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)

We studied the effect of prostaglandin (PG) F(2alpha)-AGN 190851 on farrowing induction and compared it with that of PGF(2alpha)-oxytocin. Eighty crossbred, multiparous sows were randomly assigned to the following 4 treatment groups of 20 sows each: 1) control, saline-saline; 2) PGF(2alpha) (10 mg/sow)-oxytocin (30 IU/sow); 3) PGF(2alpha) (10 mg/sow)-AGN 190851 (0.06 mg/kg); and 4) PGF(2alpha) (10 mg/sow)-AGN 190851 (0.1 mg/kg). Either PGF(2alpha) or saline was administered intramuscularly on Day 111 of gestation at 11:30 h; AGN 190851, oxytocin or saline was administered intramuscularly 20 h after the first injection. The PGF(2alpha)-AGN 190851 (0.1 mg/kg) treated sows had the shortest mean farrowing interval (2.1 +/- 1.6 h, mean +/- SD) compared with the remaining treatment groups (control: 67.1 +/- 26.2 h; PGF(2alpha)-oxytocin: 5.6 +/- 6.7 h; PGF(2alpha)-AGN 190851 [0.06 mg/kg]: 3.0 +/- 2.8 h). Duration of farrowing, litter size, litter weight and interval from weaning to first estrus in sows were not significantly changed by these treatments. The PGF(2alpha)-oxytocin group had a significantly higher stillbirth rate than the control group, whereas the PGF(2alpha)-AGN 190851 (0.1 mg/kg) group had the lowest number of pigs born dead and stillbirth rate among the 4 treatment groups. These results suggested that the PGF(2alpha)-AGN 190851 combination can be used as an alternative method to PGF(2alpha)-oxytocin for synchronizing farrowing.
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PMID:Farrowing induction with a combination of prostaglandin F(2alpha) and a peripherally acting alpha(2)--adrenergic agonist AGN 190851 and a combination of prostaglandin F(2alpha) and oxytocin. 1672 92

The aim of the present study was to investigate transcript localization of the oxytocin receptor (OTR) gene in different cells of the porcine uterus during luteolysis and early pregnancy (days 14-16) using in situ hybridization (ISH). OTR mRNA was localized in the uterine luminal epithelium (LEC), glandular epithelium (GEC), stromal cells (SC) of the endometrium, in the longitudinal muscle layer (LM) and circular muscle layer (CM) of the myometrium. The OTR transcript was quantified by optical density units of silver grains. The OTR transcript levels in the endometrium and myometrium were statistically higher during luteolysis than during early pregnancy (P<0.05). Besides, during luteolysis, the mRNA level was higher in the LEC, GEC of the endometrium and LM of the myometrium compared to that observed in the SC of endometrium and CM of the myometrium, respectively (P<0.05). In summary: 1) the level of OTR mRNA in uterine tissues is higher during luteolysis compared to early pregnancy, 2) the OTR transcript level in endometrial cells did not correspond to the sensitivity of these cells to oxytocin (OT), 3) the myometrial expression of the OTR gene is appropriate to control contractile activity and secretion of PG during luteolysis.
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PMID:Relative transcript abundance of oxytocin receptor gene in porcine uterus during luteolysis and early pregnancy. 1713 99

