The Experts below are selected from a list of 24372 Experts worldwide ranked by ideXlab platform
Wenda Wu - One of the best experts on this subject based on the ideXlab platform.
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potential roles for calcium sensing receptor casr and transient receptor potential ankyrin 1 trpa1 in murine anorectic response to deoxynivalenol vomitoxin
Archives of Toxicology, 2017Co-Authors: Hui Ren Zhou, Wenda Wu, James J PestkaAbstract:Food contamination by the trichothecene mycotoxin deoxynivalenol (DON, vomitoxin) has the potential to adversely affect animal and human health by suppressing food intake and impairing growth. In mice, the DON-induced anorectic response results from aberrant Satiety hormone secretion by enteroendocrine cells (EECs) of the gastrointestinal tract. Recent in vitro studies in the murine STC-1 EEC model have linked DON-induced Satiety hormone secretion to activation of calcium-sensing receptor (CaSR), a G-coupled protein receptor, and transient receptor potential ankyrin-1 (TRPA1), a TRP channel. However, it is unknown whether similar mechanisms mediate DON’s anorectic effects in vivo. Here, we tested the hypothesis that DON-induced food refusal and Satiety hormone release in the mouse are linked to activation of CaSR and TRPA1. Oral treatment with selective agonists for CaSR (R-568) or TRPA1 (allyl isothiocyanate (AITC)) suppressed food intake in mice, and the agonist’s effects were suppressed by pretreatment with corresponding antagonists NPS-2143 or ruthenium red (RR), respectively. Importantly, NPS-2143 or RR inhibited both DON-induced food refusal and plasma elevations of the Satiety hormones cholecystokinin (CCK) and peptide YY3–36 (PYY3–36); cotreatment with both antagonists additively suppressed both anorectic and hormone responses to DON. Taken together, these in vivo data along with prior in vitro findings support the contention that activation of CaSR and TRPA1 contributes to DON-induced food refusal by mediating Satiety hormone exocytosis from EEC.
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potential roles for calcium sensing receptor casr and transient receptor potential ankyrin 1 trpa1 in murine anorectic response to deoxynivalenol vomitoxin
Archives of Toxicology, 2017Co-Authors: Hui Ren Zhou, Wenda Wu, James J PestkaAbstract:Food contamination by the trichothecene mycotoxin deoxynivalenol (DON, vomitoxin) has the potential to adversely affect animal and human health by suppressing food intake and impairing growth. In mice, the DON-induced anorectic response results from aberrant Satiety hormone secretion by enteroendocrine cells (EECs) of the gastrointestinal tract. Recent in vitro studies in the murine STC-1 EEC model have linked DON-induced Satiety hormone secretion to activation of calcium-sensing receptor (CaSR), a G-coupled protein receptor, and transient receptor potential ankyrin-1 (TRPA1), a TRP channel. However, it is unknown whether similar mechanisms mediate DON’s anorectic effects in vivo. Here, we tested the hypothesis that DON-induced food refusal and Satiety hormone release in the mouse are linked to activation of CaSR and TRPA1. Oral treatment with selective agonists for CaSR (R-568) or TRPA1 (allyl isothiocyanate (AITC)) suppressed food intake in mice, and the agonist’s effects were suppressed by pretreatment with corresponding antagonists NPS-2143 or ruthenium red (RR), respectively. Importantly, NPS-2143 or RR inhibited both DON-induced food refusal and plasma elevations of the Satiety hormones cholecystokinin (CCK) and peptide YY3–36 (PYY3–36); cotreatment with both antagonists additively suppressed both anorectic and hormone responses to DON. Taken together, these in vivo data along with prior in vitro findings support the contention that activation of CaSR and TRPA1 contributes to DON-induced food refusal by mediating Satiety hormone exocytosis from EEC.
James J Pestka - One of the best experts on this subject based on the ideXlab platform.
