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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intravenously administered oxytocin was found to increase plasma insulin and glucagon levels. To explore if the same effects could be obtained by nonparenteral routes of administration, oxytocin was given by nasal instillation in normal conscious dogs. Plasma glucose, insulin, and glucagon levels all increased to levels which previously were shown to cause increased glucose production and utilization. Vasopressin infusion had no effect on these measurements. This is the first report of the effectiveness of oxytocin to evoke insulin and glucagon secretion by the nasal route of administration.
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PMID:Intranasal instillation of oxytocin increases insulin and glucagon secretion. 703 64

Reabsorption and/or degradation of proteins or peptides are functions of the proximal tubule. Large polypeptides or proteins are reabsorbed by luminal endocytosis and hydrolyzed by lysosomal enzymes. Our recent studies indicate that small linear peptides are hydrolyzed at the luminal membrane, with reabsorption of metabolites. The renal transport and hydrolysis of radiolabeled Al, All, BKN, oxytocin, glucagon, insulin, and LHRH were studied. Techniques for in vivo microinfusion of surface tubules in rats, arterial infusion in filtering and nonfiltering rat kidneys in vivo, and in vitro microperfusion of isolated rabbit nephron segments were used. Reabsorption of radiolabeled material was measured and the intact peptide or its metabolites were identified and quantified in urine, renal venous blood, bathing medium, and/or collection fluid. In addition, peptides were incubated in the presence of isolated renal membrane preparations to identify a probably cellular site of hydrolysis. The findings indicate that in proximal, but not distal tubules, radiolabeled Al, All, BKN, glucagon, and LHRH are hydrolyzed by brush border enzymes at the luminal membrane, followed by reabsorption of metabolites. In addition, it was found that, similar to the small intestine, the proximal tubule reabsorbed small peptide fragments, which were further degraded intracellurarly, In vivo inhibition studies with excess peptides revealed that hydrolysis is a more specific process than studies with excess peptides revealed that hydrolysis is a more specific process than reabsorption of metabolites. Large or small, complex peptides like insulin, oxytocin, or vasopressin that contain disulfide bridges are not hydrolyzed at the luminal brush border of the proximal tubule. In vivo sequestration and slow degradation of insulin by rat tubules suggest that this peptide is reabsorbed by endocytosis and degraded in lysosomes. Thus, as the molecular complexity or weight of a peptide increases, the mechanism for renal tubular degradation, instead of depending on luminal membrane hydrolysis, may primarily involve endocytosis and lysosomal digestion. This recently described mechanism for hydrolysis and transport of small linear peptides in the proximal nephron is characterized by having a high capacity and is analogous to membrane hydrolysis described for intestinal microvilli. The process may be biologically important to (1) conserve amino acids, (2) inactivate toxic peptides, and (3) help regulate circulating levels of peptide hormones.
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PMID:Renal tubular processing of small peptide hormones. 704 58

Sixteen peptides were injected intracerebroventricularly to test their effects on rectal temperature of rabbits in a thermoneutral environment. In initial tests 5 micrograms alpha-MSH, ACTH(1--24), oxytocin, vasopressin and glucagon altered body temperature while ACTH(1--10), cholecystokinin, contraceptive tetrapeptide, gastrin, insulin, interferon, leupeptin, LHRH, panhibin (somatostatin), and proctolin did not. Bombesin also altered body temperature but in no consistent direction. In further tests on the effective peptides 1.25--5.0 micrograms alpha-MSH and ACTH(1--24) produced dose-related decreases in rectal temperature as great as 1.0 degrees C. The same doses of oxytocin and glucagon produced small, prolonged hyperthermias which did not exceed 0.4 degrees C. Vasopressin caused rapid development of small increases in rectal temperature; temperature returned to normal in 2--3 hr. The results suggest that five of the peptides tested may have roles in central mediation of normal body temperature, hypothermia, hyperthermia and fever.
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PMID:Central administration of peptides alters thermoregulation in the rabbit. 724 7

The endocrine pancreas from 2 genera of lacertid lizards (Pedioplanis and Meroles) was investigated immunocytochemically for the presence of immunoreactivity to mammalian antisera to insulin (I), glucagon (G), pancreatic polypeptide (PP), peptide tyrosine tyrosine (PYY), neuropeptide tyrosine (NPY), somatostatin 14 (SRIF 14) and somatostatin 28 (SRIF 28), pancreastatin (Pst), galanin (Gl), oxytocin (OT). Cells immunoreactive (IR) to all the antisera used, and nerve fibers IR only to anti-galanin were found. Moreover, three types of colocalized immunoreactivities were detected: type 1 (PP/PYY/NPY), type 2 (G/PP/PYY/NPY), and type 3 (G/PYY/NPY/Pst).
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PMID:The endocrine pancreas of lacertids: an immunocytochemical study of the genera Pedioplanis and Meroles. 754 43

