Relevant bibliographies by topics / GPR109a

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Academic literature on the topic 'GPR109a'

Author: Grafiati
Published: 4 June 2021
Last updated: 2 February 2022

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Journal articles on the topic "GPR109a"

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Docampo, Melissa D., Christoph K. Stein-Thoeringer, Amina Lazrak, Marina D. Burgos da Silva, