Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endocrine abnormalities in patients with chronic renal failure are well documented. The present study aimed to assess the influence of long-term erythropoietin (EPO) therapy on endocrine abnormalities in haemodialyzed patients. Two groups of haemodialyzed patients, each of which comprised 17 subjects, were examined. The first one treated by EPO (EPO group) while the second one did not receive this hormone (NO-EPO group). A complete biochemical and hormonal check-up was performed before and at the 3, 6, 9 and 12 months of the study period. Normal values for the estimated parameters were obtained in appropriately selected sex and age-matched healthy subjects. After EPO therapy an increase of the haematocrit value from 21.8 +/- 0.9% to 32.6 +/- 0.9% was observed which was accompanied by a significant decline of plasma ferritin and saturation of transferrin. In patients of the NO-EPO group a significant although less marked rise of the haematocrit value (21.4 +/- 0.4% to 24.2 +/- 0.6%) was also noticed. EPO therapy did not change electrolytes (Na, K, Ca, inorganic phosphate), osteocalcin, creatinine, glucose and alkaline phosphatase plasma levels as well as plasma concentrations of calcium related hormones (PTH, calcitonin, 1.25(OH)2D3) and vasopressin (AVP). EPO treatment induced a significant decline of somatotropin (HGH), prolactin (PRO), follitropin (FSH), lutropin (LH), ACTH, cortisol, plasma renin activity, aldosterone, insulin (IRI), glucagon (IR-G), pancreatic polypeptide (PP) and gastrin plasma levels and an increase of plasma estradiol, testosterone and atrial natriuretic peptide (ANP). These EPO induced endocrine alterations were restricted mostly to the first 6 months of EPO administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of long-term erythropoietin therapy on endocrine abnormalities in haemodialyzed patients. 145 6

The distributions of atrial natriuretic peptide (ANP) clearance receptors in human umbilical cord and placenta were investigated by using des[Gln18,Ser19,Gly20,Leu21,Gly22]ANP-(4-2 3) (C-ANP) as a specific ligand of this receptor to displace bound alpha-125I-labeled ANP. alpha-125I-ANP bound reversibly to umbilical venous and arterial intima and to fetal placental and maternal decidual tissues, with dissociation constants of 1.24 +/- 0.51, 0.58 +/- 0.19, 1.86 +/- 0.51, and 1.07 +/- 0.25 mM, respectively. Binding was reversed by 1 microM unlabeled alpha-ANP but not by unrelated peptides such as gastrin. The 1 microM C-ANP displaced bound alpha-125I-ANP from the intima of umbilical artery but not that of the vein. The specific reversible binding of alpha-125I-ANP to placental decidua but not to fetal placenta was also displaced by 1 microM C-ANP. Therefore high-affinity binding sites for alpha-ANP on the intima of the umbilical artery and on placental decidua differ from those on the umbilical vein and on fetal placental tissue; the binding sites of the intima of the umbilical artery and of the decidua in humans are consistent with clearance receptors for alpha-ANP.
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PMID:Heterogeneous binding sites for alpha-atrial natriuretic peptide in human umbilical cord and placenta. 165 41

The distribution of atrial natriuretic peptide (ANP) clearance receptors in rat kidney was investigated by in vitro autoradiography using des[Gln18,Ser19,Gly20,Leu21,Gly22]-ANP-(4- 23) (C-ANP) and 125I-Tyr0-ANP-(5-25) as relatively specific ligands of this receptor. Alpha-125I-ANP (100 pM) bound reversibly but with high affinity to glomeruli, outer medullary vasa recta bundles, and inner medulla. C-ANP (10 microM) inhibited greater than 60% of this glomerular binding but did not inhibit the binding of alpha-125I-ANP to medullary tissues. Alpha-125I-ANP also bound reversibly to the renal arteries up to the glomerulus. This arterial binding was only partly inhibited by 10 microM C-ANP. In the presence of 10 microM C-ANP, increasing concentrations of alpha-125I-ANP bound to a residue of glomerular sites with apparent dissociation constants of 0.82 +/- 0.16 to 2.73 +/- 1.20 nM at different cortical levels. 125I-Tyr0-ANP-(5-25) bound significantly to glomeruli and intrarenal arteries but not to vasa recta bundles or inner medulla. This glomerular binding also occurred with nanomolar dissociation constants. It was completely inhibited by 1 microM alpha-ANP and 10 microM C-ANP, but not by unrelated peptides such as gastrin. These results suggest that renal ANP clearance receptors are restricted in vivo to the glomeruli and renal arterial system of the rat.
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PMID:Autoradiographic localization of atrial natriuretic peptide receptor subtypes in rat kidney. 216 58

