Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood-glucose concentration is tested in male volunteers before and on the 1st, 3rd, 7th, 15th, 20th, 30th and 60th min after intravenous administration of oxytocin in doses of 0.1 IU/kg. In the first minutes after the injection there is a hypoglycaemic tendency in the changes of the blood glucose concentration, maintained in 60 per cent of the cases, while in the remaining subjects slight hyperglycaemia after the 7th min is observed. Simultaneously, hyperemia of the skin, moderate decrease in the diastolic blood pressure and tachycardia are observed. The effect of oxytocin is associated with increased influx of blood in the adipose tissue, where the glucose is metabolized with the involvement of the specific oxytocin receptors. The late hypoglycaemia is associated with oxytocin-inhibited insulin decomposition, the hyperglycaemia--with the domination of the sympathoadrenal activation in some of the subjects examined. A conclusion is reached that the effect of oxytocin on carbohydrate metabolism is physiologically unimportant.
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PMID:Effect of oxytocin on the blood glucose concentration. 72 14

While the modern approach to management of diabetic pregnancy has reduced the perinatal mortality significantly, the neonatal morbidity remains high. This study has investigated factors which may account for the persisting high neonatal morbidity when birth trauma has been virtually eliminated and the incidence of respiratory distress syndrome (RDS) considerably reduced. Major congenital malformations emerge not only as the leading cause of perinatal losses but also as an important cause of morbidity. Delivery before 37 weeks increased the incidence of RDS and hypocalcemia, and it is suggested that, when strict metabolic control is used and with the help of facilities to monitor the fetus closely in the last weeks of pregnancy, the number of infants delivered at this early date can be further reduced. The present study also indicates that normoglycemia should also be encouraged on the day of delivery as maternal hyperglycemia at this stage increases the incidence of neonatal hypoglycemia. Jaundice, which very commonly affects newborn infants of diabetic mothers, is influenced by the use of oxytocin for vaginal delivery and by infant overweight (greater than 90th percentile) at birth, factors which are not beyond control. Finally, route of delivery per se may not be important in relation to neonatal morbidity.
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PMID:Neonatal morbidity among infants of diabetic mothers. 72 47

Arginine vasopressin (AVP) and oxytocin (OT) responses during an insulin (0.15 IU/kg body weight) tolerance test (ITT) were evaluated in normal men while they were infused with normal saline, glucose or fructose. Insulin-induced hypoglycemia produced significant plasma AVP and OT increments in the control test. The infusion of fructose was unable to change the posterior pituitary hormonal responses to hypoglycemia. In contrast, AVP and OT responses during ITT were completely abolished when the concomitant infusion of glucose prevented insulin-induced hypoglycemia. These data exclude a direct role of hyperinsulinemia in the mechanism underlying the AVP and OT responses during ITT. Furthermore, since glucose, but not fructose, crosses the blood-brain barrier (BBB), the posterior pituitary hormone responses to hypoglycemia appear to be generated by stimulations of glucosensitive areas located inside the BBB.
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PMID:Hypoglycemia-induced arginine vasopressin and oxytocin release is mediated by glucoreceptors located inside the blood-brain barrier. 132 55

Glucocorticoids are known to reduce both ACTH and arginine vasopressin responses to insulin-induced hypoglycemia in normal men. The present study was undertaken in order to establish whether glucocorticoids are capable of modifying the oxytocin (OT) response to hypoglycemia. For this purpose, 8 normal men (28-33 yr) were tested with insulin (0.15 IU/kg in an iv bolus) [insulin tolerance test (ITT)] with and without pretreatment with dexamethasone (2 or 4 mg in an iv bolus 10 min before insulin). Eight different subjects (29-35 yr) were tested with dexamethasone alone. The administration of dexamethasone (2 or 4 mg) alone changed neither ACTH nor OT concentrations in the plasma during the next hour. Insulin produced similar hypoglycemic responses, regardless of dexamethasone treatment. ACTH levels rose significantly in response to insulin-induced hypoglycemia, with a mean peak response at 45 min (p less than 0.01 vs baseline). Two and four mg dexamethasone produced similar significant reductions of the ACTH response to hypoglycemia (p less than 0.02 at 45 min, p less than 0.05 at 30 and 60 min vs ITT). In the ITT, OT levels rose significantly in response to hypoglycemia, with a mean peak response at 45 min (p less than 0.01 vs basal value). The pretreatment with 2 or 4 mg dexamethasone reduced in a similar manner the hypoglycemia-induced OT rise (p less than 0.05 at 30 and 45 min vs ITT). These findings show a partial inhibition by dexamethasone of the OT response to hypoglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibitory effect of dexamethasone on the oxytocin response to insulin-induced hypoglycemia in normal men. 132 51