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potential roles for calcium sensing receptor casr and transient receptor potential ankyrin 1 trpa1 in murine anorectic response to deoxynivalenol vomitoxin
Archives of Toxicology, 2017Co-Authors: Hui Ren Zhou, Wenda Wu, James J PestkaAbstract:Food contamination by the trichothecene mycotoxin deoxynivalenol (DON, vomitoxin) has the potential to adversely affect animal and human health by suppressing food intake and impairing growth. In mice, the DON-induced anorectic response results from aberrant Satiety hormone secretion by enteroendocrine cells (EECs) of the gastrointestinal tract. Recent in vitro studies in the murine STC-1 EEC model have linked DON-induced Satiety hormone secretion to activation of calcium-sensing receptor (CaSR), a G-coupled protein receptor, and transient receptor potential ankyrin-1 (TRPA1), a TRP channel. However, it is unknown whether similar mechanisms mediate DON’s anorectic effects in vivo. Here, we tested the hypothesis that DON-induced food refusal and Satiety hormone release in the mouse are linked to activation of CaSR and TRPA1. Oral treatment with selective agonists for CaSR (R-568) or TRPA1 (allyl isothiocyanate (AITC)) suppressed food intake in mice, and the agonist’s effects were suppressed by pretreatment with corresponding antagonists NPS-2143 or ruthenium red (RR), respectively. Importantly, NPS-2143 or RR inhibited both DON-induced food refusal and plasma elevations of the Satiety hormones cholecystokinin (CCK) and peptide YY3–36 (PYY3–36); cotreatment with both antagonists additively suppressed both anorectic and hormone responses to DON. Taken together, these in vivo data along with prior in vitro findings support the contention that activation of CaSR and TRPA1 contributes to DON-induced food refusal by mediating Satiety hormone exocytosis from EEC.
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potential roles for calcium sensing receptor casr and transient receptor potential ankyrin 1 trpa1 in murine anorectic response to deoxynivalenol vomitoxin
Archives of Toxicology, 2017Co-Authors: Hui Ren Zhou, Wenda Wu, James J PestkaAbstract:Food contamination by the trichothecene mycotoxin deoxynivalenol (DON, vomitoxin) has the potential to adversely affect animal and human health by suppressing food intake and impairing growth. In mice, the DON-induced anorectic response results from aberrant Satiety hormone secretion by enteroendocrine cells (EECs) of the gastrointestinal tract. Recent in vitro studies in the murine STC-1 EEC model have linked DON-induced Satiety hormone secretion to activation of calcium-sensing receptor (CaSR), a G-coupled protein receptor, and transient receptor potential ankyrin-1 (TRPA1), a TRP channel. However, it is unknown whether similar mechanisms mediate DON’s anorectic effects in vivo. Here, we tested the hypothesis that DON-induced food refusal and Satiety hormone release in the mouse are linked to activation of CaSR and TRPA1. Oral treatment with selective agonists for CaSR (R-568) or TRPA1 (allyl isothiocyanate (AITC)) suppressed food intake in mice, and the agonist’s effects were suppressed by pretreatment with corresponding antagonists NPS-2143 or ruthenium red (RR), respectively. Importantly, NPS-2143 or RR inhibited both DON-induced food refusal and plasma elevations of the Satiety hormones cholecystokinin (CCK) and peptide YY3–36 (PYY3–36); cotreatment with both antagonists additively suppressed both anorectic and hormone responses to DON. Taken together, these in vivo data along with prior in vitro findings support the contention that activation of CaSR and TRPA1 contributes to DON-induced food refusal by mediating Satiety hormone exocytosis from EEC.
Hui Ren Zhou - One of the best experts on this subject based on the ideXlab platform.