Several factors are involved in the persistence of endocrine alterations after renal transplantation, among which the following are to be mentioned: (1) duration of chronic uraemia before renal transplantation; (2) residual function of the patients' native kidneys; (3) quality of function of the renal graft; (4) modulation of secretion, transport, and degradation of hormones, and/or (5) altered target organ responsiveness to hormones induced by immunosuppressive drugs (glucocorticoids, azathioprine, cyclosporin A) or altered internal environment. In kidney transplant patients the following endocrine abnormalities are to be mentioned: dissociation of the physiological relationship between aldosterone synthesis and function of the renin-angiotensin system, abnormal volumetric regulation of arginine vasopressin secretion, suppressed responsiveness of cortisol secretion to stimulatory manoeuvres, persistent secondary hyperparathyroidism, relative deficiency of insulin (induced by glucocorticoid therapy), with consequent carbohydrate intolerance or even diabetes mellitus, suppressed response of gastrin and pancreatic hormone secretion to a test meal, and reduced responsiveness of atrial natriuretic peptide secretion to central hypervolaemia. Episodes of acute graft rejection are characterized by endocrine alterations similar to those seen in patients with acute or chronic renal failure.
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PMID:Endocrine alterations in kidney transplant patients. 219 17

Twenty-two different humoral parameters including stress-, gastrointestinal- and volume-regulating hormones were measured before and within 45 min after parabolic flight maneuvers of twenty healthy adult subjects. We compared hormonal data of motion sickness-affected participants with those unaffected. Changes in cortisol and vasoactive intestinal peptide plasma levels were significantly different (p less than 0.002 and p less than 0.004) between the two groups with increasing plasma levels of both hormones during motion sickness but decreasing levels within the control group. Growth hormone and prolactin plasma levels increased by 400% and 115% within the motion sickness-affected group and to a smaller degree (120% and 40% increases, respectively) within the control group, while ACTH levels were almost unchanged within both groups. Pancreatic polypeptide and gastrin plasma levels as well as plasma levels of insulin and C-peptide were significantly decreased within both groups after the parabolic flight. Plasma renin, aldosterone, atrial natriuretic peptide and cyclic GMP levels were unchanged within the control group. Within the motion sickness-affected group, plasma renin and aldosterone levels were decreased and atrial natriuretic peptide levels increased after the flight. Humoral parameters of the thyroid gland were neither changed within the groups nor different between the groups. The present data confirm previous results that increases in plasma levels of certain stress hormones participate in motion sickness. Furthermore, increases in vasoactive intestinal peptide levels participate in motion sickness. These increases could explain some of the gastrointestinal symptoms in motion sickness and might serve as markers for a discrimination between regular stress and motion sickness.
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PMID:Hormonal changes after parabolic flight: implications on the development of motion sickness. 224 48

In order to elucidate the mechanism of postoperative intestinal dysfunction and the effects of Dachengqui Decoction (DCQD) on it, somatostatin (SS), gastrin (GAS), vasoactive intestinal polypeptide (VIP), substance P (SP), motilin (MOT) and atrial natriuretic peptide (ANP) were determined, frequency and spectrum of peristaltic sound were simultaneously analyzed in 31 subjects undergoing cholecystectomy, the value of pre-, post-operation and post-medication were compared. Plasma SS and MOT decreased postoperatively (P < 0.05), DCQD elevated SS and MOT to higher level than preoperation, VIP, SP increased for half fold (P < 0.05). Gurgling sound diminished after operation, whereas DCQD normalized it. Peak frequency (Fmax) of gurgling ranging from 234.4 to 468.2 Hz preoperatively, mean frequency (FA) was 341.8 +/- 30.9 Hz postoperatively. FA reduced to 322.3 +/- 79.4, DCQD elevated it to 374.2 +/- 57.1 Hz. The result suggested that intestinal motility was disturbed after cholecystectomy, bowel was in dystonic status, accompanying with decreased plasma MOT, DCQD promoted intestinal peristalsis and enhanced it's tonus. The influence of gut peptides might be one of the important pathway that DCQD works.
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PMID:[Effects of dachengqi decoction on gut hormones and intestinal movement after cholecystectomy]. 753 83

Endocrine abnormalities in patients with chronic renal failure are well documented. The present study aimed to assess the influence of long-term erythropoietin (EPO) therapy on endocrine abnormalities in hemodialyzed patients. Two groups of hemodialyzed patients, each of which comprised 17 subjects, were examined. The first group was treated by EPO (EPO group) while the second one did not receive this hormone (No-EPO group). A complete biochemical and hormonal check-up was performed before and at the 3, 6, 9, and 12 month points of the study period. Normal values for the estimated parameters were obtained in appropriately selected sex- and age-matched healthy subjects. After EPO therapy, an increase of the hematocrit value from 21.8 +/- 0.9 to 32.6 +/- 0.9% was observed, which was accompanied by a significant decline of plasma ferritin and saturation of transferrin. In patients of the No-EPO group, a significant although less marked rise of the hematocrit value (21.4 +/- 0.4 to 24.2 +/- 0.6%) was also noticed. EPO therapy did not change plasma levels of electrolytes (Na, K, Ca, inorganic phosphate), osteocalcin, creatinine, glucose, and alkaline phosphatase as well as plasma concentrations of calcium-related hormones (PTH, calcitonin, 1,25[OH]2D3), vasopressin, and triiodothyronine. EPO treatment induced a significant decrease in somatotropin, prolactin, follitropin, lutropin, ACTH, cortisol, plasma renin activity, aldosterone, noradrenaline, adrenaline, dopamine, glucagon, pancreatic polypeptide, and gastrin plasma levels and an increase in plasma insulin, estradiol, testosterone, atrial natriuretic peptide, thyrotropin, and thyroxine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Function of endocrine organs in hemodialyzed patients of long-term erythropoietin therapy. 762 22

