UNIPROT:P01275 - FACTA Search

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

The endocrine status of the pancreas and the hypothalamic neurosecretory nuclei were studied by radioimmunoassay, immunocytochemical, morphometric and histochemical methods in Wistar rats of both sexes with experimental diabetes mellitus. The development of diabetes mellitus was characterized by beta-cell destruction and insulin concentrations reduction in these cells and the blood, by increase of glucagon and somatostatin levels in the alpha- and delta-cells, respectively, as well as by the growth of these substances concentrations in the peripheral blood. These changes were parallelled by activation of the vasopressin-, oxytocin and corticoliberin-synthesizing neurones of the paraventricular and supraoptic nuclei of the hypothalamus, as evidenced by morphometric findings and by increase of the blood vasopressin and corticoliberin concentrations and oxytocin level in the hypothalamus. Experimental diabetes mellitus was found to be characterized by activation of the hypothalamo-hypophyseo-adrenal system. Functional differences in the contribution of vasopressin- and oxytocin-synthesizing neurones of the hypothalamic nuclei in the pathogenesis of the disease is shown, as are their sex-specific reactions.
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PMID:[Status of vasopressin-, oxytocin- and corticoliberin-synthesizing structures of the hypothalamus in experimental diabetes mellitus in rats of different sexes]. 805 64

The present study assessed the possible role of oxytocin in the deterioration of glucose tolerance in gestational diabetes. Plasma levels of oxytocin, insulin, glucagon and glucose were measured at the time of a 400-kcal breakfast meal tolerance test in 12 women with gestational diabetes and 12 normal pregnant women in the third trimester. The gestational diabetic women had higher basal levels of insulin and an enhanced, delayed and prolonged insulin response to the breakfast. The same differences occurred in the glucose levels. There was no significant difference in the glucagon levels between the two groups. In the normal pregnant women, a significant (p < 0.05) though small rise in glucagon levels occurred 30 min after the ingestion of the breakfast. Oxytocin levels were not affected by the breakfast, and there was no clear difference between the two groups. The metabolic differences between the normal pregnant and gestational diabetic women were not related to any differences in oxytocin levels. In conclusion, we found no evidence of a role of oxytocin in the alteration of glucose metabolism in women with gestational diabetes. However, since alterations in oxytocin levels of possible significance for an impaired glucose tolerance are found in type 1 diabetic and extremely obese patients, further studies are needed in women with gestational or manifest diabetes.
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PMID:Is oxytocin involved in the deterioration of glucose tolerance in gestational diabetes? 822 52

Antidiuretic hormone and parathyroid hormone (PTH) inhibit HCO3- absorption by the rat medullary thick ascending limb (MTAL). Studies were performed on rat MTAL tubule suspension to specify the H(+)-HCO3- membrane transporters affected by these hormones and the implicated intracellular second messengers. Arginine vasopressin (AVP) and PTH stimulated cell adenosine 3',5'-cyclic monophosphate (cAMP) production with a relative rank order potency of AVP > rat PTH-(1-34) > bovine PTH-(1-84). Significant cell acidification in HCO3- -CO2-free medium, monitored in 2'7'-bis(carboxyethyl)-5(6')-carboxyfluorescein-loaded cells, was caused by 0.1 nM AVP, 1 nM rat PTH-(1-34), but not by < 100 nM bovine PTH-(1-84), as well as by 10(-4) M 8-bromo-cAMP and 2 x 10(-5) M forskolin; 10 nM AVP or rat PTH-(1-34) did not alter the intracellular pH when Na+/H+ antiport was inhibited by 2 mM amiloride. Prostaglandin E2 (PGE2, 10(-6) M), which inhibited AVP-stimulated cell cAMP production, reduced by 35% the cell acidification response to 10 nM AVP. AVP and 8-bromo-cAMP inhibited Na+/H+ antiport-dependent cell pH recovery from intracellular acidification, which was explained by a decrease in the Vmax of the antiporter. AVP did not directly affect K(+)-HCO3- cotransport and plasma membrane H(+)-ATPase of rat MTAL cells. Cytosolic calcium ([Ca2+]i), monitored in fura-2-loaded cells, was unaffected by up to 1 nM AVP, 100 nM PTH, glucagon, calcitonin, and oxytocin, and 1 microM PGE2; however, 100 nM AVP, but not 1-desamino-8-D-AVP (dDAVP), caused a peak increase in [Ca2+]i, even in the absence of extracellular Ca2+, and stimulated cell accumulation of [3H]inositol phosphates.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:cAMP-dependent control of Na+/H+ antiport by AVP, PTH, and PGE2 in rat medullary thick ascending limb cells. 838 52

