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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

To examine the possible link between endocrine status and perinatal problems related to cattle cloning, plasma concentrations of cortisol, adrenocorticotropic hormone (ACTH) and components of the insulin-like growth factor (IGF) system were compared between 13 somatic cell cloned and seven control Japanese Black calves (five produced by artificial insemination [AI] and two produced from in vitro fertilized embryos [IVP]) immediately after birth. Five cloned calves required delivery by cesarean section (C-section), while all of control calves were delivered by spontaneous vaginal delivery. The C-section delivered clones were heavier at birth, followed by vaginally delivered clones and IVP controls, and AI controls were the lightest. The neonatal mortality (death within the 1st week) of C-section delivered clones was also high (4/5) compared to that of vaginally delivered clones (1/8) or controls (0/7). Plasma concentrations of cortisol and IGF-I were lower in the clones than control calves although the plasma ACTH level was not different between the groups. A striking difference was observed in plasma IGF binding protein (IGFBP) profile in which cloned calves had a greater relative abundance of IGFBP-2 compared with controls. Observed differences suggest that insufficient prepartum rise in plasma cortisol of cloned calves failed to initiate the switch to an adult mode of the IGF system during late gestation and therefore parturition was not spontaneous. Inappropriate developmental changes in endocrine system may be partly responsible for the fetal overgrowth and perinatal complications associated with the cloning technology.
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PMID:Endocrine characteristics of cloned calves. 1239 7

The development and function of the primate adrenal cortex are characterized by rapid growth, high steroidogenic activity, and a particular morphological appearance. The fetal adrenal glands grow rapidly and exponentially and at term are similar in weight to adult adrenals. From birth to 1 year their mass is reduced as they undergo a process of differentiation. Growth then remains slow until age 7 years. Thereafter, growth accelerates and the adrenals reach adult weight by the end of puberty. In the first trimester of gestation, fetal adrenal growth is thought to be independent of adrenocorticotropic hormone (ACTH), but after 15 weeks, ACTH is absolutely required for normal morphological and functional development. Other factors of fetal and/or placental origin, acting independently of or in conjunction with ACTH, are also required. Basic fibroblast growth factor, epidermal growth factor/transforming growth factor beta, and insulin-like growth factor (IGF)-I and -II, all acting in an autocrine and/or paracrine fashion, have been postulated to stimulate fetal adrenal cell proliferation. Corticotropin-releasing hormone may also play an important role in primate fetal adrenal function, primarily at the end of gestation. Finally, the estrogens are also important in the development of the pituitary-adrenal axis in primates.
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PMID:Development and function of the human fetal adrenal cortex. 1251 Sep 85

Ghrelin is a novel GH (growth hormone)-releasing peptide isolated from the stomach. The cardiovascular and hormonal effects of the subcutaneous administration of ghrelin in humans remain unknown. Six healthy volunteers each received subcutaneous administration of three doses of ghrelin (1, 5 or 10 microg/kg) and placebo; the order of administration was randomized, and separate doses were given at least 24 h apart. The serum GH level dose-dependently increased from 0.5 +/- 0.4 to 3.6 +/- 2.1 ng/ml (1 microg/kg ghrelin; P=0.99 compared with baseline), 27.1 +/- 12.0 ng/ml (5 microg/kg; P<0.01 compared with baseline) and 45.4 +/- 12.8 ng/ml (10 microg/kg; P<0.01 compared with baseline) 30 min after ghrelin administration. Subcutaneous administration of ghrelin did not significantly alter circulating levels of corticotropin, cortisol, insulin-like growth factor-1, noradrenaline or adrenaline, although 10 microg/kg ghrelin slightly increased the prolactin level. No significant changes in heart rate or mean arterial pressure were observed. In contrast, the left ventricular ejection fraction, as assessed by echocardiography, increased dose-dependently from 63.5 +/- 0.6% to 65.1 +/- 0.9% (1 microg/kg ghrelin; P=0.97 compared with baseline), 69.6 +/- 1.3% (5 microg/kg; P<0.01 compared with baseline) and 71.5 +/- 0.9% (10 microg/kg; P<0.01 compared with baseline) 30 min after ghrelin administration. These haemodynamic and hormonal changes were still apparent 60 min after ghrelin injection. In conclusion, subcutaneous administration of ghrelin dose-dependently induced relatively specific GH release and enhanced cardiac performance in humans.
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PMID:Cardiovascular and hormonal effects of subcutaneous administration of ghrelin, a novel growth hormone-releasing peptide, in healthy humans. 1277 96

