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)

In humans, the syndrome of cortisol resistance is characterized by the absence of signs and symptoms of Cushing's syndrome, elevated total and unbound plasma cortisol concentrations, and increases in urinary free cortisol excretion and plasma adrenocorticotropic hormone. In one family, a severely affected member had hypertension and hypokalemic alkalosis associated with increased plasma concentrations of corticosterone and deoxycorticosterone. These patients are resistant to suppression of the pituitary-adrenal axis by dexamethasone. Dexamethasone therapy, however, effectively corrected hypertension and hypokalemic alkalosis in the severely affected patient, without causing signs of glucocorticoid excess. The glucocorticoid receptor from these patients has a low affinity for glucocorticoids and is unstable during thermal activation. Both the molecular weight of the glucocorticoid receptor and the size of the corresponding mRNA are similar to those of normal controls. Transformation of B-lymphocytes with Epstein-Barr virus leads to induction of glucocorticoid receptors. Receptor induction, however, is lower in patient cells than those obtained from normal controls. This decreased induction parallels decreased expression of glucocorticoid receptor mRNA. Thus, in this form of glucocorticoid resistance the glucocorticoid receptor is abnormal and leads to diminished target organ responsiveness. Many New World primates exhibit glucocorticoid "resistance," without apparent pathology. These species have markedly elevated plasma cortisol, both total and unbound concentrations, increased urinary free cortisol excretion, and marked increases in plasma adrenocorticotropic hormone and beta-endorphin. The glucocorticoid receptors of these primates have decreased affinity for glucocorticoids, are thermolabile, and are not induced by Epstein-Barr virus transformation as indicated by specific binding and mRNA expression. Both the molecular weight of the glucocorticoid receptor and the size of the corresponding mRNA are similar to those of normal controls. Despite the high plasma cortisol concentrations in these primates, there is no sodium retention and aldosterone levels are actually increased. The kidney aldosterone receptor cross-reacts poorly with cortisol, explaining the absence of sodium retention. New World primates also have progesterone, estrogen, aldosterone, and vitamin D insensitivity, suggesting a common factor linking steroid hormone receptors.
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PMID:Glucocorticoid resistance in humans and nonhuman primates. 264 36

Subcutaneous injection of nonspecific irritants such as magnesium silicate (talc) provokes granulomatous inflammation in the rat. Part of the acute phase response (APR) in these animals is the loss of trabecular bone at sites distant from the site of inflammation. To assess the possible involvement of vitamin D in the bone loss, we studied the development of the acute phase response in vitamin D-deprived rats. The serum APR provoked by subcutaneous inflammation in rachitic rats consisted of hypozincemia, hypercupremia, increased alkaline phosphatase activity and adrenocorticotropic hormone (ACTH) concentration, and was similar to that in control animals except for the absence of hypoferremia. Control rats with talc-induced subcutaneous inflammation also had splenomegaly and decreased total and mononuclear peripheral blood cell counts, while subcutaneous inflammation did not induce spleen changes in rachitic rats. Subcutaneous inflammation induced the loss of trabecular bone and decreased the osteoblastic cell count in tibial metaphyses in control animals. Rachitic rats had abundant osteoid on trabecular surfaces, and the number of osteoblasts and osteoclasts was comparable to that of the controls. Subcutaneous inflammation did not affect any of the bone parameters in rachitic rats. These results indicate that vitamin D plays an important role in the generation of the acute phase response during inflammation, particularly in the induction of spleen and bone cell changes. The discrepancy of the blood on one hand and bone and spleen indices of the APR on the other, indicate that they may be divergent pathways in the generation of the inflammatory response, some of which may be dependent on vitamin D.
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PMID:Role of 1,25-dihydroxyvitamin D3 in the generation of the acute-phase response in rats with talc-induced granulomatosis. 835 76

The results of analysis of interloci associations between two pairs of syntenic loci (transferrin and ceruloplasmin, receptor for vitamin D and kappa-casein) and two non-syntenic ones (amylase-1 and post-transferrin 2) in two cattle groups of Red Steppe breed (infected and uninfected by bovine leukosis virus) and in two groups of Black-and-White Holsteins (from relatively "pure" zone and from the 10 km zone of Chernobyl NPP) were presented. It is found that "linkage disequilibrium" between loci is observed independent of their synteny. The data obtained allowed the authors to suppose, that the interloci associations are rather controlled by different factors of artificial and natural selection than by the genetic linkages between genes.
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PMID:[Interlocus associations and their variability in cattle]. 959 47

