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)

The object of this study was to investigate the effect of maternal metabolic state on the activity of lipoprotein lipase (LPL) in human milk. Although the total LPL activity in milk was not significantly affected by up to three cycles of freezing and thawing, the amount of LPL associated with the cream fraction of the milk increased from an average of less than 10% to about 70% after this treatment. The enzyme was relatively stable when the milk was stored on ice, losing activity at a rate of about 1% per hour. At 37 degrees C degradation was more rapid, about 7% per hour. When LPL activity was measured in samples taken at hourly intervals by breast pump, using oxytocin to achieve a complete letdown at each pumping, activity was found to double from the first to the third pumping. Thereafter the activity was stable under fasting conditions. Hyperglycemic and euglycemic, hyperinsulinemic glucose clamp protocols were used to evaluate the effects of glucose and insulin. Both high plasma glucose and high plasma insulin in the presence of normal glucose significantly increased LPL activity within 4 hours. We conclude that, like adipose, tissue LPL, mammary LPL is regulated by plasma insulin.
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PMID:Lipoprotein lipase in human milk: compartmentalization and effect of fasting, insulin, and glucose. 206 61

Microinjections of oxytocin and of an oxytocin antagonist into the dorsal vagal complex of the medulla oblongata were performed in order to study the possible role of the oxytocin containing axons that innervate this region in the regulation of pancreatic insulin secretion. No significant effect was produced by the intramedullary injection of the oxytocin vehicle alone or of 0.04 pM oxytocin. Injections of 4 and 20 pM oxytocin produced a reversible decrease of plasmatic insulin levels which fall to 59% of basal levels 15 min after the injection. Such an effect was abolished when 4 pM oxytocin was injected to animals which have been previously bilaterally vagotomized. In contrast to oxytocin, intramedullary injection of a specific antagonist of oxytocin to intact animals induced a marked increase of plasmatic insulin levels which raised 131% of basal levels 15 min after the injection. In animals receiving such an injection of oxytocin antagonist, a secondary injection of 4 pM oxytocin produced a slight but not significant decrease of plasmatic insulin levels. These data strongly suggest that the hypothalamic neurons producing oxytocin that densely project to the dorsal vagal complex may be involved in an inhibitory control of the vagal preganglionic neurons that innervate the pancreas.
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PMID:Microinjection of oxytocin into the dorsal vagal complex decreases pancreatic insulin secretion. 207 Feb 58

Incubation of isolated rat adipocytes with insulin, vasopressin, or oxytocin increased plasma membrane-bound protein kinase C (PKC) activity by 100-400%. PKC activity was assayed by a procedure that is virtually background-free, thus permitting assay of protein kinase activity in highly diluted samples of solubilized membranes. Hormone-dependent increases in PKC activity were limited to plasma membranes. Stimulation of the kinase was half-maximal with 70 pM insulin, and the hormone effect was rapid. Oxytocin and vasopressin produced effects on PKC similar to insulin, but the magnitude of the vasopressin stimulation exhibited seasonal variations. Treatment of cells with phorbol 12-myristate 13-acetate (PMA) resulted in a loss of PKC activity from the cytosol and a gain in plasma membrane activity, indicative of translocation of the enzyme. With activity measurements it was not possible to determine if insulin stimulated a translocation of the kinase. However, Western blot analysis of plasma membranes with polyclonal antibodies directed against PKC suggest that at least some of the insulin-stimulated PKC activity resulted from enzyme translocation.
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PMID:Insulin, oxytocin, and vasopressin stimulate protein kinase C activity in adipocyte plasma membranes. 210 94

Two selective radioligands for oxytocin receptors, [3H]-[4-threonine,7-glycine]oxytocin [( 3H]-[Thr4,Gly7]OT) and 125I-[1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine, 4-threonine, 8-ornithine, 9-tyrosine amide]-oxytocin (125I-OTA), were used to characterize oxytocin receptors from two pig kidney-derived cell lines, LLC-PK1 and LLC-PK1L. [3H]-[Thr4,Gly7]OT and 125I-OTA bind with high affinity (mean Kd values of 14 and 0.06 nM, respectively) to the same population of sites on LLC-PK1 cell membranes [maximum binding (Bmax) of 100 fmol/mg membrane protein]. These sites had the expected ligand selectivity of oxytocin receptors. [3H]-[Thr4,Gly7]OT and 125I-OTA binding sites could be distinguished from V2 vasopressin receptors present on LLC-PK1 and LLC-PK1L cells on the basis of clearly different maximal capacities and ligand selectivities, different sensitivities to insulin and serum, and absence of heterologous downregulation. Oxytocin receptors from LLC-PK1 cells have no functional relationship with adenylate cyclase. [Thr4,Gly7]OT affected neither the basal adenosine 3',5'-cyclic monophosphate (cAMP) content nor the vasopressin-induced cAMP accumulation by LLC-PK1 cells. Xenopus laevis oocytes injected with LLC-PK1 cell mRNA responded to [Thr4,Gly7]OT by an increase in 45Ca2+ outflux; this effect is antagonized by a highly selective oxytocin antagonist.
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PMID:Oxytocin receptors from LLC-PK1 cells: expression in Xenopus oocytes. 215 46