The aim of the present study was to investigate how oxytocin given subcutaneously (SC) and intracerebroventricularly (ICV) influences the secretion of insulin, glucagon and glucose and to investigate whether the effect on these variables of suckling in lactating rats is mediated by oxytocinergic mechanisms. Male rats were given oxytocin in doses of 2 or 20 ng (SC) or 2 or 200 ng (ICV). Trunk blood was collected and hormone analysis performed by radioimmunoassay. Subcutaneous injections of oxytocin increased insulin, glucagon and glucose levels significantly. Two nanograms oxytocin given ICV had no effect on glucagon and glucose levels but caused a significant rise in insulin levels at this time point. This effect was abolished by atropine. The oxytocin antagonist 1-deamino-2-D-Tyr-(OEt)-4-Thr-8-Orn-oxytocin administered ICV increased insulin levels itself and therefore the effect on oxytocin-induced insulin secretion was difficult to evaluate. Intracerebroventricular injections of 200 ng oxytocin caused a significant rise not only of insulin but also of glucagon and glucose levels. Since this dose of oxytocin also caused a substantial rise of circulating oxytocin levels, these effects on glucose and glucagon may have been exerted at a peripheral site. Suckling in lactating rats was followed by a significant increase of glucose and glucagon levels. These effects were completely abolished by pretreatment with an oxytocin antagonist. In conclusion, oxytocin seems to influence pancreatic hormone secretion by two different mechanisms. Elevated circulating levels of oxytocin-e.g. as seen in response to suckling in lactating rats-are accompanied by a rise of glucagon and glucose levels which is blocked by the oxytocin antagonist. In contrast, nanogram amounts of oxytocin administered ICV cause a rise of insulin levels. Since this effect was blocked by atropine, it is likely to involve activation of vagal cholinergic neurons, innervating pancreatic beta-cells.
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PMID:Evidence of a peripheral and a central effect of oxytocin on pancreatic hormone release in rats. 873 93

The biotinyl-tyramide substrate of the horseradish peroxidase enzyme has been recently introduced to amplify immunohistochemical signals. We applied either fluorochromeor biotin-conjugated tyramine to improve the detection of different antigens in sections of rat stomach, pancreas, and hypothalamus. A ten- to 100-fold increase in staining efficiency was achieved, depending on the antibody, with either fluorescent or peroxidase detection systems. The amplification method was particularly useful for increasing a weak signal of conventional immunostaining caused by suboptimal tissue fixation. At a very low concentration of the primary antibody, the antigen can no longer be detected by a conventional fluorescent secondary antibody but is still detectable after amplification. When an antibody is used at this very low concentration and is detected by a fluorescent amplification method, another primary antibody, raised in the same host species, can be used and demonstrated with a different fluorochrome in subsequent conventional immunostaining of the same section. In this way it becomes possible to immunostain the same section with two different primary antibodies raised in the same host species. Samples for such double immunostaining are demonstrated here using pairs of monoclonal antibodies (to tyrosine hydroxylase and oxytocin) in the hypothalamus and polyclonal antibodies (to glucagon and neurofilament M) in sections of rat pancreas. Because in many cases the availability of antibodies is limited, the amplification method can be a quick and efficient tool for double immunostaining with antibodies from the same host species.
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PMID:Immunohistochemical signal amplification by catalyzed reporter deposition and its application in double immunostaining. 898 27