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potential roles for calcium sensing receptor casr and transient receptor potential ankyrin 1 trpa1 in murine anorectic response to deoxynivalenol vomitoxin
Archives of Toxicology, 2017Co-Authors: Hui Ren Zhou, Wenda Wu, James J PestkaAbstract:Food contamination by the trichothecene mycotoxin deoxynivalenol (DON, vomitoxin) has the potential to adversely affect animal and human health by suppressing food intake and impairing growth. In mice, the DON-induced anorectic response results from aberrant Satiety hormone secretion by enteroendocrine cells (EECs) of the gastrointestinal tract. Recent in vitro studies in the murine STC-1 EEC model have linked DON-induced Satiety hormone secretion to activation of calcium-sensing receptor (CaSR), a G-coupled protein receptor, and transient receptor potential ankyrin-1 (TRPA1), a TRP channel. However, it is unknown whether similar mechanisms mediate DON’s anorectic effects in vivo. Here, we tested the hypothesis that DON-induced food refusal and Satiety hormone release in the mouse are linked to activation of CaSR and TRPA1. Oral treatment with selective agonists for CaSR (R-568) or TRPA1 (allyl isothiocyanate (AITC)) suppressed food intake in mice, and the agonist’s effects were suppressed by pretreatment with corresponding antagonists NPS-2143 or ruthenium red (RR), respectively. Importantly, NPS-2143 or RR inhibited both DON-induced food refusal and plasma elevations of the Satiety hormones cholecystokinin (CCK) and peptide YY3–36 (PYY3–36); cotreatment with both antagonists additively suppressed both anorectic and hormone responses to DON. Taken together, these in vivo data along with prior in vitro findings support the contention that activation of CaSR and TRPA1 contributes to DON-induced food refusal by mediating Satiety hormone exocytosis from EEC.
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potential roles for calcium sensing receptor casr and transient receptor potential ankyrin 1 trpa1 in murine anorectic response to deoxynivalenol vomitoxin
Archives of Toxicology, 2017Co-Authors: Hui Ren Zhou, Wenda Wu, James J PestkaAbstract:Food contamination by the trichothecene mycotoxin deoxynivalenol (DON, vomitoxin) has the potential to adversely affect animal and human health by suppressing food intake and impairing growth. In mice, the DON-induced anorectic response results from aberrant Satiety hormone secretion by enteroendocrine cells (EECs) of the gastrointestinal tract. Recent in vitro studies in the murine STC-1 EEC model have linked DON-induced Satiety hormone secretion to activation of calcium-sensing receptor (CaSR), a G-coupled protein receptor, and transient receptor potential ankyrin-1 (TRPA1), a TRP channel. However, it is unknown whether similar mechanisms mediate DON’s anorectic effects in vivo. Here, we tested the hypothesis that DON-induced food refusal and Satiety hormone release in the mouse are linked to activation of CaSR and TRPA1. Oral treatment with selective agonists for CaSR (R-568) or TRPA1 (allyl isothiocyanate (AITC)) suppressed food intake in mice, and the agonist’s effects were suppressed by pretreatment with corresponding antagonists NPS-2143 or ruthenium red (RR), respectively. Importantly, NPS-2143 or RR inhibited both DON-induced food refusal and plasma elevations of the Satiety hormones cholecystokinin (CCK) and peptide YY3–36 (PYY3–36); cotreatment with both antagonists additively suppressed both anorectic and hormone responses to DON. Taken together, these in vivo data along with prior in vitro findings support the contention that activation of CaSR and TRPA1 contributes to DON-induced food refusal by mediating Satiety hormone exocytosis from EEC.
Bradford B Lowell - One of the best experts on this subject based on the ideXlab platform.