The discovery of leptin (LEP) shed new light on mechanisms regulating body fat mass (BFM). In this aspect, interactions between LEP and glucocorticoids at hypothalamic level may be of great importance. Factors that influence plasma LEP levels have not been fully recognized and available data on LEP levels are often inconsistent. The aim of this study was to evaluate absolute and BFM-corrected plasma LEP levels and their diurnal variation, as well as to assess the relationship between LEP levels, body fat distribution, and hormones influencing body fat in subjects with various levels of endogenous cortisol and different nutritional status. Group I was composed of 14 women aged 14-58 yrs, BMI of 23.9-37.1 kg/m2, with hypercortisolism due to ACTH-dependent and ACTH-independent Cushing's syndrome (CUS). 17 women with visceral obesity (OTY) and normal or disturbed carbohydrate metabolism, i.e. impaired glucose tolerance (IGT) and diabetes mellitus (DM), aged 24 do 50 yrs, BMI 30.0-46.1 kg/m2, were included in group II. Group III consisted of 14 women with Addison's disease (AD), aged 18 do 63 yrs, BMI 15.4-31.6 kg/m2. The control group IV (KON) included 17 healthy women with normal BMI. BMI, WHR, body composition, and body fat distribution (DEXA method) were assessed in all subjects. Basal plasma levels of LEP, beta-endorphin (B-EP), cortisol (F), insulin-like growth factor-1 (IGF-1) were measured with RIA test kits. Plasma adrenocorticotrophin (ACTH) levels, serum levels of insulin (IRI) and growth hormone (GH) were measured with IRMA test kits. Blood glucose (G) concentration was determined with an enzymatic method. Adiposity-corrected LEP levels were expressed as LEP/BFM and LEP/%BF indices. Fasting insulin resistance index (FIRI) was also calculated. Higher BFM and %BF values were found in the OTY group as compared with CUS KON and AD groups. BFM distribution did not differ in KON and AD groups whereas CUS subjects exhibited a higher accumulation of fat in the trunk when compared to OTY subjects. Absolute LEP levels were correlated with trunk BF in CUS patients whereas in KON and AD groups these levels were correlated only with limb fat. Absolute LEP levels in CUS and OTY groups were comparable, whereas LEP/BFM and LEP/%BF indices were higher in the CUS group (Table 1) reflecting upregulation of LEP levels (Figs. 1, 2). BFM-corrected LEP levels were comparable in groups with normal cortisolemia, i.e. in OTY and KON groups, whereas in the AD group both absolute and BFM-corrected LEP levels were lower than in controls. No correlation was found between plasma levels of F and LEP in CUS and AD groups. This correlation was negative in KON (Fig. 3) and positive in OTY groups (Fig. 4). Moreover, KON and AD groups demonstrated a negative correlation between plasma ACTH and LEP levels. CUS patients showed positive, BFM-independent correlations between LEP levels, FIRI and G values, and a positive, BFM-dependent correlation between IRI and LEP levels. OTY patients exhibited a BFM-dependent positive correlation between FIRI and LEP levels. In these and in AD patients, a positive, BFM-independent correlation between IRI and LEP levels was found. Moreover, a negative, BFM-dependent correlation between GH and LEP levels was found in OTY patients. In this group, B-EP levels were positively correlated with LEP/BFM and LEP/%BF indices (Fig. 5). A negative correlation between LEP levels, LEP/BFM and LEP/%BF indices was ascertained in the AD group. In CUS, OTY, and KON groups, but not in the AD group, a midnight increase in leptin levels was observed. In conclusion, upregulation of leptin levels in relation to body fat in Cushing's syndrome is independent of the source of hypercortisolism. Apparently, it results from insulin resistance and hyperglycaemia and contributes to coexisting metabolic abnormalities. In Addison's disease, downregulation of leptin may reflect an adaptation mechanism to cortisol deficiency and result from low insulin and extremely high adrenocorticotrophin levels. In women with normal cortisol levels, irrespectively of nutritional status; leptin levels reflect body fat content. In obese subjects, leptin levels may be influenced by cortisol levels, high levels of insulin, IGF-1, and beta-endorphin as well as low levels of growth hormone. Disturbed function of hypothalamic-pituitary-adrenal axis (CUS, AD) does not directly influence diurnal variation in plasma leptin levels. In Cushing's syndrome, visceral fat may be a predominant source of leptin, whereas in women with normal or low cortisol levels peripherally accumulated fat may determine leptin secretion.
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PMID:[Evaluation of leptin levels in plasma and their reliance on other hormonal factors affecting tissue fat levels in people with various levels of endogenous cotisol]. 1460 84

