The Experts below are selected from a list of 81 Experts worldwide ranked by ideXlab platform
Didier F. Pisani - One of the best experts on this subject based on the ideXlab platform.
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Oxytocin reverses osteoporosis in a sex-dependent manner.
Frontiers in Endocrinology, 2014Co-Authors: Guillaume E Beranger, Mansour Djedaini, Christian H Roux, Severine Battaglia, Marcel Scheideler, Dominique Heymann, Ez-zoubir Amri, Didier F. PisaniAbstract:The increase of life expectancy has led to the increase of age-related diseases such as osteoporosis. Osteoporosis is characterized by bone weakening promoting the occurrence of fractures with defective bone regeneration. Men aged over 50 have a prevalence for osteoporosis of 20%, which is related to a decline in sex hormones occurring during andropause or surgical orchidectomy. As we previously demonstrated in a mouse model for menopause in women that treatment with the Neurohypophyseal Peptide hormone oxytocin (OT) normalizes body weight and prevents the development of osteoporosis, herein we addressed the effects of OT in male osteoporosis. Thus, we treated orchidectomized mice, an animal model suitable for the study of male osteoporosis, for 8 weeks with OT and then analyzed trabecular and cortical bone parameters as well as fat mass using micro-computed tomography. Orchidectomized mice displayed severe bone loss, muscle atrophy accompanied by fat mass gain as expected in andropause. Interestingly, OT treatment in male mice normalized fat mass as it did in female mice. However, although OT treatment led to a normalization of bone parameters in ovariectomized mice, this did not happen in orchidectomized mice. Moreover, loss of muscle mass was not reversed in orchidectomized mice upon OT treatment. All of these observations indicate that OT acts on fat physiology in both sexes, but in a sex specific manner with regard to bone physiology.
Quentin J. Pittman - One of the best experts on this subject based on the ideXlab platform.
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Vasopressie-induced sensitization: involvement of Neurohypophyseal Peptide receptors
European journal of pharmacology, 1995Co-Authors: Paule Poulin, Daniel M. Dorsa, Patricia Szot, Quentin J. PittmanAbstract:Abstract Rats pretreated with an intracerebroventricular (i.c.v.) injection of 10 pmol of vasopressin or vasoprcssin analogs, including deamino- d -vasopressin, [pGlu1,Cyt6]vasopressin, [pGlu-Asn-Cys(Cys)]Pro-Leu-Gly-NH2, des-Gly-NH92-vasopressin, Pro-Leu-Gly-NH2, Pro-Arg-Gly-NH2, became markedly hyper-responsive to the motor effects, 24 h later, to a subsequent challenge dose of vasopressin, but not vasopressin-related Peptides. A vasopressin V1 receptor antagonist, [d(CH2)15, Tyr(Me)2]vasopressin. but not the vasopressin V2 receptor antagonist, [d(CH2)15, Tyr(Et)2,Val4]vasopressin, or a more selective vasopressin V2 receptor antagonist, [d(CH2)15, d -Ile2,Ile4]vasopressin, or the oxytocin receptor antagonist, [d(CH2)15, Tyr(Me)2, Thr4,Orn8, Tyr-NH92]vasotocin ([d(CH2)15,Tyr(Me)2,Thr4,Tyr-NH92]OVT), blocked vasopressin and vasopressin analog-induced sensitization. Furthermore, both vasopressin V2 receptor antagonists were found to sensitize the brain to a subsequent vasopressin injection. This vasopressin V2 receptor antagonist-induced sensitization was also blocked by the vasopressin V1 receptor antagonist. Next. we wanted to determine if this sensitization process could involve the release of endogenous vasopressin in the brain as reflected in an amplification of vasopressin mRNA expression. However pretreatment of rats with an i.c.v. vasopressin injection was not associated with an increase in vasopressin mRNA expression in the bed nucleus of the stria terminalis, medial amygdala or the paraventricular nucleus of the hypothalamus when measured 0, 1, 3, 7, 12, or 24 h after the first vasopressin injection. As many vasopressin analogs can induce sensitization, we suggest that a novel type of receptor may be involved in the sensitization process.
David De Wied - One of the best experts on this subject based on the ideXlab platform.
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barrel rotation induced by central arginine8 vasopressin treatment involvement of Neurohypophyseal Peptide receptors
Pharmacology Biochemistry and Behavior, 1994Co-Authors: Michaela Diamant, Gábor L. Kovács, Annemarie M Baars, David De WiedAbstract:Abstract Two series of experiments were done to investigate the mechanism underlying arginine 8 -vasopressin (AVP)-induced barrel rotation in rats. In the first series, the effect of intracerebroventricular (ICV) administration of various Neurohypophyseal hormone antagonists on AVP-induced barrel rotation was studied. The more vasopressin was given, the more the rats exhibited barrel rotation. ICV pretreatment with a V 1 vasopressin receptor antagonist, d(CH 2 ) 5 [Tyr(Me) 2 ]AVP, prevented barrel rotation, while similar treatment with a V 2 -antagonist, d(CH 2 ) 5 [dIle 2 Ile 4 ]AVP, did not affect vasopressin-induced barrel rotation. However, Des-Gly,NH 2 d(CH 2 ) 5 [Tyr)Me 2 )Thr 4 Orn 8 ]-vasotocin, a specific oxytocin antagonist, potentiated the effect of AVP on barrel rotation. The second experiment was performed in rats equipped with a telemetry system to measure heart rate (HR), core temperature (CT), and gross locomotor activity. Also, in this experiment the incidence of AVP-induced barrel rotation was dose-dependent, as was the number of rats that died. Barrel rotation was accompanied by a significant decrease in CT and HR, while rats that did not develop hypothermia did not show barrel rotation. These results suggest that a V 1 receptor is involved in barrel rotation. Since AVP-induced hypothermia is also mediated by a V 1 receptor, it is postulated that hypothermia is a prerequisite for barrel rotation to occur. Further experiments are needed to substantiate this hypothesis.