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a rapidly acting glutamatergic arc pvh Satiety circuit postsynaptically regulated by α msh
Nature Neuroscience, 2017Co-Authors: Henning Fenselau, Bhavik P. Shah, Joseph C Madara, John N Campbell, Anne M J Verstegen, Jon M Resch, Zongfang Yang, Yael Mandelblatcerf, Yoav Livneh, Bradford B LowellAbstract:Arcuate nucleus (ARC) neurons sense the fed or fasted state and regulate hunger. Agouti-related protein (AgRP) neurons in the ARC (ARCAgRP neurons) are stimulated by fasting and, once activated, they rapidly (within minutes) drive hunger. Pro-opiomelanocortin (ARCPOMC) neurons are viewed as the counterpoint to ARCAgRP neurons. They are regulated in an opposite fashion and decrease hunger. However, unlike ARCAgRP neurons, ARCPOMC neurons are extremely slow in affecting hunger (many hours). Thus, a temporally analogous, rapid ARC Satiety pathway does not exist or is presently unidentified. Here we show that glutamate-releasing ARC neurons expressing oxytocin receptor, unlike ARCPOMC neurons, rapidly cause Satiety when chemo- or optogenetically manipulated. These glutamatergic ARC projections synaptically converge with GABAergic ARCAgRP projections on melanocortin-4 receptor (MC4R)-expressing Satiety neurons in the paraventricular hypothalamus (PVHMC4R neurons). Transmission across the ARCGlutamatergic→PVHMC4R synapse is potentiated by the ARCPOMC neuron-derived MC4R agonist, α-melanocyte stimulating hormone (α-MSH). This excitatory ARC→PVH Satiety circuit, and its modulation by α-MSH, provides insight into regulation of hunger and Satiety.
Bhavik P. Shah - One of the best experts on this subject based on the ideXlab platform.
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a rapidly acting glutamatergic arc pvh Satiety circuit postsynaptically regulated by α msh
Nature Neuroscience, 2017Co-Authors: Henning Fenselau, Bhavik P. Shah, Joseph C Madara, John N Campbell, Anne M J Verstegen, Jon M Resch, Zongfang Yang, Yael Mandelblatcerf, Yoav Livneh, Bradford B LowellAbstract:Arcuate nucleus (ARC) neurons sense the fed or fasted state and regulate hunger. Agouti-related protein (AgRP) neurons in the ARC (ARCAgRP neurons) are stimulated by fasting and, once activated, they rapidly (within minutes) drive hunger. Pro-opiomelanocortin (ARCPOMC) neurons are viewed as the counterpoint to ARCAgRP neurons. They are regulated in an opposite fashion and decrease hunger. However, unlike ARCAgRP neurons, ARCPOMC neurons are extremely slow in affecting hunger (many hours). Thus, a temporally analogous, rapid ARC Satiety pathway does not exist or is presently unidentified. Here we show that glutamate-releasing ARC neurons expressing oxytocin receptor, unlike ARCPOMC neurons, rapidly cause Satiety when chemo- or optogenetically manipulated. These glutamatergic ARC projections synaptically converge with GABAergic ARCAgRP projections on melanocortin-4 receptor (MC4R)-expressing Satiety neurons in the paraventricular hypothalamus (PVHMC4R neurons). Transmission across the ARCGlutamatergic→PVHMC4R synapse is potentiated by the ARCPOMC neuron-derived MC4R agonist, α-melanocyte stimulating hormone (α-MSH). This excitatory ARC→PVH Satiety circuit, and its modulation by α-MSH, provides insight into regulation of hunger and Satiety.
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a neural basis for melanocortin 4 receptor regulated appetite
Nature Neuroscience, 2015Co-Authors: Bhavik P. Shah, Alastair S Garfield, Chia Li, Joseph C Madara, Emily Webber, Jennifer S Steger, John N Campbell, Oksana GavrilovaAbstract:Melanocortin 4 receptors (MC4Rs) are critical to the promotion of homeostatic Satiety. The authors established paraventricular hypothalamus (PVH) MC4R-expressing neurons as a functional target for orexigenic arcuate nucleus agouti-related peptide–expressing neurons and identify an explicit PVH MC4R-expressing neuron to lateral parabrachial nucleus Satiety-promoting circuit, the activation of which encodes positive valence in calorically depleted mice.