Hypopituitarism is an increasingly recognized complication of traumatic brain injury that can have significant potential to impair recovery and rehabilitation in affected survivors. Although posttraumatic cranial diabetes insipidus is known to be transient in many cases, recovery of established anterior pituitary hormone deficiency is thought to be a very rare event. We report the case of a 25-yr-old man who incurred severe traumatic brain injury in 1997. Sixteen months later, dynamic pituitary stimulation tests revealed severe growth hormone and adrenocorticotropin hormone deficiency. He was treated with recombinant human growth hormone and hydrocortisone. Five years after traumatic brain injury, repeat neuroendocrine assessment, prompted by an increasing serum insulin-like growth factor-1 level, showed normal growth hormone and adrenocorticotropin hormone responses. This is the first case report, to our knowledge, to show that adult posttraumatic growth hormone deficiency can be reversible. The recognition that anterior pituitary dysfunction can recover after traumatic brain injury has implications for the follow-up of patients with hypopituitarism secondary to head trauma to avoid unnecessary, expensive, and potentially harmful therapy.
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PMID:Spontaneous recovery from posttraumatic hypopituitarism. 1582 86

The adenohypophysial hormones have been believed to have evolved from several ancestral genes by duplication followed by evolutionary divergence. To understand the origin and evolution of the endocrine systems in vertebrates, we have characterized adenohypophysial hormones in an agnathan, the sea lamprey Petromyzon marinus. In gnathostomes, adrenocorticotropin (ACTH) and melanotropin (MSH) together with beta-endorphins (beta-END) are encoded in a single gene, designated as proopiomelanocortin (POMC), however in sea lamprey, ACTH and MSH are encoded in two distinct genes, proopoicortin (POC) gene and proopiomelanotropin (POM) gene, respectively. The POC and POM genes are expressed specifically in the rostral pars distalis (RPD) and the pars intermedia (PI), respectively. Consequently, the final products from both tissues are the same in all vertebrates, i.e., ACTH from the PD and MSH from the PI. The POMC gene might have been established in the early stages of invertebrate evolution by internal gene duplication of the MSH domains. The ancestral gene might be then inherited in lobe-finned fish and tetrapods, while internal duplication and deletion of MSH domains as well as duplication of whole POMC gene took place in lamprey and gnathostome fish. Sea lamprey growth hormone (GH) is expressed in the cells of the dorsal half of the proximal pars distalis (PPD) and stimulates the expression of an insulin-like growth factor (IGF) gene in the liver as in other vertebrates. Its gene consists of 5 exons and 4 introns spanning 13.6 kb, which is the largest gene among known GH genes. GH appears to be the only member of the GH family in the sea lamprey, which suggests that GH is the ancestral hormone of the GH family that originated first in the molecular evolution of the GH family in vertebrates and later, probably during the early evolution of gnathostomes. The other member of the gene family, PRL and SL, appeared by gene duplication. A beta-chain cDNA belonging to the gonadotropin (GTH) and thyrotropin (TSH) family was cloned. It is expressed in cells of the ventral half of PPD. Since the expression of this gene is stimulated by lamprey gonadotropin-releasing hormone, it was assigned to be a GTHbeta. This GTHbeta is far removed from beta-subunits of LH, FSH, and TSH in an unrooted tree derived from phylogenetic analysis, and takes a position as an out group, suggesting that lampreys have a single GTH gene, which duplicated after the agnathans and prior to the evolution of gnathostomes to give rise to LH and FSH.
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PMID:The dawn and evolution of hormones in the adenohypophysis. 1635 98