A novel relaxin sensitive cell line of apparent smooth muscle origin has been established from a newborn rhesus monkey uterus (NRMU). NRMU cells respond to relaxin, in the presence of 1 microM forskolin, by producing intracellular adenosine 3', 5'-cyclic monophosphate (cAMP). The increase in cAMP levels is dose, time and cell density dependent, reaching peak levels at 10 min when cells are seeded at 1 X 10(5) cells/well. Specificity was demonstrated by neutralization of the relaxin activity with anti-relaxin monoclonal and polyclonal antibodies, degradation of cAMP in the presence of phosphodiesterase, and confirmation of the absence of cGMP. Three synthetic analogs of human relaxin generated a dose-related cAMP response as did synthetic native human relaxin. Natural relaxin purified from human corpora lutea tissue also generated a response similar to synthetic human relaxin. Porcine and rat relaxins also increased levels of cAMP. Insulin, but not IGF I or IGF II, was capable of increasing cAMP levels in NRMU cells, however, 200 ng/mL were required to achieve cAMP levels comparable to 6.25 ng/ml relaxin. Combinations of relaxin with insulin, IGF I or IGF II did not increase cAMP levels above levels obtained with relaxin alone. The effect on NRMU cells of other hormones, growth factors and drugs potentially present in cell culture systems or serum samples was evaluated. In combination with relaxin, oxytocin significantly decreased the cAMP production below the levels induced by relaxin alone, whereas progesterone and prostaglandin E2 resulted in additive increases in cAMP. These data suggest that the NRMU cell line is an appropriate target tissue for studying relaxin-mediated biological responses in vitro as well as functioning as the primary component of a relaxin in vitro bioassay.
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PMID:Increase in cyclic AMP levels by relaxin in newborn rhesus monkey uterus cell culture. 216 18

To examine the secretion of oxytocin (OT) and progesterone (P) from a homogeneous population of cells during luteinization, we developed a serum-free culture technique for granulosa cells, obtained from individual preovulatory bovine follicles. Granulosa cells from earlier stages of the follicle development did not have the capability to secrete OT under the in vitro conditions used. For optimal stimulation of the cells the medium (a 1:1 mixture of Dulbecco's modified Eagle's medium and Ham's F-12) was supplemented with bovine serum albumin (BSA) and insulin. OT was detectable from day 1 of culture reaching a maximum level between days 2 and 4 and then declined towards day 5. In the absence of insulin OT declined from day 1 onwards and was undetectable from day 4. When cells were cocultured with theca tissue or theca-conditioned medium (TCM), there was an enhancement in OT secretion, but not in P secretion. Other tissues including liver, kidney, aorta, muscle and adrenal incubated with the cells induced a similar increase in OT production. In the presence of insulin progesterone secretion was increased and was correlated with OT production, but did not show a consistent pattern among follicles. We conclude that (a) culture of granulosa cells from an individual follicle in a serum-free medium can be used to study the secretion of OT and P from bovine granulosa cells, (b) insulin is essential for the optimal production of OT and P by these cells, and (c) the addition of theca or other tissues enhanced OT secretion by a mechanism not understood.
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PMID:Oxytocin and progesterone secretion by bovine granulosa cells of individual preovulatory follicles cultured in serum-free medium. 218 57

In animals, there is sexual dimorphism of both neurohypophysial peptide secretion in response to stressful stimuli and to the inhibitory effects of opioids. In men, endogenous opioids inhibit the release of oxytocin when AVP secretion is stimulated by insulin-induced hypoglycemia. We have now investigated the role of endogenous opioids in the AVP and oxytocin response to insulin-induced hypoglycemia in women. Twelve subjects, 6 in the follicular and 6 in the luteal phase of the menstrual cycle, were infused on 2 occasions with naloxone (4 mg bolus and 6 mg/h) or saline. Soluble insulin (Human Actrapid, 0.15 mu/kg, iv) was given and serial blood samples taken. Blood sugar fell significantly (p less than 0.05) and similarly in all groups. In the follicular phase hypoglycemia led to a rise in plasma AVP from 1.3 +/- 0.2 to 1.8 +/- 0.2 pmol/l in the saline-infused subjects (NS), and from 1.0 +/- 0.1 to 2.0 +/- 0.2 pmol/l in the naloxone-infused (p less than 0.05). AVP rose similarly from 0.6 +/- 0.1 to 1.6 +/- 0.5 pmol/l (p less than 0.05) in the luteal phase controls and from 0.8 +/- 0.1 to 1.5 +/- 0.3 pmol/l (p less than 0.05) in naloxone-infused subjects in the luteal phase. There were no significant differences between any of these groups. There were no significant changes in plasma oxytocin in any group. We therefore conclude that in women, unlike men, endogenous opioids do not modulate oxytocin or vasopressin release during insulin-induced hypoglycemia.
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PMID:Neurohypophysial secretion to insulin-induced hypoglycemia and its regulation by endogenous opioids in women. 218 2