Acting in vivo, adrenalin and noradrenalin cause a statistically significant and permanent decrease in the motility of mouse spermatozoa remaining in the vas deferens. Intratesticular injection of vasopressin, oxytocin, insulin, and glucagon results in a decrease in spermatozoa motility in vas deferens, removal the spermatozoa to PBS in vitro, and an increase in percentage of motile spermatozoa on incubation medium. Thyroxine, calcytonin, and TRH did not affect motility of mouse spermatozoa in vivo.
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PMID:Effects of selected hormones on the motility of spermatozoa in the mouse vas deferens. 785 64

Hypothalamic mechanisms of neurohormone regulation of endocrine pancreas in diabetes mellitus, adaptation to hypoxia and their combination were studied on Wistar rats. To evaluate the condition of supraoptic nucleus (SON) secretory function, paraventricular subnuclei (PVH) of hypothalamus and endocrine pancreas, we used radioimmunoassay, immunocytochemical, morphometrical and histochemical methods. Hyperglycemia, hypoinsulinemia, glucagon and somatostatin synthesis and secretion intensification in diabetes mellitus is accompanied by marked reorganization of hypothalamic neurohormones (CRF, vasopressin, oxytocin) secretion with corresponding signs of activity increase of synthesizing their hypothalamus nuclei and subnuclei and also ACTH, corticosterone, cortisol rise in blood. Adaptation to hypoxia caused hypoglycemia, activated insulin biosynthesis, changed glucagon and somatostatin synthesis and secretion. CRF concentration, corticosterone and cortisol, ACTH in blood was not changed, vasopressin concentration lowered, oxytocin in median eminence of hypothalamus increased to a higher degree than in diabetes. Adaptation to hypoxia corrected impaired hormone balance and state of Langerhans islets (beta-cells destruction process inhibition, insulin biosynthesis stimulation, glucagon and somatostatin secretion decrease) in diabetes mellitus, hypothalamic neurohormones participating in this process.
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PMID:[The vasopressin-, oxytocin- and corticoliberin-synthesizing structures of the hypothalamus in rats with diabetes mellitus under hypoxic exposures]. 790 84

Hyperglycemia, hypoinsulinemia, and an increase of glucagon and somatostatin concentration under diabetes mellitus are accompanied by intensification of secretion of hypothalamic neurohormones (CRF, vasopressin, oxytocin, somatostatin) with the corresponding signs of the increase in activity of hypothalamus nuclei and subnuclei secreting them as well as ACTH, corticosterone and cortisol rise in blood. Adaptation to hypoxia has caused hypoglycemia, activated insulin biosynthesis, changed glucagon and somatostatin synthesis and secretion. CRF corticosterone, cortisol and ACTH concentration in blood was not changed, vasopressin concentration lowered, somatostatin and oxytocin amount (in hypothalamus) increased to a higher degree than under diabetes. Adaptation to hypoxia corrected impaired hormone balance and state of Langerhans islets (beta-cells destruction process inhibition, insulin biosynthesis stimulation, glucagon and somatostatin secretion decrease) under diabetes mellitus, hypothalamus neurohormones participating in this process.
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PMID:[Hypothalamic mechanisms of neurohormone regulation of the endocrine part of the pancreas]. 790 82

Previous studies have shown that infusion of oxytocin into normal dogs increased plasma levels of insulin and glucagon. These responses were accompanied by increased rates of glucose production and overall glucose uptake. The purpose of the present study was to determine whether, conversely, changes in glucose metabolism would result in changes in oxytocin secretion. In normal dogs, injection of insulin (0.1 U/kg/iv) resulted in increased secretion of oxytocin which coincided with the hypoglycemic nadir, and the oxytocin levels remained elevated for the remaining 60 min, during which time plasma glucose levels were returning to normal. In dogs made diabetic with streptozocin, injection of insulin (1 U/kg/iv) evoked increased oxytocin secretion which began as the plasma glucose levels were falling from the control value of 400 mg/dl to about 170 mg/dl; the oxytocin levels remained above initial values for at least 90 min, during which period plasma glucose returned to normal glycemic values. In normal dogs, infusion of 2-deoxyglucose, which causes intracellular glucopenia, caused a prompt and sustained increase in plasma oxytocin levels. The data suggest that abrupt decreases in availability of glucose in the central nervous system, as induced experimentally by administration of 2-deoxyglucose or by a rapid fall in peripheral glucose levels, evokes secretion of oxytocin.
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PMID:Oxytocin secretion is stimulated by changes in glucose metabolism. 793 34

