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21 results for “Neuropeptide Y”
Figure 4 in Perinatal exposure to a high-fat diet alters proopiomelanocortin, neuropeptide Y and dopaminergic receptors gene expression and the food preference in offspring adult rats
Figure 4. Body weight on the 120th offspring from mothers submitted the control diet or the high-fat diet. Values are presented as mean ± SEM using two-way ANOVA followed by the Bonferroni multiple-comparison test. *p<0,05; **p<0,005.
Figure 3 in Perinatal exposure to a high-fat diet alters proopiomelanocortin, neuropeptide Y and dopaminergic receptors gene expression and the food preference in offspring adult rats
Figure 3. Body weight on the second day life's of offspring from mothers submitted the control diet (C) or the high-fat diet (H). Values are presented as mean + SEM using Student t-test. C: n = 23; H: n = 23.
Figure 2 in Perinatal exposure to a high-fat diet alters proopiomelanocortin, neuropeptide Y and dopaminergic receptors gene expression and the food preference in offspring adult rats
Figure 2. Pomc (A) and npy (B) gene expression in the hypothalamus of offspring exposed or not to a control diet or high-fat diet during perinatal and/or postnatal period. Values are presented as mean ± SEM using two-way ANOVA followed by the Bonferroni multiplecomparison test. Level of significance: *p<0,05; "a": compared to CC, "b": compared to CH; "c": compared to HC; "d": compared to HH.
Figure 1. Drd1 in Perinatal exposure to a high-fat diet alters proopiomelanocortin, neuropeptide Y and dopaminergic receptors gene expression and the food preference in offspring adult rats
Figure 1. Drd1 (A) and drd2 (B) gene expression in the nucleus accumbens of offspring exposed or not to a control diet or high-fat diet during perinatal and/or postnatal period. Values are presented as mean ± SEM using two-way ANOVA followed by the Bonferroni multiplecomparison test. Level of significance: *p<0,05; "a": compared to CC, "b": compared to CH; "c": compared to HC; "d": compared to HH.
Table 2 in Perinatal exposure to a high-fat diet alters proopiomelanocortin, neuropeptide Y and dopaminergic receptors gene expression and the food preference in offspring adult rats
<p><b>Table 2.</b> Relative food intake of the high-fat diet and control diet during the food preference study in offspring exposed or not a control diet or high-fat diet during perinatal and/or postnatal period.</p><table><tbody><tr><th></th><th><i>High-fat diet (g/100 g body weight)</i></th><th></th></tr></tbody><tbody><tr><th></th><td><i>102º day</i></td><td><i>110º day</i></td><td><i>116º day</i></td></tr><tr><th><i>CC</i></th><td>12.6 ± 0.6</td><td>11.3 ± 0.2</td><td>11.1 ± 0.7</td></tr><tr><th><i>CH</i></th><td>12.8 ± 0.6</td><td>12.4 ± 0.3</td><td>11.4 ± 0.4</td></tr><tr><th><i>HC</i></th><td>16.7 ± 1.1 <b>a.b*</b></td><td>13.7 ± 0.9</td><td>10.0 ± 0.5</td></tr><tr><th><i>HH</i></th><td>15.3 ± 0.7 <b>a.b*</b></td><td>11.7 ± 0.9</td><td>10.7 ± 0.5</td></tr><tr><th></th><td><i>Control diet (g/100 g body weight)</i></td><td></td></tr><tr><th></th><td><i>102º day</i></td><td><i>110º day</i></td><td><i>116º day</i></td></tr><tr><th><i>CC</i></th><td>1.4 ± 0.2</td><td>1.1 ± 0.1</td><td>1.1 ± 0.3</td></tr><tr><th><i>CH</i></th><td>2.1 ± 0.2</td><td>1.5 ± 0.3</td><td>0.9 ± 0.1</td></tr><tr><th><i>HC</i></th><td>1.8 ± 0.2</td><td>1.0 ± 0.3</td><td>1.0 ± 0.3</td></tr><tr><th><i>HH</i></th><td>1.9 ± 0.2</td><td>1.1 ± 0.2</td><td>0.7 ± 0.1</td></tr></tbody></table><p>Values are presented as mean + SEM using two-way ANOVA followed by the Bonferroni multiple-comparison test. *p<0,005; “a”: compared to CC, “b”: compared to CH; “c”: compared to HC; “d”: compared to HH.</p>
Table 1 in Perinatal exposure to a high-fat diet alters proopiomelanocortin, neuropeptide Y and dopaminergic receptors gene expression and the food preference in offspring adult rats
<p><b>Table 1.</b> Experimental design. The rats were fed commercial standard diet for rodents control diet or high-fat diet during pregnancy, lactation and post-weaning (up to 100 days of life).During the feeding period, rats consumed both diets (control diet and high-fat diet). The numbers in parentheses indicate the animals number in each nutritional group.</p><table><tbody><tr><th><b>Experimental Design</b></th></tr></tbody><tbody><tr><th><b>Genitors (n)</b></th><td><b>Gestation and lactation</b></td><td><b>Offspring during lactation (n)</b></td><td><b>Offspring (n)</b></td><td><b>Post-weaning (21-100° life’s day)</b></td><td><b>Food preference (102-116º life’s day)</b></td></tr><tr><th></th><td></td><td></td><td>CC (12)</td><td>Control diet</td><td>Control diet</td></tr><tr><th></th><td></td><td></td><td></td><td></td><td>High-fat diet</td></tr><tr><th>GC (5)</th><td>Control diet</td><td>C (23)</td><td>CH (11)</td><td>High-fat diet</td><td>Control diet</td></tr><tr><th></th><td></td><td></td><td></td><td></td><td>High-fat diet</td></tr><tr><th></th><td></td><td></td><td>HC (11)</td><td>Control diet</td><td>Control diet</td></tr><tr><th></th><td></td><td></td><td></td><td></td><td>High-fat diet</td></tr><tr><th>GH (5)</th><td>High-fat diet</td><td>H (23)</td><td>HH (12)</td><td>High-fat diet</td><td>Control diet</td></tr><tr><th></th><td></td><td></td><td></td><td></td><td>High-fat diet</td></tr></tbody></table>
Intranasal Administration of Neuropeptide Y in Healthy Male Volunteers
ClinicalTrials.gov study NCT00748956. IPD Sharing: Not stated. Countries: 1. Publications: 9.