Pharmacological doses of insulin (3-25 U/kg sc) elicited feeding and increased gastric motility in rats. In contrast, the glucose analogue 2-deoxy-D-glucose (2-DG), given ip in doses known to increase food intake, had dose-dependent effects on gastric motility: 100 and 200 mg/kg 2-DG increased gastric motility, whereas 500 mg/kg 2-DG virtually eliminated gastric contractions. This latter result resembled the known effects on gastric motility of cholecystokinin (CCK) and LiCl. Moreover, like CCK and LiCl, 500 mg/kg 2-DG stimulated pituitary oxytocin (OT) secretion, and its effects on gastric motility and OT secretion were potentiated by pretreatment with the opioid antagonist naloxone. In contrast, OT secretion was not affected by insulin-induced hypoglycemia with or without naloxone pretreatment. These results suggest that there are two components to the effects of 2-DG on gastric motility: an insulin-like excitatory component and a CCK-LiCl-like inhibitory component. The latter inhibitory component may be mediated by the paraventricular nucleus of the hypothalamus, which has already been implicated in the inhibitory control of gastric motility.
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PMID:Effects of glucoprivation on gastric motility and pituitary oxytocin secretion in rats. 220 80

The presence of the classical neurohypophyseal hormone oxytocin has recently been described in the human pancreas in considerably higher concentrations than those found in peripheral plasma. Evidence in animals and man suggests that oxytocin can directly stimulate the secretion of glucagon from pancreatic islets. In order to investigate a possible paracrine role for oxytocin in the regulation of glucagon secretion we have studied the effect of oxytocin on the plasma glucagon response to insulin-induced hypoglycaemia in 10 lean fasted male subjects. Intravenous insulin tests were performed in random order with or without oxytocin infusion (2 U bolus injection; 111 mU/min for 2 hours). Blood sugar nadir occurred at the onset of symptoms (time S) with no significant differences between oxytocin and saline infusions (saline S = 24 +/- 2.3 min; oxytocin S = 23.3 +/- 2.7 min). There was no significant change in peripheral plasma oxytocin concentrations during saline infusion. During the oxytocin infusion plasma oxytocin concentrations rose from 1.05 +/- 0.1 (mean +/- SEM) pmol/l to a peak of 632 +/- 179 pmol/l and remained elevated throughout the study. Peak plasma glucagon concentrations occurred at S + 10 mins with no significant differences in peak values (saline 200 +/- 26.3 pg/ml; oxytocin 207 +/- 23.6 pg/ml) between saline and oxytocin infusions. The data suggest that oxytocin at concentrations up to 6.3 X 10(-10) M has no effect on the decline or recovery of blood glucose concentrations or on the plasma glucagon response to insulin-induced hypoglycaemia.
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PMID:The effect of oxytocin on the plasma glucagon response to insulin-induced hypoglycaemia in man. 221 21

In the present investigation it was studied whether oxytocin administered directly in the pancreas of the rat stimulates the release of insulin and glucagon. In order to study such effects in vivo, a new experimental model applying the microdialysis technique was developed. To test the validity of the method, glucose or arginine were infused i.v. and it was shown that perfusate concentrations of insulin and glucagon increased significantly to 344 and 292% of basal overflow, respectively. Administration of oxytocin via the dialysis probe into the splenic portion of the pancreas resulted in significant elevations of insulin and glucagon concentrations to 210 (P less than 0.05) and 528% (P less than 0.01), respectively. The present study also includes a combined autoradiographic and immunohistochemical investigation of binding sites for oxytocin in the rat pancreas. A high density of [3H]oxytocin binding was present in the periphery of the islets of Langerhans, corresponding to the localization of the glucagon-producing alpha-cells. Both oxytocin and arginine(A)-vasopressin displaced [3H]oxytocin. The IC50 values were 10 and 180 nM, respectively. In conclusion, the oxytocin-induced release of insulin and glucagon as previously demonstrated in a number of species, may be due to a stimulation exerted by the peptide directly within the pancreas.
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PMID:Effects of oxytocin on in vivo release of insulin and glucagon studied by microdialysis in the rat pancreas and autoradiographic evidence for [3H]oxytocin binding sites within the islets of Langerhans. 221 8


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