Oxytocin (OT) and vasopressin (AVP) stimulate insulin and glucagon release from the pancreas, and evoke insulin secretion from the rat insulinoma cell line, RINm5F. To determine which AVP/OT receptor subtype is expressed in RINm5F cells, we used PCR with degenerate primers to two transmembrane domains of the AVP (V1a, V1b (or V3), V2) and OT receptors (OTRs). The single PCR fragment identified was used to obtain a full length cDNA from a RINm5F cDNA library. Comparison of the deduced amino acid sequence of this clone with uterine OTR sequences from several species (human, sheep, bovine) and to the pig kidney epithelial cell (LLC-PK1) OTR reveals a very high degree of homology. After the RIN cell OTR cDNA was stably transfected into CHO cells (CHO-OTR), the cell membranes bound iodinated oxytocin antagonist with an apparent Kd comparable to that of RIN cell membranes and those from other OT target cells. Comparison of the ligand specificities of CHO-OTR and RIN cells membranes showed that the relative Ki values of a series of OT analogues were approximately equivalent in both preparations. The rank order of apparent Ki values also corresponded to published values for the rat myometrium, where OT elicits intracellular calcium transients, and increases inositol phosphate production. In uterin endometrium and amnion cells, OT stimulates prostaglandin release. Stimulation of CHO-OTR cells with OT caused an increase in cytosolic calcium concentration originating from both intracellular and extracellular sources, and a dose-dependent increase in inositol phosphate levels. Arachidonic acid release and PGE2 synthesis were also stimulated by OT. These findings (amino acid sequence homology, binding specificity, and signal transduction/second messenger production) suggest that OTRs from RINm5F cells are indistinguishable from OTRs that have been described in other tissues. The expression of OTR in pancreatic cells implies that OT plays a role in pancreatic function.
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PMID:Molecular cloning and functional characterization of the oxytocin receptor from a rat pancreatic cell line (RINm5F). 900 55

The effects of the posterior-pituitary peptides oxytocin (OT), arginine-vasopressin (AVP) and lysine-vasopressin (LVP) on insulin and glucagon secretion were examined in adult sheep. Each peptide was injected intravenously at doses from 1 to 3000 pmol kg-1. All three peptides increased plasma insulin and glucagon concentrations, but their dose-response relationships revealed differences between them. The maximal insulin responses induced by OT and AVP were very similar, but the threshold and maximal doses of AVP for increasing plasma insulin were higher than those of OT. OT and AVP had the same activity for stimulating glucagon secretion in respect of the threshold and maximal doses and the maximal hormone response. LVP also increased plasma insulin and glucagon concentrations, but it had the weakest activity for stimulating both hormones. These results suggest that in sheep posterior-pituitary peptide may play a role in regulating nutrient metabolism by influencing pancreatic hormone secretion.
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PMID:Effects of oxytocin, arginine-vasopressin and lysine-vasopressin on insulin and glucagon secretion in sheep. 924 6

Within the central nervous system, glucagon-like peptide-1-(7-36) amide (GLP-1) acts as a transmitter, inhibiting feeding and drinking behavior. Hypothalamic neuroendocrine neurons are centrally involved in the regulatory mechanisms controlling these behaviors, and high densities of GLP-1 binding sites are present in the rat hypothalamus. In the present study we have, over a period of 4 h, followed the effect of centrally injected GLP-1 on plasma levels of the neurohypophysial hormones vasopressin and oxytocin. Plasma levels of corticosterone and glucose were also followed across time after central administration of GLP-1. In conscious, freely moving, and unstressed rats, central injection of GLP-1 significantly elevated plasma levels of vasopressin 15 and 30 min after administration (basal, 0.8 +/- 0.2 pg/ml; 15 min, 7.5 +/- 2.0 pg/ml; 30 min, 5.6 +/- 1.1 pg/ml; mean +/- SEM) and elevated corticosterone 15 min after administration (52 +/- 13 vs. 447 +/- 108 ng/ml, basal vs. 15 min; mean +/- SEM). In contrast, plasma oxytocin levels were unaffected by intracerebroventricular (icv) injections of GLP-1 over a period of 4 h after the injection. The animals given a central injection of GLP-1 developed transient hypoglycemia 20 min after the injection, which was fully restored to normal levels at 30 min. Furthermore, we used c-fos immunocytochemistry as an index of stimulated neuronal activity. The distribution and quantity of GLP-1-induced c-fos immunoreactivity were evaluated in a number of hypothalamic neuroendocrine areas, including the magnocellular neurons of the paraventricular (PVN) and supraoptic (SON) nuclei and the parvicellular neurons of the medial parvicellular subregion of the PVN. The number of c-fos-expressing nuclei in those areas was assessed 30, 60, and 90 min after icv administration of GLP-1. Intracerebroventricular injection of GLP-1 induced c-fos expression in the medial parvicellular subregion of the PVN as well as in magnocellular neurons of the PVN and SON. A slight induction of c-fos expression was seen in the arcuate nucleus and the nucleus of the solitary tract, including the area postrema. In contrast, the subfornical organ, which is a rostrally situated circumventricular organ, was free of c-fos-positive cells after central administration of GLP-1. When the GLP-1 antagonist exendin-(9-39) was given before the GLP-1, c-fos expression in these neuroendocrine areas was almost completely abolished, suggesting that the effect of GLP-1 on c-fos expression is mediated via specific receptors. A dual labeling immunocytochemical technique was used to identify the phenotypes of some of the neurons containing c-fos-immunoreactive nuclei. Approximately 80% of the CRH-positive neurons in the hypophysiotropic medial parvicellular part of the PVN coexpressed c-fos 90 min after icv GLP-1 administration. In contrast, very few (approximately 10%) of the vasopressinergic magnocellular neurons of the PVN/SON contained c-fos-positive nuclei, whereas approximately 38% of the magnocellular oxytocinergic neurons expressed c-fos-positive nuclei in response to GLP-1 administration. This study demonstrates that central administration of the anorectic neuropeptide GLP-1 activates the central CRH-containing neurons of the hypothalamo-pituitary-adrenocortical axis as well as oxytocinergic neurons of the hypothalamo-neurohypophysial tract. Therefore, we conclude that GLP-1 activates the hypothalamo-pituitary-adrenocortical axis primarily through stimulation of CRH neurons, and this activation may also be responsible for the inhibition of feeding behavior.
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PMID:Central administration of glucagon-like peptide-1 activates hypothalamic neuroendocrine neurons in the rat. 932 62