Intranasal Neuropeptide Y in Clinical Trial in Level Two Trauma Patients for PTSD and Acute Stress Disorder
ClinicalTrials.gov study NCT04071600. IPD Sharing: NO. Countries: 1. Publications: 3.
A Dose Escalation Study of Intranasal Neuropeptide Y in Post Traumatic Stress Disorder (PTSD)
ClinicalTrials.gov study NCT01533519. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Neuropeptide Y Regulates Neurogenic Pulp Inflammation
ClinicalTrials.gov study NCT06606236. IPD Sharing: NO. Countries: 1. Publications: 13.
pH-dependent structural dynamics of the neuropeptide Y in aqueous solution
Open the record for dataset details and reuse information.
ABCA7-dependent induction of neuropeptide Y is required for synaptic resilience in Alzheimer's disease through BDNF/NGFR signaling
GEO Series GSE244550. Danio rerio. 4 samples. Type: Expression profiling by high throughput sequencing.
Neuropeptide Y (NPY) Regulation of Nociceptors
ClinicalTrials.gov study NCT00596193. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Sex Differences in Neuropeptide Y Serum, But Not in Fat Intake and Body Mass Index
ClinicalTrials.gov study NCT04650308. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Neuropeptide Y and Sympathovagal Balance
ClinicalTrials.gov study NCT03933787. IPD Sharing: UNDECIDED. Countries: 1. Publications: 0.
mTOR-neuropeptide Y signaling sensitizes nociceptors to drive neuropathic pain development
GEO Series GSE184014. Mus musculus. 17 samples. Type: Expression profiling by high throughput sequencing.
Moxonidine Effects on Neuropeptide Y
ClinicalTrials.gov study NCT05147753. IPD Sharing: NO. Countries: 0. Publications: 0.
A key role for neuropeptide Y in lifespan extension and cancer suppression by dietary restriction
GEO Series GSE42761. Mus musculus. 8 samples. Type: Expression profiling by array.
An epithelial paracrine pathway that induces an asthmatic phenotype through a neuropeptide-Y induced mechanism
GEO Series GSE64774. Mus musculus. 6 samples. Type: Expression profiling by array.
Dataset related to the article "Neuropeptide Y promotes adipogenesis of human cardiac mesenchymal stromal cells in arrhythmogenic cardiomyopathy"
<p>This record contains raw data related to the article “Neuropeptide Y promotes adipogenesis of human cardiac mesenchymal stromal cells in arrhythmogenic cardiomyopathy"</p> <p><strong>Background: </strong>Arrhythmogenic Cardiomyopathy (AC) is a familial cardiac disease, mainly caused by mutations in desmosomal genes. AC hearts show fibro-fatty myocardial replacement, which favors stress-related life-threatening arrhythmias, predominantly in the young and athletes. AC lacks effective therapies, as its pathogenesis is poorly understood. Recently, we showed that cardiac Mesenchymal Stromal Cells (cMSCs) contribute to adipose tissue in human AC hearts, although the underlying mechanisms are still unclear.</p> <p><strong>Purpose: </strong>We hypothesize that the sympathetic neurotransmitter, Neuropeptide Y (NPY), participates to cMSC adipogenesis in human AC.</p> <p><strong>Methods: </strong>For translation of our findings, we combined in vitro cytochemical, molecular and pharmacologic assays on human cMSCs, from myocardial biopsies of healthy controls and AC patients, with the use of existing drugs to interfere with the predicted AC mechanisms. Sympathetic innervation was inspected in human autoptic heart samples, and NPY plasma levels measured in healthy and AC subjects.</p> <p><strong>Results: </strong>AC cMSCs expressed higher levels of pro-adipogenic isotypes of NPY-receptors (i.e. Y1-R, Y5-R). Consistently, NPY enhanced adipogenesis in AC cMSCs, which was blocked by FDA-approved Y1-R and Y5-R antagonists. AC-associated PKP2 reduction directly caused NPY-dependent adipogenesis in cMSCs. In support of the involvement of sympathetic neurons (SNs) and NPY in AC myocardial remodeling, patients had elevated NPY plasma levels and, in human AC hearts, SNs accumulated in fatty areas and were close to cMSCs.</p> <p><strong>Conclusions: </strong>Independently from the disease origin, AC causes in cMSCs a targetable gain of responsiveness to NPY, which leads to increased adipogenesis, thus playing a role in AC myocardial remodeling.</p>
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