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)

Several polypeptide hormones of apparently diverse structure and function have a number of similarities which suggest that there may be common features in their mechanism of action. These hormones are all composed of a single linear sequence of about 30 amino acids; their hydrophobic amino acids are regularly spaced at every third or fourth amino acid residue, allowing them to form amphipathic structures which can interact with phospholipids; a fragment at or near their N-terminus is required for biological activity. These hormones include glucagon, beta-endorphin, parathyroid hormone and calcitonin. A model is proposed in which all regions of the hormone bind to the receptor with comparable affinity except for a small segment which, when intact, triggers a conformational change in the receptor resulting in a further stabilization of the hormone-receptor complex. The activity of partial sequences and chemically modified forms of beta-endorphin, parathyroid hormone and glucagon are discussed in relation to this model.
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PMID:Relationships among several different non-homologous polypeptide hormones. 631 22

A set of commercially available peptides suitable for use as standards in denaturing isoelectric focusing (IEF) is described. The peptides N-procalcitonin fragment 1-57 (pI 3.98), Gln11-amyloid beta-protein fragment 1-28 (pI 5.76), gastric inhibitory polypeptide (pI 7.14), parathyroid hormone fragment 1-34 (pI 8.64) and human beta-endorphin (pI 9.49) can be focused to their isoelectric point in the presence of 8 M urea and 2% Nonidet P-40, and subsequently fixed and stained in polyacrylamide gels. The peptides give a linear standard curve in close agreement with a slope determined with a surface pH electrode. Under the same conditions some proteins focus to positions significantly at odds with their theoretical isoelectric point. The origins of these discrepancies and the implications for the determination of isoelectric points of unknown proteins by denaturing IEF are discussed.
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PMID:Peptides as standards for denaturing isoelectric focusing. 753 58

The mechanisms that control lipolysis in intra-abdominal fat cells from various primate species, the marmoset (Callithrix jacchus), the baboon (Papio papio), and the macaque (Macaca fascicularis), were compared to those of human intraabdominal fat cells. Selective beta 1- or beta 2-adrenoceptor agonists induced lipolysis in all species. Selective beta 3-agonists (BRL 37344, CL 316243, and SR 58611) acted as partial agonists in marmoset but were inefficient in other primates, including humans. alpha 2-Adrenoceptor number ([3H]RX 8210002 binding) equalized (baboon) or exceeded (other primates) beta 1/beta 2-adrenoceptors ([3H]CGP 12177 binding). Baboon fat cell membranes expressed similar amounts of coupled beta- and alpha 2-adrenoceptors. In all species, norepinephrine- or epinephrine-induced lipolysis did not reach the lipolytic effect of isoproterenol but their effects were enhanced after alpha 2-adrenoceptor blockade. N6-phenylisopropyladenosine (PIA) induced a full antilipolytic effect in baboon, macaque, and human adipocytes through adenosine receptors ([3H]DPCPX binding). Peptide YY (PYY) weakly inhibited lipolysis in baboon. Adrenocorticotropic hormone (ACTH) was inactive whereas parathyroid hormone (PTH) partially stimulated lipolysis in primates. Histamine was partially lipolytic in marmoset only. This study emphasizes the similarities of the mechanisms controlling the lipolysis in nonhuman primate and in human adipocytes and suggests that the baboon and the macaque should provide unique models for the study of the regulation of lipolysis.
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PMID:Control of lipolysis in intra-abdominal fat cells of nonhuman primates: comparison with humans. 777 57