The historical picture of the endocrine system as a set of discrete hormone-producing organs has been substituted by organs regarded as organized communities in which the cells emit, receive and coordinate molecular signals from established endocrine organs, other distant sources, their neighbors, and themselves. In this wide sense, the human skin and its tissues are targets as well as producers of hormones. Although the role of hormones in the development of human skin and its capacity to produce and release hormones are well established, little attention has been drawn to the ability of human skin to fulfil the requirements of a classic endocrine organ. Indeed, human skin cells produce insulin-like growth factors and -binding proteins, propiomelanocortin derivatives, catecholamines, steroid hormones and vitamin D from cholesterol, retinoids from diet carotenoids, and eicosanoids from fatty acids. Hormones exert their biological effects on the skin through interaction with high-affinity receptors, such as receptors for peptide hormones, neurotransmitters, steroid hormones and thyroid hormones. In addition, the human skin is able to metabolize hormones and to activate and inactivate them. These steps are overtaken in most cases by different skin cell populations in a coordinated way indicating the endocrine autonomy of the skin. Characteristic examples are the metabolic pathways of the corticotropin-releasing hormone/propiomelanocortin axis, steroidogenesis, vitamin D, and retinoids. Hormones exhibit a wide range of biological activities on the skin, with major effects caused by growth hormone/insulin-like growth factor-1, neuropeptides, sex steroids, glucocorticoids, retinoids, vitamin D, peroxisome proliferator-activated receptor ligands, and eicosanoids. At last, human skin produces hormones which are released in the circulation and are important for functions of the entire organism, such as sex hormones, especially in aged individuals, and insulin-like growth factor-binding proteins. Therefore, the human skin fulfils all requirements for being the largest, independent peripheral endocrine organ.
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PMID:Human skin: an independent peripheral endocrine organ. 1159 11

We report here a 47-year-old woman with isolated adrenocorticotropin (ACTH) deficiency (IAD). She presented impaired renin-angiotensin-aldosterone (R-A-A) system and suppressed parathyroid hormone (PTH)-vitamin D system. She showed severe hyponatremia due to secondary adrenocortical insufficiency, which was deteriorated by hypoaldosteronism. She also showed hyperphosphatemia and relative hypercalcemia with suppressed PTH-vitamin D axis. Moreover, she showed hypothyroidism, which was thought to be important to maintain normal Ca levels under secondary hypoadrenalism via decrease in bone resorption by T3. Replacement with glucocorticoid completely normalized PTH-vitamin D axis and R-A-A system. Thus, the present case implicates that severe adrenocortical deficiency due to IAD might affect both R-A-A system and PTH-vitamin D axis. These findings suggest that the ACTH-cortisol axis has an important role in mineral metabolism in vivo.
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PMID:Isolated adrenocorticotropin deficiency presenting with impaired renin-angiotensin-aldosterone system and suppressed parathyroid hormone-vitamin D axis. 1213 25

From experience in six cases the anabolic steroid hormones, especially long-acting testosterone and estrogen preparations, are the treatment of choice in Paget's disease, as in postmenopausal osteoporosis. Details of the management of three patients over a period of four years are presented. Roughly 4 per cent of the population, mostly persons over 40, show some evidence of Paget's disease. Only a small number of them, however, have severe manifestations requiring treatment, such as pain, howing or fracture of the bones, pressure on nerves or heart failure. In rare cases malignant changes occur in the involved bone. Since the cause of Paget's disease is not known, treatment in the past has been largely empirical. Reifenstein and Albright had advocated the therapeutic use of calcium, vitamin D and ascorbic acid, and, in postmenopausal women, administration of estrogens; but with fractures or immobilization, intake of calcium-containing foods, such as milk, must be restricted to avoid dangerous piling up of calcium and kidney stones, and fluids must be forced. In recent years anabolic steroid hormones, principally oral androgens and estrogens, have been employed by Gordan and others to promote bone repair, lessen bone pain and decrease urinary excretion of calcium. While these hormones probably do not arrest the disease, they seem to stabilize it and bring relief of symptoms. More recently, Albright and Henneman demonstrated that very large doses of corticotropin (ACTH) or cortisone resulted in immediate cessation of bone pain, decrease in urinary excretion of calcium and histologic evidence of regression of the disease process. The large doses required, however, also produce dangerous side effects, such as psychosis and osteoporosis, indicating that such treatment probably should not be continued over long periods.
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PMID:Paget's disease; changes occurring following treatment with newer hormonal agents. 1441 Jun 71

