Last update 09 Oct 2024
NPY receptor
32 Drugs associated with NPY receptor
34 Clinical Trials associated with NPY receptor
100 Clinical Results associated with NPY receptor
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100 Translational Medicine associated with NPY receptor
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3,144 Literatures (Medical) associated with NPY receptor
Article
Author: Eickhoff, Hans ; Monteiro-Alfredo, Tamaeh ; Viana, Sofia ; Botelho, Maria Filomena ; Lopes, Eduardo ; Pires, Ana Salomé ; Seiça, Raquel ; Abrantes, Ana Margarida ; Matafome, Paulo ; Reis, Flávio ; Rosendo-Silva, Daniela ; Falcão-Pires, Inês
OBJECTIVE: Obesity is linked to perturbations in energy balance mechanisms, including ghrelin and leptin actions at the hypothalamic circuitry of neuropeptide Y (NPY) and melanocortin. However, information about the regulation of this system in the periphery is still scarce. Our objective was to study the regulation of the NPY/melanocortin system in the adipose tissue (AT) and evaluate its therapeutic potential for obesity and type 2 diabetes.
METHODS: The expression of the NPY/melanocortin receptors' levels was assessed in the visceral AT of individuals with obesity and altered metabolism. Protein levels of these receptors were evaluated in cultured adipocytes incubated with ghrelin (30 and 100 ng/mL) and leptin (1 and 10 nM) and in the AT of an animal model with a mutation in the leptin receptor (ZSF1 rat), to understand their regulation by leptin and ghrelin. The vertical sleeve gastrectomy animal model was used to evaluate the putative therapeutic potential of the NPY/melanocortin system.
RESULTS: In this study, we unravelled that leptin (1 nM and 10 nM) selectively reduced the levels of NPY5R and MC3R but no other NPYR/MCRs in cultured adipocytes. In turn, acylated ghrelin (100 ng/mL) significantly increased NPY1R, but the inhibition of its receptor also abrogates MC3R levels. However, in the Lepr-deficient ZSF1 rat, both NPY5R and MC3R levels were reduced, along with other NPYRs and MCRs, suggesting that leptin resistance negatively affects NPY and melanocortin signalling. In human adipose tissue, we found a downregulation of genes encoding the NPY and melanocortin receptors in the visceral AT of individuals with obesity and insulin resistance, being correlated with genes regulating metabolic activity. Additionally, diabetic obese rats submitted to vertical sleeve gastrectomy showed increased levels of NPY, melanocortin, ghrelin, and leptin receptors in the AT, including MC3R, suggesting it may constitute a therapeutic target in obesity.
CONCLUSIONS: Our results suggest that the AT NPY/melanocortin system, particularly the MC3R, may be involved in the neuroendocrine regulation of adipocyte metabolism. Altogether, our work shows MC3R is under the control of the ghrelin/leptin duo, is reduced in patients with obesity and prediabetes, and may constitute a therapeutic target in obesity.
Author: Haun, Harold L ; Boyt, Kristen M ; Thiele, Todd E ; Flanigan, Meghan E ; Kash, Thomas L ; Méndez, Hernán G ; Neira, Sofia
While there are numerous brain regions that have been shown to play a role in this AUD in humans and animal models, the central nucleus of the amygdala (CeA) has emerged as a critically important locus mediating binge alcohol consumption. In this study, we sought to understand how relative gene expression of key signaling molecules in the CeA changes during different periods of abstinence following bouts of binge drinking. To test this, we performed drinking in the dark (DID) on two separate cohorts of C57BL/6J mice and collected CeA brain tissue at 1 day (acute) and 7 days (protracted) abstinence after DID. We used qRTPCR to evaluate relative gene expression changes of 25 distinct genes of interest related to G protein-coupled receptors (GPCRs), neuropeptides, ion channel subunits, and enzymes that have been previously implicated in AUD. Our findings show that during acute abstinence CeA punches collected from female mice had upregulated relative mRNA expression of the gamma-aminobutyric acid receptor subunit alpha 2 (Gabra2), and the peptidase, angiotensinase c (Prcp). CeA punches from male mice at the same time point in abstinence had upregulated relative mRNA encoding for neuropeptide-related molecules, neuropeptide Y (Npy) and somatostatin (Sst), as well as the neuropeptide Y receptor Y2 (Npyr2), but downregulated Glutamate ionotropic receptor NMDA type subunit 1 (Grin1). After protracted abstinence, CeA punches collected from female mice had increased mRNA expression of corticotropin releasing hormone (Crh) and Npy. CeA punches collected from male mice at the same timepoint had upregulated relative mRNA expression of Npy2r, Npy, and Sst. Our findings support that there are differences in how the CeA of male and female mice respond to binge-alcohol exposure, highlighting the need to understand the implications of such differences in the context of AUD and binge drinking behavior.
Author: Yoo, Ji Youn ; Dutra, Samia Valeria Ozorio ; Wilson, Ronee ; Urmi, Shaheda ; Awomolo, Adeola ; Campos, Adriana ; Louis-Jacques, Adetola ; Villarreal, Xuban Palau ; Groer, Maureen
INTRODUCTION: Cortisol is a biological marker of stress, and its levels reflect the hypothalamic-pituitary-adrenal (HPA) axis response to stress over time. Saliva, blood, and urine cortisol reflect acute stress, whereas assessment of hair cortisol is a better reflection of chronic stress. There is limited information on hair cortisol concentration (HCC) in the perinatal period, particularly, in the preconception and postpartum periods. In addition to being a biomarker for stress, high levels of cortisol are typically associated with poor psychosocial outcomes, and adverse pregnancy outcomes. The objectives of this study were: (1) to measure HCC from six months preconception to six months postpartum; (2) to examine the relationship between HCC and demographic characteristics, depressive symptoms, and perceived stress in the first six months postpartum period; (3) and to assess the associations between HCC and systemic inflammatory markers in the first six months postpartum.
METHODS: The analysis included 96 women from a longitudinal study with up to 3 study visits in the first six months postpartum. Blood and hair samples were collected at 1-2 months (PP1), 3-4 months (PP2), and 5-6 months (PP3) postpartum. We obtained sociodemographic information, depressive symptoms, and perceived stress scores at PP1-PP3. To quantify cortisol levels over time, 8 segments were derived corresponding to 6 (PC1) and 3 (PC2) months preconception as well as for each trimester (T1-T3) and postpartum (PP1-PP3). Eight cytokines (Granulocyte-macrophage colony-stimulating factor (GM-CSF), Interferon- gamma [IFN- γ], Interleukin [IL]-10, IL-2, IL-4, IL-6, IL-8, and Tumor necrosis factor-alpha (TNF- α) were measured in plasma in the postpartum samples. Univariate, bivariate, correlations, and linear mixed modelling were performed using SAS 9.4. Multiple testing correction was conducted for correlations using false discovery rate and a Q value of <0.05 was deemed significant.
RESULTS: Median HCC varied over time peaking in the third trimester and declining in the postpartum. Significant differences were noted in median cortisol levels by race with Black/African American postpartum women experiencing higher levels at all timepoints. Significantly, higher median cortisol levels were also observed at PP1 and PP2 for mothers who reported their relationship status as single. Ethnicity, education, median age, depressive symptoms, and perceived stress were not associated with median cortisol levels. Pro-inflammatory cytokines IFN- γ (q= 0.01;