Oxytocin has been shown to influence insulin, glucagon and blood glucose levels in various experimental situations. The present study was performed in order to obtain support for a possible interaction of glucose and oxytocin under physiological conditions. We therefore studied whether or not short-term food deprivation (24 hours) affects basal oxytocin levels in male, female and lactating rats, since this is a situation when glucose is mobilized to prevent hypoglycaemia. Secondly, we studied whether oxytocin levels rise in a situation when blood glucose levels fall, i.e. following i.p. injection of insulin (20 U kg-1). In order to explore the role of oxytocin more directly, we investigated whether i.p. injection of the oxytocin antagonist 1-deamino-2-D-Tyr-(OEt)-4-Thr-8-Orn-oxytocin affects blood glucose levels. Plasma levels of oxytocin, insulin and glucagon were measured with radioimmunoassay in samples obtained after decapitation. We found that oxytocin levels were significantly increased following short-term food deprivation in lactating rats. We also found that insulin-induced hypoglycaemia could elevate plasma levels of oxytocin in female and male rats. In addition, administration of an oxytocin antagonist cause a small, but significant decrease in blood glucose levels after 30 min. These data imply that oxytocin may be one of several factors that take part in the control of blood glucose regulation.
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PMID:Plasma levels of oxytocin after food deprivation and hypoglycaemia, and effects of 1-deamino-2-D-Tyr-(OEt)-4-Thr-8-Orn-oxytocin on blood glucose in rats. 158 19

Arginine vasopressin, oxytocin and ACTH are released from the pituitary gland in response to acute hypoglycemia. To investigate the role of alpha-adrenergic mechanisms in mediating this response, 6 non-diabetic subjects were studied during hypoglycemia induced by 0.15 IU/kg i.v. insulin under control conditions, and during non-selective alpha-adrenergic blockade with phentolamine. In the control study plasma arginine vasopressin rose from 1.6 +/- 0.8 pmol/l (mean +/- SEM) basally to a maximum of 2.5 +/- 0.8 pmol/l following hypoglycemia (p less than 0.05). An exaggerated response was found during phentolamine blockade, with a maximum plasma vasopressin of 11.5 +/- 0.4 pmol/l (by analysis of variance, p less than 0.05). The plasma oxytocin response to hypoglycemia was similarly increased during phentolamine compared to control. Plasma growth hormone rose to 94 +/- 19 mU/l, and during blockade with phentolamine the response was significantly reduced reaching a peak of 34 +/- 7 mU/l (by analysis of variance, p less than 0.05). ACTH and prolactin both increased in response to hypoglycemia, but the increases were not affected by phentolamine. An alpha-adrenergic mechanism appears to inhibit the release of arginine vasopressin and oxytocin in response to hypoglycemia, but does not appear to affect the secretion of ACTH.
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PMID:Effect of alpha-adrenergic blockade on pituitary hormonal responses to insulin-induced hypoglycemia in humans. 168 2

Gastric acid output was examined following oxytocin injection into the hypothalamic paraventricular nucleus (PVN) or into the vagus nucleus (X) of the medulla in rats with insulin-hypoglycemia. Gastric acid output was reduced following the injection of nanomolar quantities of oxytocin into these nuclei, and the response was dose-dependent. It was also noted that there was a synergistic action on the response by the peptide between PVN and X. The acid response was blocked by section of the vagus nerve at the subdiaphragmatic level or by prior administration of atropine sulfate. These observations suggest that oxytocin in the PVN is active in suppressing gastric acid secretion, and the vagal response is characteristic of activation of the PVN and X.
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PMID:Secretion of gastric acid inhibited by oxytocin injected into the hypothalamic paraventricular nucleus in the rat. 176 66

The present study was performed in order to establish whether angiotensin II (ANG II) and/or insulin-induced hypoglycemia exert their oxytocin (OT)-releasing effects by interacting with a GABAergic pathway. For this purpose, in 14 normal men the OT responses to ANG II (infusion for 60 min of successively increasing doses of 4, 8 and 16 ng/kg.min, each dose for 20 min; n = 7) or to insulin (0.15 IU/kg)-induced hypoglycemia (n = 7) were evaluated with or without previous treatment with the GABAergic agonist sodium valproate (600 mg in 3 divided doses, p.o.). In all subjects insulin produced a similar hypoglycemic response regardless of sodium valproate administration. Both ANG II and insulin-induced hypoglycemia produced significant increases in plasma OT levels (mean peaks were about 60% higher than baseline). The pretreatment with sodium valproate was unable to change the OT response to hypoglycemia, whereas it abolished the ANG-II-induced OT rise. These data suggest that in man a GABAergic mechanism is involved in the regulation of the OT response to ANG II, but not in the mediation of poglycemia-induced OT release.
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PMID:Different effects of the GABAergic agent sodium valproate on the oxytocin responses to angiotensin II and insulin-induced hypoglycemia in normal men. 181 97