Kiyoshi Shimada - One of the best experts on this subject based on the ideXlab platform.
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effects of naloxone on Neurohypophyseal Peptide release by hypertonic stimulation in chicks
General and Comparative Endocrinology, 1999Co-Authors: Noboru Saito, Mitsuhiro Furuse, Takeshi Sasaki, Koji Arakawa, Kiyoshi ShimadaAbstract:The effects of opioid Peptides on the osmotic release of Neurohypophyseal hormones, arginine vasotocin (AVT) and mesotocin (MT), were determined in 2-day-old chicks. Experiment 1 examined the effect of a variety of doses of naloxone, an opioid antagonist, on chicks administered isotonic or hypertonic solution. Plasma osmolality in chicks administered hypertonic solution was significantly higher than that in groups administered isotonic solution. None of the doses of naloxone affected plasma osmolality in response to isotonic and hypertonic solution. Plasma levels of AVT increased in hypertonic solution and this response was further enhanced by naloxone injection as the doses increased. The hypertonic solution alone did not affect plasma levels of MT, but additional treatment with naloxone slightly increased plasma levels of MT. Experiment 2 examined the effect of DAMGO ([d-Ala(2), N-Me-Phe(4),Gly-ol]-enkepha lin), a specific mu receptor agonist. Relatively high plasma osmolality caused by hypertonic solution was not affected by additional treatment with DAMGO. Plasma levels of AVT in response to hypertonic solution and to additional treatment with naloxone were reduced by higher doses of DAMGO. Experiment 3 examined the effect of naloxone on chicks administered different concentrations of NaCl. Administration of hypertonic solution resulted in an increase in plasma osmolality and plasma levels of AVT. Naloxone administration enhanced the increase in plasma AVT levels in response to hypertonic solution. Experiment 4 examined the effect of naloxone on different kinds of hypertonic solution, 0.15 M NaCl, 1.5 M NaCl, 2.55 M urea, and 1.95 M sucrose. The increases in plasma osmolality resulting from the administration of the urea and sucrose solutions were the same as those in the chicks injected with 1.5 M NaCl. In sucrose-treated chicks, plasma levels of AVT increased in chicks administered naloxone but not in chicks injected with normal saline. In contrast, no significant changes in plasma levels of AVT were observed in urea treatment with or without naloxone. In Experiments 3 and 4, plasma levels of MT after administration of hypertonic solutions did not change. However, naloxone administration enhanced plasma levels of MT in osmotically stimulated chicks. The results of the present study suggest that opioid Peptides attenuate the increase in plasma AVT and MT in hypertonic states.
Guillaume E Beranger - One of the best experts on this subject based on the ideXlab platform.
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Oxytocin reverses osteoporosis in a sex-dependent manner.
Frontiers in Endocrinology, 2014Co-Authors: Guillaume E Beranger, Mansour Djedaini, Christian H Roux, Severine Battaglia, Marcel Scheideler, Dominique Heymann, Ez-zoubir Amri, Didier F. PisaniAbstract:The increase of life expectancy has led to the increase of age-related diseases such as osteoporosis. Osteoporosis is characterized by bone weakening promoting the occurrence of fractures with defective bone regeneration. Men aged over 50 have a prevalence for osteoporosis of 20%, which is related to a decline in sex hormones occurring during andropause or surgical orchidectomy. As we previously demonstrated in a mouse model for menopause in women that treatment with the Neurohypophyseal Peptide hormone oxytocin (OT) normalizes body weight and prevents the development of osteoporosis, herein we addressed the effects of OT in male osteoporosis. Thus, we treated orchidectomized mice, an animal model suitable for the study of male osteoporosis, for 8 weeks with OT and then analyzed trabecular and cortical bone parameters as well as fat mass using micro-computed tomography. Orchidectomized mice displayed severe bone loss, muscle atrophy accompanied by fat mass gain as expected in andropause. Interestingly, OT treatment in male mice normalized fat mass as it did in female mice. However, although OT treatment led to a normalization of bone parameters in ovariectomized mice, this did not happen in orchidectomized mice. Moreover, loss of muscle mass was not reversed in orchidectomized mice upon OT treatment. All of these observations indicate that OT acts on fat physiology in both sexes, but in a sex specific manner with regard to bone physiology.