The aim of this study was to investigate the role of vagal nerve activity for the release of oxytocin, prolactin and gastrointestinal (GI) hormones during suckling as well as for the secretion of milk in lactating rats. We have therefore performed experiments on vagotomized lactating rats. The animals were decapitated and trunk blood was collected from nonsuckling rats and from suckling rats in connection with milk ejection. Oxytocin, prolactin, vasoactive intestinal polypeptide (VIP), somatostatin, insulin, glucagon and glucose levels in plasma were measured by RIA-technique. In addition, maternal weight as well as the weight of the litters were recorded 7 d after vagotomy. As expected, oxytocin and prolactin levels rose in response to suckling in sham-operated controls. In vagotomized animals the suckling-induced increase of oxytocin was blocked and prolactin levels were significantly decreased. VIP levels in plasma increased following suckling in sham-operated animals and failed to respond after vagotomy. In contrast, somatostatin levels that rose significantly in sham-operated rats were even more significantly raised in vagotomized animals. In addition, insulin but not glucagon levels were increased by suckling. The insulin response, however, persisted after vagotomy. Interestingly, suckling was followed by a lowering of blood-glucose levels in vagotomized, but not in sham-operated animals. The vagotomized rats ate as much and increased in weight as sham-operated rats during the 7 d of vagotomy. The litters of vagotomized rats, however, gained significantly less weight in comparison with control litters. In conclusion, this study shows that vagal nerve activity is of importance for the release of oxytocin, prolactin, vasoactive intestinal polypeptide and somatostatin during suckling.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of vagal nerve activity during suckling. Effects on plasma levels of oxytocin, prolactin, VIP, somatostatin, insulin, glucagon, glucose and of milk secretion in lactating rats. 797 18

Because of the enormous growth over the last three decades of research on the role of peptides in the brain, the need became apparent to determine the status of these compounds in terms of their current research interest. Since 1965, over a quarter of a million research papers have been published on peptides that have since been classified as neuroactive. The present study was undertaken to analyze systematically the yearly trends of research emphasis in neuroactive peptides as reflected by their individual frequency of publication by year, beginning in 1966. A computer analysis of the publication characteristics was carried out using the Medline data base in which the citation search was limited to the topic brain crossed with the topic mammal. One criterion for the inclusion of a given peptide in the analysis was a frequency of 25 or more citations following its discovery, as related to the mammalian brain. The 42 peptides that met this criterion were: adrenocorticotropic hormone, angiotensin II, atrial natriuretic factor, bombesin, bradykinin, calcitonin, calcitonin gene-related peptide, carnosine, beta-casomorphin, cholecystokinin, corticotropin-releasing factor, delta sleep-inducing peptide, dynorphin, beta-endorphin, Leu-enkephalin, Met-enkephalin, galanin, gastrin, glucagon, growth hormone, growth hormone-releasing factor, insulin, kyotorphin, beta-lipotropin, luteinizing hormone-releasing factor, melanocyte-stimulating hormone release inhibitory factor-1, alpha-melanocyte-stimulating hormone, motilin, neurokinin A, neurokinin B, neuropeptide Y, neurotensin, oxytocin, pituitary adenylate cyclase activating polypeptide, peptide HI, prolactin, secretin, somatostatin, substance P, thyroid-releasing hormone, vasopressin, and vasoactive intestinal peptide. An overall analysis of the 298,105 papers published on these 42 peptides since 1965 revealed that the research activity of 24,742, or 8.30%, of the studies, focused on their neuroactive properties. Taken as a whole, the research on neuroactive peptides reached a peak in 1986, as reflected by the total of 1793 papers published during that year. Although the level of publication has fluctuated between 1548 and 1774 research papers over the last 6 years, it is now clear that the trend in research on neuroactive peptides has reached an asymptote today that shows no sign of deviation. A temporal analysis year by year of individual publication profiles revealed three distinct trends: 1) peptides showed a slow development in research interest and did not exceed more than 15-30 publications per year; 2) peptides exhibited a steady increase in research activity over the years that continues today; and 3) peptides displayed an initial, often intense, research emphasis that inexplicably declined, in some cases precipitously, in the mid 1980s.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neuroactive peptides: unique phases in research on mammalian brain over three decades. 800 41


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