Gastric electrical stimulation (GES) has been proposed as a therapeutic option for obesity. However, its clinical efficacy is not proven, and its mechanisms remain largely unknown. To compare the peripheral and central neural and behavioral effects in rats of GES with a pulse width currently used in clinical trials (GES-A: 6 mA, 0.3 ms, 40 Hz, 2 s on, 3 s off) and GES with a wider pulse (GES-B: same as GES-A, except that the pulse width is 3 ms). Experiment 1: assessing gastric volume changes as a result of GES. Experiment 2: recording the extracellular potentials of a single neuron in the paraventricular nucleus (PVN) with GES. Experiment 3: determining the effects of GES on oxytocin-immunoreactive (OT-IR) neuron expression in the hypothalamus. Experiment 4: determining the effects of GES on food intake and body weight. GES-B, but not GES-A, significantly increased gastric volume. GES-B activated a higher percentage of gastric distention-responsive neurons in the PVN (93% vs. 81%, P = 0.021) and elicited more intensive neuronal responses than GES-A. The number of OT-IR neurons was significantly increased in the PVN and supraoptic nucleus with both methods of GES compared with control groups. The increase in OT-IR neurons in the PVN was higher with GES-B than with GES-A. A 1-week GES treatment significantly reduced daily food intake and body weight. GES-B was more potent than GES-A in producing weight loss (P < 0.001). The effects of GES depend on the stimulation pulse width. GES with a wider pulse is more effective both peripherally and centrally and more potent in reducing body weight in rats.
Obesity (Silver Spring) 2009 Mar
PMID:Gastric electrical stimulation for obesity: the need for a new device using wider pulses. 1905 30

Abstract The peptide hormone oxytocin has an important role in parturition, lactation and maternal behavior. The present study employed in situ hybridization histochemistry to determine whether oxytocin messenger ribonucleic acid (mRNA) levels in cells in the medial preoptic area, a brain area known to control maternal behavior, change during pregnancy and lactation in the rat. Female rats were perfused on either Day 18 or 22 of pregnancy or Day 5 of lactation. Ovariectomized female rats were included as an additional control group. Cells expressing oxytocin mRNA were detected by in situ hybridization using an [(125) l]-labeled 38 base synthetic oligodeoxynucleotide probe complementary to the C-terminal coding region of the preprooxytocin. Relative differences in oxytocin mRNA levels were determined by silver grain counting of labeled cells. A group of oxytocin neurons in the dorsal medial preoptic area, called the lateral subcommissural nucleus, showed elevated oxytocin mRNA levels in lactating animals relative to ail other groups. Oxytocin mRNA levels in the neurons of the periventricular nucleus of the preoptic area did not change across pregnancy and lactation. This result extends the findings of others showing elevated oxytocin mRNA levels in magnocellular nuclei of lactating animals. The results are discussed in terms of the possible role of oxytocin cells in the medial preoptic area in the expression of maternal behavior.
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PMID:Oxytocin Messenger Ribonucleic Acid Levels in the Medial Preoptic Area are Increased During Lactation. 1921 97

Oxytocin (Oxt) is secreted both peripherally and centrally and is involved in several functions including parturition, milk let-down reflex, social behavior, and food intake. Recently, it has been shown that mice deficient in Oxt receptor develop late-onset obesity. In this study, we characterized a murin model deficient in Oxt peptide (Oxt(-/-)) to evaluate food intake and body weight, glucose tolerance and insulin tolerance, leptin and adrenaline levels. We found that Oxt(-/-) mice develop late-onset obesity and hyperleptinemia without any alterations in food intake in addition to having a decreased insulin sensitivity and glucose intolerance. The lack of Oxt in our murin model also results in lower adrenalin levels which led us to hypothesize that the metabolic changes observed are associated with a decreased sympathetic nervous tone. It has been shown that Oxt neurons in the paraventricular nucleus (PVN) are a component of a leptin-sensitive signaling circuit between the hypothalamus and caudal brain stem for the regulation of food intake and energy homeostasis. Nevertheless, the lack of Oxt in these mice does not have a direct impact on feeding behavior whose regulation is probably dependent on the complex interplay of several factors. The lack of hyperphagia evident in the Oxt(-/-) mice may, in part, be attributed to the developmental compensation of other satiety factors such as cholecystokinin or bombesin-related peptides which merits further investigation. These findings identify Oxt as an important central regulator of energy homeostasis.
Obesity (Silver Spring) 2009 May
PMID:Low sympathetic tone and obese phenotype in oxytocin-deficient mice. 1924 73


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