differentiated rat hepatocytes (RL-PR-C) was evaluated for its usefulness as an in vitro system for studying the regulation of the insulin receptor. 2. Insulin rapidly reversibly and specifically bound to RL-PR-C hepatocytes. Binding of tracer 125I-labeled insulin, which was competitively inhibited by native insulin as well as by proinsulin and analogs of insulin and proinsulin in proportion to their biological activity, was not influenced by glucagon, corticotropin, or human growth hormone. Anti-insulin receptor serum from a patient with Acanthosis Nigricans Type B competed with 125I-labeled insulin for binding to cell surface sites. 3. Trypsinization destroyed insulin binding sites, but these were restored by incubation under growth conditions; a 75% restoration of binding sites was achieved by one cell population doubling. 4. RL-PR-C hepatocytes responded to insulin binding by an increase in glycogen synthesis from glucose. The insulin effect was maximal at 85 nM, but was detectable at lower, more physiological, concentrations. 5. Chronic exposure (for at least 3h) of hepatocytes to insulin (10(-10)--(10(-8) M) reduced by up to 60% the number of binding sites for insulin (down-regulation). Down-regulation was prevented by cycloheximide at concentration (10 micron) sufficient to inhibit markedly protein synthesis from tracer isoleucine. Recovery from down-regulation induced by native insulin at 10(-7 M or lower concentrations was complete by 18 h under growth conditions. 6. Although RL-PR-C hepatocytes spontaneously transform after about 90 population doublings, no significant differences between normal and transformed cells were observed in insulin binding characteristics and in interaction of cells with anti-insulin receptor serum. However, transformed cells exhibited a substantially reduced (maximum of 20%) down-regulation response to insulin. 7. RL-PR-C rat hepatocytes appear, for these reasons, to be a useful model system for studying the regulation of the insulin receptor.
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PMID:Hormone receptors. 7. Characteristics of insulin receptors in a new line of cloned neonatal rat hepatocytes. 56 93

The bibliography concerning the interaction of the thymus with other endocrines is summarized. The thymus, the lymph nodes and the spleen of Sprague-Dawley rats were extracted with the method of Bezssonoff and Comsa and the extracts fractionated with the method of Bernardi and Comsa. The animals were (1) normal, (2) adrenalectomized, (3) adrenalectomized and substituted with one or several corticosteroids, (4) adrenalectomized and thymectomized, (5) thyroidectomized, (6) thyroidectomized and substituted with thyroxine, (7 and 8) castrated (males or females), (9 and 10) castrates substituted with sexual hormones, (11) castrated and adrenalectomized, (12) castrated and thyroidectomized, (13) castrated, adrenalectomized and thyroidectomized, (14) hypophysectomized, and (15) hypophysectomized and substituted with one hypophyseal hormone. In the Bernardi-Comsa preparations hormone was determined by UV-spectrophotometry. Adrenalectomy resulted in a significant decrease of the hormone content of the thymus (which was still more attenuated by cortisol) and its increase in the lymph nodes and the spleen. Corticosterone and desoxycorticosterone increased the hormone content in all three tissues, whilst aldosterone increased it in the thymus and decreased it in the lymph nodes and the spleen. Thyroidectomy resulted in a significant decrease of the hormone in the thymus and its quasi-disappearance from the lymph nodes and the spleen. This was prevented by thyroxine therapy. Castration resulted in an increase of the hormone content in all three tissues. This was prevented by sexual hormone therapy. Hypophysectomy resulted in decrease of the hormone content in all three tissues. This was prevented by injections with growth hormone, corticotropin and thyrotrophin. These results were compared with those of histological examinations of thymus, lymph nodes and spleen in the corresponding experimental groups. The consistency was found satisfactory.
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PMID:Hormonal influences on the secretion of the thymus. 57 3