The localization and distribution of neuropeptides in the central nervous system of the pig roundworm, Ascaris suum, have been determined by an indirect immunofluorescence technique in conjunction with confocal microscopy. Antisera to 25 vertebrate peptides and two invertebrate peptides were used to screen the worm for immunoreactivity (IR). Immunostaining was obtained with antisera to pancreatic polypeptide (PP), peptide YY (PYY), neuropeptide Y (NPY), gastrin, cholecystokinin (CCK), substance P (SP), atrial natriuretic peptide (ANP), salmon gonadotropin-releasing hormone (SGnRH), mammalian gonadotropin-releasing hormone (MGnRH), chromogranin A (CGA) and FMRFamide. The most extensive patterns of IR occurred with antisera to PYY, FMRFamide and gastrin. IR was evident in nerve cells and fibres in the ganglia associated with the anterior nerve ring and in the main nerve cords and their commissures; IR to FMRFamide also occurred in the posterior nerve ring. Immunostaining for the other peptides was confined to the nerve cords, with the number of immunoreactive nerve fibres varying from peptide to peptide.
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PMID:Immunocytochemical demonstration of neuropeptides in the central nervous system of the roundworm, Ascaris suum (Nematoda: Ascaroidea). 768 85

Several factors are involved in the persistence of endocrine alterations after renal transplantation, among which the following are to be mentioned: 1) duration of chronic uraemia before renal transplantation; 2) residual function of the patients' native kidneys; 3) quality of function of the renal graft; 4) modulation of secretion, transport, and degradation of hormones, and/or 5) altered target organ responsiveness to hormones induced by immunosuppressive drugs (glucocorticoids, azathioprine, cyclosporin A) or altered internal environment. In kidney transplant patients the following endocrine abnormalities are to be mentioned: dissociation of the physiological relationship between aldosterone synthesis and function of the renin-angiotensin system, abnormal volumetric regulation of arginine vasopressin secretion, suppressed responsiveness of cortisol secretion to stimulatory manoeuvres, persistent secondary hyperparathyroidism, relative deficiency of insulin (induced by glucocorticoid therapy), with consequent carbohydrate intolerance or even diabetes mellitus, suppressed response of gastrin and pancreatic hormone secretion to a test meal, and reduced responsiveness of atrial natriuretic peptide secretion to central hypervolaemia. Episodes of acute graft rejection are characterized by endocrine alterations similar to those seen in patients with acute or chronic renal failure.
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PMID:Function of endocrine organs in kidney transplant patients. 986 33

Dwyer has suggested that peptide receptors evolved from self-aggregating peptides so that peptide receptors should incorporate regions of high homology with the peptide ligand. If one considers self-aggregation to be a particular manifestation of molecular complementarity in general, then it is possible to extend Dwyer's hypothesis to a broader set of peptides: complementary peptides that bind to each other. In the latter case, one would expect to find homologous copies of the complementary peptide in the receptor. Thirteen peptides, 10 of which are not known to self-aggregate (amylin, ACTH, LHRH, angiotensin II, atrial natriuretic peptide, somatostatin, oxytocin, neurotensin, vasopressin, and substance P), and three that are known to self-aggregate (insulin, glucagon, and gastrin), were chosen. In addition to being self-aggregating, insulin and glucagon are also known to bind to each other, making them a mutually complementary pair. All possible combinations of the 13 peptides and the extracellular regions of their receptors were investigated using bioinformatic tools (a total of 325 combinations). Multiple, statistically significant homologies were found for insulin in the insulin receptor; insulin in the glucagon receptor; glucagon in the glucagon receptor; glucagon in the insulin receptor; and gastrin in gastrin binding protein and its receptor. Most of these homologies are in regions or sequences known to contribute to receptor binding of the respective hormone. These results suggest that the Dwyer hypothesis for receptor evolution may be generalizable beyond self-aggregating to complementary peptides. The evolution of receptors may have been driven by small molecule complementarity augmented by modular evolutionary processes that left a "molecular paleontology" that is still evident in the genome today. This "paleontology" may allow identification of peptide receptor sites.
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PMID:Molecular complementarity III. peptide complementarity as a basis for peptide receptor evolution: a bioinformatic case study of insulin, glucagon and gastrin. 1229 71


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