Previous research in our laboratory demonstrated marked increases in phytate P utilization when P-deficient corn-soybean meal diets were supplemented with 1a-hydroxycholecalciferol [1alpha-(OH) D3] and fed to chicks. Our objective was to determine if 1alpha-(OH) D3 would improve phytate P utilization when supplemented to vitamin D-adequate laying hen diets. The five experimental treatments were 1) P-deficient corn-soybean basal diet [17% CP, 3.8% Ca, and 0.10% nonphytate NPP)], 2) basal with 2.5 microg/kg 1alpha-(OH) D3, 3) basal with 5 microg/kg 1alpha-(OH) D3, 4) basal with 10 microg/kg 1alpha-(OH) D3, and 5) basal with 0.35% supplemental inorganic P (0.45% NPP, positive control). Diets were fed to six replicate groups of 12 HyLine W-98 White Leghorn laying hens from 44 to 52 wk of age. Hen-day egg production was significantly depressed by 47 wk of age for the basal diet treatment and by 47, 49, and 48 wk of age, respectively, for the 2.5, 5, and 10 microg/kg of 1alpha-(OH) D3 treatments compared to the positive control diet. Supplementation with 5 or 10 microg/kg 1alpha-(OH) D3 did improve (P < 0.05) egg production, but egg production for those treatments was much lower than that for the 0.45% NPP treatment. Our results indicate that 1alpha-(OH) D3 did not substantially improve P utilization in laying hens fed corn-soybean meal diets.
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PMID:1alpha-hydroxycholecalciferol has little effect on phytate phosphorus utilization in laying hen diets. 1465 75

We review the evidence indicating a possible beneficial role for UVR on three Th1-mediated autoimmune diseases: multiple sclerosis, type 1 diabetes and rheumatoid arthritis in relation to recent developments in photoimmunology. Recent work suggests that UVR exposure may be one factor that can attenuate the autoimmune activity leading to these three diseases through several pathways involving UVB and UVA irradiation, UVR-derived vitamin D synthesis and other routes such as alpha-melanocyte-stimulating hormone, calcitonin gene related peptide and melatonin. Ecological features, particularly a gradient of increasing prevalence of multiple sclerosis and type 1 diabetes with higher latitude, provide some support for a beneficial role of UVR. Analytical studies provide additional support, particularly as low vitamin D has been prospectively associated with disease onset for all three diseases, but are not definitive. Randomized controlled trial data are required. Further, we discuss how associated genetic studies may assist the accumulation of evidence with regard to the possible causal role of low UVR exposure and/or low vitamin D status in the development of these diseases.
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PMID:UVR, vitamin D and three autoimmune diseases--multiple sclerosis, type 1 diabetes, rheumatoid arthritis. 1597 32

Hormones influence the development and function of human skin which also produces and releases hormones. Recently attention has been focused on identifying and understanding the complex endocrine properties of human skin, such as expression and function of specific hormone receptors, synthesis of hormones from major classes of compounds used by the body for general purposes, organized metabolism, activation, inactivation and elimination of the hormones in specialized cells of the tissue, exertion of biological activity and release of tissue hormones in the circulation. Specifically, hormones exert their biological effects on the skin through interaction with high-affinity receptors, such as several receptors for peptide hormones and neurotransmitters, steroid and thyroid hormones. Hormones exhibit a wide range of biological activities on the skin with distinct effects caused by growth hormone/insulin-like growth factor-I, neuropeptides, sex steroids, glucocorticoids, retinoids, vitamin D, peroxisome proliferator-activated receptor ligands, eicosanoids, melatonin and serotonin. Human skin produces, activates or inactivates metabolically numerous hormones which are probably important for skin functions but also for functions of the entire human organism, such as sex hormones, especially in aged individuals, insulin-like growth factor and -binding proteins, neuropeptides, prolactin, catecholamines, retinoids, steroids, vitamin D and eicosanoids. These functions are undertaken in most cases by different skin cell populations in a coordinated way, indicating the endocrine autonomy of the skin. Characteristic examples are the metabolic pathways of the corticotropin-releasing hormone/propiomelanocortin axis, steroidogenesis, vitamin D and retinoids. The human skin is, thus, the largest, peripheral endocrine organ.
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PMID:The human skin as a hormone target and an endocrine gland. 1698 74

Male offspring of neonatally vitamin A or D treated (hormonally imprinted) rat dams were studied for hormone (adrenocorticotrophine [ACTH], beta-endorphin, histamine, triiodothyronine [T3]) content in immune cells, by using immunocytochemical methods for flow cytometry and confocal microscopy. ACTH and T3 were almost doubled in the lymphocytes of vitamin A treated mothers' offspring, while histamine decreased to a one-third in the histamine content of vitamin D treated mothers' offspring. Part of the animals received vitamin treatment again 24 hours before measurement, however, only endorphin content elevated moderately. In the offspring of untreated dams administered with vitamin D 24 hours before measurement, each cell type studied (lymphocyte, monocyte-granulocyte group, mast cell) had a one-third lower T3 content, which shows that vitamin D treatment can influence hormone content of immune cells. The experiments call attention to the transgenerational effect of perinatal treatment with lipid-soluble, intracellular receptor-bound vitamins.
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PMID:Transgenerational effect of neonatal vitamin A or D treatment (hormonal imprinting) on the hormone content of rat immune cells. 1737 34


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