Implantation of a mammotropic tumor (MtTF4), secreting growth hormone, prolactin, and corticotropin, in female rats of Fischer F344 strain causes hypertension, vasculitis, renal and cardiac hypertrophy, and extensive renal and cardiac lesions. When rats of the same strain were implanted with the MtTF4 tumor but sodium was withheld from the diet, systolic blood pressure rose more slowly but by six weeks reached the same values recorded in the animals implanted with the tumor and allowed to consume sodium ad libitum. In the rats, on sodium deficient diet, however, the vascular damage as well as the renal and cardiac lesions were minimal or absent. Implantation of the tumor caused adrenal cortical dysfunction, and elevated levels of deoxycorticosterone were seen in the peripheral plasma of the rats of all three groups. Nonetheless, plasma deoxycorticosterone was significantly lower in rats on a sodium deficient diet as compared with those having sodium added to the diet. Light microscopic and ultrastructural studies of the adrenal glands revealed that the lack of dietary sodium largely prevented the extensive damage of the zona fasciculata cells usually seen in the tumor-bearing rats, consuming sodium ad libitum. Both hypertensive MtT tumor-bearing animals and normotensive controls on a sodium deficient diet had a conspicuous increase of renal content of renin. It is evident that hypertension may be produced in rats bearing the MtTF4 tumor even in the virtual absence of dietary sodium. It does not appear that the hypersecretion of renal renin sustains the hypertension in these rats, since high levels of this substance were seen in the kidney of normotensive controls on the same sodium deficient diet. Elevated levels of plasma DOC may possibly explain the hypertension. In addition, it is likely that the animals may also have elevated levels of glucocorticoids.
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PMID:Deveolpment of hypertension in rats maintained on a sodium deficient diet and bearing a mammotropic tumor (MtTF4). 81 73

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

A 20 year old patient with generalized sarcoidosis is described. Sudden cessation of growth, and failure of development of secondary sex characteristics were noted at age 16. Tests of hypothalamic-pituitary function documented a deficiency of growth hormone and adrenocorticotropin reserve. The patient has osteolytic lesions in the calvarium of his skull, a previously unreported finding in patients with hypopituitarisim seconary to sarcoidosis. This is the 29th reported case of sarcoidosis and hypopituitarism, and the first in which growth hormone deficiency is documented. The literature pertaining to sarcoidosis and hypopituitarism, and sarcoid involvement of the skull is reviewed.
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PMID:Partial hypopituitarism and possible hypothalamic involvement in sarcoidosis: report of a case and review of the literature. 84 60

Adrenocortical function and plasma growth hormone pattern were investigated in 15 patients with chronic obstructive lung disease, in a period of acute respiratory failure and again after recovery. During the acute period, secretion rate and plasma concentrations of cortisol were markedly enhanced; urinary excretion of cortisol metabolites was only slightly increased, suggesting an alteration of the catabolism of cortisol under these conditions; adrenocortical sensitivity to corticotropin and capacity of maximal adrenal secretion were normal. The increase of cortisol secretion was probably due to hypoxemia and/or hypercapnia acting through the hypothalamo-pituitary axis. During the chronic phase of respiratory insufficiency, adrenocortical secretion and responsiveness were within the normal range. Finally, respiratory failure did not stimulate the secretion of growth hormone.
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PMID:Adrenocortical and somatotrophic secretions in acute and chronic respiratory insufficiency. 114 86

The effect of acute administration of human growth hormone (HGH) and of alpha-melanocyte stimulating hormone (alpha-MSH) on plasma aldosterone, cortisol, corticosterone and growth hormone has been studied in normal man and in patients with panhypopituitarism. There is no acute effect of exogenous HGH on plasma levels of aldosterone, cortisol and corticosterone in normal man and in patients with panhypopituitarism. The plasma level of immunoreactive HGH measured during acute HGH infusion in man does not seem to be proportional to the dose administred in our study. Alpha-MSH raises the concentartion of plasma HGH, BYT THIS STIMULATION IS NOT DOSE-DEPENDENT. Aldosterone, cortisol and corticosterone concentrations are not influenced by the elevation of HGH mediated by alpha-MSH in normal man. Although in some patients with panhypopituitarism an elevation of plasma aldosterone concenntration following alpha-MSH infusion is observed, it is unlikely that MSH is directly involved in the acute regulation of aldosterone secretion in healthy subjects.
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PMID:Influence of acute administration of human growth hormone and alpha-MSH on plasma concentrations of aldosterone, cortisol, corticosterone and growth hormone in man. 117 3