To understand endocrine function and to determine which endocrine systems are likely to be affected, 6 patients with mitochondrial encephalomyopathies were studied. Three patients had myoclonus epilepsy and ragged-red fibers, and the other 3 patients had mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes. Clinically, short stature (5/6), amenorrhea (2/3), impotency (3/3), and poor development of secondary sexual characteristics (4/6) were noted. The endocrinological studies including triiodothyronine, tetraiodothyronine, thyrotropin, adrenocorticotropin, cortisol, parathyroid hormone and blood sugar were normal. However, there were low serum concentrations of estradiol (2), and progesterone (2) in 3 female patients. Two patients (1 man and 1 woman) had growth hormone deficiency and 1 had low testosterone level. Hypothalamopituitary dysfunction was confirmed after a series of stimulation tests. We conclude that patients with mitochondrial encephalomyopathies are common to have gonadal dysfunction. Although target organ may play a role, hypothalamopituitary lesion may be responsible for this abnormality.
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PMID:Gonadal dysfunction in mitochondrial encephalomyopathies. 854 17

To assess daily rhythms of salt appetite, we measured spontaneous 300 mM NaCl intake of male Sprague-Dawley rats fed a diet containing 150 or 25 mmol Ca2+/kg. Both groups drank most NaCl at night, but, as the dark period progressed, intakes of controls remained constant or diminished, whereas intakes of rats fed low-Ca2+ diet increased. During the late dark period, when the difference in NaCl intake between the two dietary groups was greatest, rats fed a low-Ca2+ diet lost more corticosterone and sodium in urine, had lower plasma osmolarity, and had higher plasma adrenocorticotropic hormone (ACTH) and corticosterone concentrations than did controls. Over the 24-h cycle, rats fed the low-Ca2+ diet excreted less Ca2+ and more corticosterone in urine than did controls. They also had consistently lower plasma concentrations of Ca2+ and renin activity and consistently higher plasma phosphorus, arginine vasopressin, parathyroid hormone, thyroxine, calcitonin, and 1,25-dihydroxyvitamin D3. These findings support the hypothesis that salt appetite induced by dietary Ca2+ deficiency involves a subtle dysfunction of the ACTH-corticosterone axis, but they also raise several other possibilities.
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PMID:Daily rhythm of NaCl intake in rats fed low-Ca2+ diet: relation to plasma and urinary minerals and hormones. 878 Feb 14

The effect of biologically active peptides (adrenocorticotropin, parathyroid hormone, calcitonin, prolactin) and steroids (aldosterone, progesterone, testosterone) hormones on NMR-relaxation proton of tissue water of kidney have been investigated in vitro. Results of this study suggest that peptide hormones caused dehydration of tissues via sodium regulation. Steroids, quite on the contrary, caused the hydration of kidney tissue independent of the movement of osmotic active electrolyte.
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PMID:[Action of biologically active peptides and steroids on nuclear magnetic resonance relaxation of protons of kidney tissue water in vitro]. 929 6

Traumatic brain injury (TBI) combined with fractures of long bones or large joints is often associated with enhanced osteogenesis (early fracture healing accompanied by hypertrophic callus formation and/or heterotopic ossifications). Humoral factors that cause enhanced osteogenesis in patients with TBI are not yet identified. The aim of this study was to reveal if post-traumatic change(s) of hormone levels in patients with TBI and bone fractures could be associated with the phenomenon of enhanced osteogenesis. The blood values of adrenocorticotropic hormone (ACTH), cortisol, growth hormone (GH), parathyroid hormone (PTH) and prolactin (PRL) were studied weekly over a period of three months after injury in patients with bone fractures only, those with TBI only or combined bone fractures and TBI (patients exerting enhanced osteogenesis). Stress-hormones, ACTH and cortisol, or the hormones related to the bone growth (GH and PTH) did not show any particular post-traumatic changes in the blood of patients with combined injury that could be associated with the enhanced osteogenesis. On the other hand, patients with combined bone fractures and TBI accompanied by enhanced osteogenesis had significantly elevated PRL levels in blood during the 5th week of the post-traumatic period. Thus, the maximal PRL values were measured at the time when in this group of patients fractures were in consolidation and hypertrophic callus or heterotopic ossifications were developing (as verified by x-ray imaging). Hence, PRL does not only influence physiology of the bone metabolism but also seems to be one of the humoral factors involved in the phenomenon of enhanced osteogenesis in patients with TBI.
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PMID:Post-traumatic hormonal disturbances: prolactin as a link between head injury and enhanced osteogenesis. 958 80