A 10-year-old uncastrated male Dalmatian dog was referred for gait abnormalities consisting of chronic progressive stiffness and rigidity. Other symptoms were polyphagia associated with weight gain, polyuria and polydipsia, excessive panting, and an inspiratory stridor. The owner had noticed progressive thickening of the skin and enlargement of the tongue over the last 3 years. Physical examination revealed thickening of the skin, redundant skin folds, and enlargement of the tongue. The only remarkable abnormalities found on routine laboratory examination were mild anaemia and an increased serum fructosamine concentration. Circulating concentrations of total thyroxine, free thyroxine, and cTSH, and the results of an ACTH stimulation test were all within reference ranges. The basal serum growth hormone (GH) concentration was markedly elevated (23microg/l) and did not decrease during a glucose tolerance test or after somatostatin administration. The serum insulin-like growth factor-1 concentration was also markedly elevated (1254microg/l). Basal serum insulin concentration was high (95mU/l) and insulin concentrations increased considerably after glucose loading, consistent with insulin resistance. Abdominal ultrasonography showed no abnormalities. Survey radiographs of the vertebral column showed severe spondylosis deformans extending from the cervical to the lumbosacral spine. CT scanning of the skull showed an enlarged pituitary gland with normal enhancement pattern. On post-mortem examination, the entire vertebral column appeared as a single and inflexible structure due to the presence of multiple fused osteophytes. The pituitary gland contained an acidophilic adenoma that immunostained positively for GH (and negatively for ACTH and alpha-MSH). In conclusion, this Dalmatian dog with acromegaly and insulin resistance represents the first case of GH hypersecretion proven to be due to a somatotroph adenoma.
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PMID:Acromegaly due to a somatroph adenoma in a dog. 1647 61

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

Few and controversial results exist on the cellular sites of insulin-like growth factor (IGF)-I synthesis and the type 1 IGF receptor (IGF-1R) in mammalian anterior pituitary. Thus, the present study analysed IGF-I and the IGF-1R in rat pituitary. Reverse transcription-polymerase chain reaction revealed IGF-I and IGF-1R mRNA expression in pituitary. The sequences of both were identical to the corresponding sequences in other rat organs. In situ hybridization localized IGF-I mRNA in endocrine cells. The majority of the growth hormone (GH) cells and numerous adrenocorticotropic hormone (ACTH) cells exhibited IGF-1R-immunoreactivity at the cell membrane. At lower densities, IGF-1 receptors were also present at the other hormone-producing cell types, indicating a physiological impact of IGF-I for all endocrine cells. IGF-I-immunoreactivity was located constantly in almost all ACTH-immunoreactive cells. At the ultrastructural level, IGF-I-immunoreactivity was confined to secretory granules in co-existence with ACTH-immunoreactivity, indicating a concomitant release of both hormones. Occasionally, IGF-I-immunoreactivity was detected in an interindividually varying number of GH cells. In some individuals, weak IGF-I-immunoreactions were also detected also in follicle-stimulating hormone and luteinizing hormone cells. Thus, IGF-I seems to be produced as a constituent in ACTH cells, possibly indicating its particular importance in stress response. Generally, IGF-I from the endocrine cells may regulate synthesis and/or release of hormones in an autocrine/paracrine manner as well as prevent apoptosis and stimulate proliferation. Production of IGF-I in GH cells may depend on the physiological status, most likely the serum IGF-I level. IGF-I released from GH cells may suppress GH synthesis and/or release by an autocrine feedback mechanism in addition to the endocrine route.
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PMID:Insulin-like growth factor I (IGF-I) and its receptor (IGF-1R) in the rat anterior pituitary. 1724 Dec 80


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