It was the aim of the present experiment to detect possible effects of branched-chain amino acids (BCAA) on the endocrine response to 1 h of continuous running. Blood samples were collected from 14 long-distance runners (age 24-42 years) in two different trials performed at 1-week intervals. In both trials (E and P) blood samples were collected at the following times: 9 a.m. (basal values sample), 10.30 a.m. (sample 90), 11.30 a.m. (sample 150), 12.30 p.m. (sample 210); the athletes performed 1 h of running at a constant predetermined speed between samples 90 and 150. Following the basal sample a mixture containing BCAA (E trial), or not containing BCAA (P trial) was ingested. In both trials no hormone basal concentrations, except insulin, were changed before exercise. In P trial, following exercise (sample 150), human growth hormone (HGH), prolactin (PRL), adrenocorticotropic hormone (ACTH) and cortisol (C) increased, while testosterone (T) decreased. In sample 210, after 1 h of rest, while ACTH, PRL and HGH had recovered to basal concentrations, C remained elevated and T displayed a further decrease. In the E trial a similar pattern of change was observed in sample 150 for HGH, PRL, ACTH and C; in sample 210 HGH and PRL displayed significantly lower values than in the corresponding P trial samples. The T was not modified by the running exercise and increased during the recovery period. It is, therefore, suggested that BCAA administration before exercise affects the response of some anabolic hormones, mainly HGH and T.
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PMID:Changes in the exercise-induced hormone response to branched chain amino acid administration. 131 74

The thymosins are a family of hormone-like products of epithelial cells of the thymus which are important in maintenance and function of the immune system. Thymosin fraction 5, a partially purified extract of calf thymus, can influence pituitary hormone release. We have studied the effects of thymosin alpha 1 (T alpha 1), the first peptide isolated from thymosin fraction 5, on thyrotropin (TSH), adrenocorticotropin (ACTH), prolactin (Prl) and growth hormone (GH) release. To evaluate its effect in vivo we injected the peptide into the third ventricle of conscious male rats and measured the concentration of the pituitary hormones in plasma at different times after the injection. Following third-ventricular injection of T alpha 1, there was a significant decrease in plasma TSH and ACTH concentrations in comparison with values of control groups injected with diluent. The decrease in plasma TSH was of longer duration and was obtained with a lower dose of T alpha 1 than that of ACTH. Also, a significant decrease in plasma Prl was observed, with the same dose as for TSH. On the other hand, there were no significant changes in plasma GH. To examine if there is any direct effect of T alpha 1 at the pituitary level, we incubated hemipituitaries from male rats in vitro with different concentrations of the peptide. In this system T alpha 1 evoked a dose-dependent release of TSH and ACTH, while there was no effect on the release of Prl and GH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of thymosin alpha-1 on pituitary hormone release. 131 3

Octreotide may act on non-growth hormone-, non-thyroid-stimulating hormone, and non-prolactin-secreting adenomas. Its efficacy was reported in some corticotropin-secreting adenomas from Nelson's syndrome and from Cushing's disease. In gonadotropin-secreting adenomas, octreotide was shown to be effective in two of eight cases. In nonfunctioning adenomas, visual improvement was observed with octreotide in 14 of 23 cases in a French multicenter study. Among the 33 patients whose tumor volume was checked, shrinkage occurred in seven, but an increase in tumor volume was observed in another seven patients. Mechanism(s) and prediction of efficacy of octreotide remain to be documented.
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PMID:The role of octreotide (Sandostatin) in non-growth hormone-, non-thyroid-stimulating hormone-, and non-prolactin-secreting adenomas. 132 96


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