Chronically hyponatremic rats were subjected to various stressors in order to evaluate the possible contribution of magnocellular neurons to the regulation of ACTH secretion, since such rats have markedly inhibited secretion and synthesis of magnocellular arginine vasopressin (AVP) and oxytocin (OT). Stress caused by a novel environment or by insulin-induced hypoglycemia resulted in moderate increases in plasma ACTH, which were of similar magnitude in both hyponatremic and normonatremic rats, and these stressors caused no increase in plasma AVP and OT levels in either group of rats. However, when exposed to ether, hyponatremic rats exhibited a significantly blunted ACTH response compared to normonatremic controls (331 +/- 49 vs. 740 +/- 124 pg/ml; P less than 0.01, respectively), and plasma AVP levels were markedly increased in the normonatremic, but not in the hyponatremic, rats. Intravenous infusion of 2 M NaCl also caused an ACTH release in hyponatremic rats that was significantly smaller than that in their normonatremic counterparts (228 +/- 52 vs. 479 +/- 85 pg/ml; P less than 0.05, respectively), and in this case both plasma AVP and OT levels were markedly increased in the normonatremic, but not in the hyponatremic, rats. However, hyponatremic rats exhibited greatly increased plasma ACTH levels 2 and 96 h after adrenalectomy (ADX), which were statistically equivalent to the increases in ACTH levels in normonatremic rats after ADX. Seven days after ADX parvocellular neurons of the paraventricular nucleus showed strongly increased CRF-41 and AVP-neurophysin, but not OT-neurophysin, immunoreactivities in both normonatremic and hyponatremic rats. These results show that parvocellular CRF-41/AVP-producing neurons in the paraventricular nucleus are not inhibited by chronic hyponatremia, in contrast to magnocellular neurons, and suggest that ACTH secretion induced by ether or hypertonic saline, but not by novel environment or insulin-induced hypoglycemia, is partially mediated by magnocellular AVP and/or OT.
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PMID:Hyponatremia-induced inhibition of magnocellular neurons causes stressor-selective impairment of stimulated adrenocorticotropin secretion in rats. 184 2

Oxytocin has been suggested to have glucoregulatory functions in rats, man and other mammals. The hyperglycemic actions of oxytocin are believed to be mediated indirectly through changes in pancreatic function. The present study examined the interaction between glucose and oxytocin in normal and streptozotocin (STZ)-induced diabetic rats, under basal conditions and after injections of oxytocin. Plasma glucose and endogenous oxytocin levels were significantly correlated in cannulated lactating rats (r = 0.44, P less than 0.01). To test the hypothesis that oxytocin was acting to elevate plasma glucose, adult male rats were injected with 10 micrograms/kg oxytocin and killed 60 min later. Oxytocin increased plasma glucose from 6.1 +/- 0.1 to 6.8 +/- 0.2 mM (P less than 0.05), and glucagon from 179 +/- 12 to 259 +/- 32 pg/ml (P less than 0.01, n = 18). There was no significant effect of oxytocin on plasma insulin, although the levels were increased by 30%. A lower dose (1 microgram/kg) of oxytocin had no significant effect on plasma glucose or glucagon. To eliminate putative local inhibitory effects of insulin on glucagon secretion, male rats were made diabetic by i.p. injection of 100 mg/kg STZ, which increased glucose to greater than 18 mM and glucagon to 249 +/- 25 pg/ml (P less than 0.05). In these rats, 10 micrograms/kg oxytocin failed to further increase plasma glucose, but caused a much greater increase in glucagon (to 828 +/- 248 pg/ml) and also increased plasma ACTH. A specific oxytocin analog, Thr4,Gly7-oxytocin, mimicked the effect of oxytocin on glucagon secretion in diabetic rats. The lower dose of oxytocin also increased glucagon levels (to 1300 +/- 250 pg/ml), but the effect was not significant. A 3 h i.v. infusion of 1 nmol/kg per h oxytocin in conscious male rats significantly increased glucagon levels by 30 min in normal and STZ-rats; levels returned to baseline by 30 min after stopping the infusion. Plasma glucose increased in the normal, but not STZ-rats. The relative magnitude of the increase in glucagon was identical for normal and diabetic rats, but the absolute levels of glucagon during the infusion were twice as high in the diabetics. To test whether hypoglycemia could elevate plasma levels of oxytocin, male rats were injected i.p. with insulin and killed from 15-180 min later. Plasma glucose levels dropped to less than 2.5 mM by 15 min. Oxytocin levels increased by 150-200% at 30 min; however, the effect was not statistically significant.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Interactions between oxytocin, glucagon and glucose in normal and streptozotocin-induced diabetic rats. 192 91


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