Secretin, glucagon, gastric inhibitory polypeptide (GIP), and parathyroid hormone (PTH) belong, together with vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase (AC)-activating polypeptide, to a family of peptides (the VIP-secretin-glucagon family), which also includes growth hormone-releasing hormone and exendins. All the members of this peptide family possess a remarkable amino-acid sequence homology, and bind to G-protein-coupled receptors, whose signaling mechanism primarily involves AC/protein kinase A and phospholipase C/protein kinase C cascades. VIP and pituitary AC-activating polypeptide play a role in the regulation of the hypothalamus-pituitary-adrenal (HPA) axis, and in this review we survey findings that also other members of the VIP-secretin-glucagon family may have the same function. Secretin and secretin receptors are expressed in the hypothalamus and pituitary gland, and secretin inhibits adrenocorticotropic hormone (ACTH) release. No evidence is available for the presence of secretin receptors in adrenal glands, but secretin selectively depresses the glucocorticoid response to ACTH of dispersed zona fasciculata-reticularis (ZF/R) cells. Glucagon and glucagon-like peptide-1 are contained in the hypothalamus, and all the components of the HPA axis are provided with glucagon and glucagons-like-1 receptors. These peptides exert a short-term inhibitory effect on stress-induced pituitary ACTH release and depress the ZF/R cell response to ACTH by inhibiting the AC/protein kinase A cascade; they also stimulate hypothalamic arginine-vasopressin release. GIP receptors are present in the ZF/R of the normal adrenals, and are particularly abundant in some types of adrenocortical adenomas and hyperplasias. GIP, through the activation of the AC/protein kinase A cascade, evokes a sizeable glucocorticoid secretagogue effect, leading to the identification of a food/GIP-dependent Cushing's syndrome. PTH and PTH-related protein are expressed in the hypothalamus and pituitary gland, and PTH and PTH-related protein receptors in all the components of the HPA axis. Both peptides enhance ACTH and arginine-vasopressin release, as well as stimulate aldosterone and glucocorticoid secretion of dispersed zona glomerulosa and ZF/R cells, respectively. The involvement of growth hormone-releasing hormone and exendins in the functional regulation of the HPA axis has not yet been extensively investigated.
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PMID:Secretin, glucagon, gastric inhibitory polypeptide, parathyroid hormone, and related peptides in the regulation of the hypothalamus- pituitary-adrenal axis. 1076 61

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

The authors report on a 44-year-old female hemodialysis (HD) patient who presented with hypercalcemia secondary to isolated adrenocorticotropic hormone (ACTH) deficiency. She had been suffering from nausea and abdominal pain caused by recurrent esophageal ulcer. Blood calcium (Ca) adjusted for serum albumin concentration was increased to 14.9 mg/dL (3.72 mmol/L) concurrently with fever and hypotension. Serum intact parathyroid hormone (PTH)-related peptide was not elevated, but serum intact PTH and 1,25-(OH)2 vitamin D3 were decreased to 31 pg/mL (ng/L) and 8.1 pg/mL (2.6 pmol/L), respectively. Endocrinologic examination found that plasma ACTH was reduced below 5.0 pg/mL (0.22 pmol/L). A single ACTH stimulation normally increased blood cortisol, whereas a single corticotropin-releasing hormone injection failed to increase plasma ACTH and cortisol. Pituitary magnetic resonance imaging disclosed no enlargement of pituitary gland. Circulating bone formation and absorption markers were not elevated. Blood Ca was normalized shortly after pamidronate disodium administration without glucocorticoid supplementation. This case suggested that secondary adrenal insufficiency caused by isolated ACTH deficiency could be an occult cause of severe hypercalcemia in HD subjects.
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PMID:Isolated adrenocorticotropic hormone deficiency presenting with hypercalcemia in a patient on long-term hemodialysis. 1290 Aug 50


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