The subcommissural organ (SCO) is a circumventricular organ of glial origin typical of all vertebrates. The SCO releases its secretion into the third ventricle to constitute Reissner's fibre (RF). Reportedly, in reptiles, SCO has cyclic secretory activity related to the reproductive cycle. In this immunocytochemical study we show that, in females of oviparous reptiles (Lacertidae: Podarcis sicula) and in a viviparous species (Scincidae: Chalcides chalcides), SCO secretion consists of hormones, in part of the oxytocin-like (OXY-like) type. The amount of OXY-like material in the cells and in the third ventricle varies according to the different stages of the reproductive cycle. In the oviparous species, OXY-like hormone secretion can be induced by FSH administration at 28 degrees C, in the period of winter reproductive stasis as well. In the viviparous skink, showing an annual single ovulatory cycle, OXY-like secretion is present in the basal region of the cells, and is released into the third ventricle only at delivery. The role of an OXY-like hormone in the SCO is here discussed in relation to the different stages of the reproductive cycle. Its influence on the hypothalamus-hypophysis-gonad axis and its role in the transport of eggs into the ducts in the oviparous species, and at delivery in the viviparous one, are also suggested.
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PMID:Production of an oxytocin like substance by the subcommissural organ (SCO), related to the reproductive cycle in oviparous and viviparous reptiles. 935 32

Receptor antagonists were used to determine which receptor mediates the effect of arginine vasopressin (AVP) and oxytocin (OT) on glucagon release from hamster glucagonoma In-R1-G9 cells. Both AVP (10(-9)-10(-6) M) and OT (10(-8)-10(-5) M) increased glucagon release from In-R1-G9 cells in a concentration-dependent manner and AVP was approximately 30-fold more potent than OT in this aspect. The antagonists with potent V1b receptor blocking activity, CL-4-84 (10(-9)-10(-6) M), dP[Tyr(Me)2]AVP and AO-2-44 (10(-8)-10(-6) M), antagonized the effect of both AVP and OT in a concentration-dependent manner. Other receptor antagonists at 10(-6) M failed to block the effect of AVP and OT; these included a highly selective OT-receptor antagonist, L-366,948 and a V1a/V2 receptor antagonist WK-3-6. However, these antagonists at higher concentrations (10(-5) and 10(-4) M) caused inhibition of AVP- and OT-induced glucagon release. The order of antagonistic potency was estimated as CL-4-84 approximately = dP[Tyr(Me)2]AVP approximately = AO-2-44 > WK 3-6 > L366,948. d[D-3-Pal]VP (10(-8)-10(-5) M), a V1b receptor agonist, also increased glucagon release in a concentration-dependent manner, which was antagonized by dP[Tyr(Me)2]AVP (10(-8)-10(-6) M) and CL-4-84 (10(-9)-10(-6) M), but not by WK-3-6 (10(-6) M) or L-366,948 (10(-6) M). Therefore, the stimulatory effects of both OT and AVP on glucagon release may be mediated by V1b receptors, but not by V1a, V2, or OT receptors.
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PMID:Effects of arginine vasopressin and oxytocin on glucagon release from clonal alpha-cell line In-R1-G9: involvement of V1b receptors. 982 65

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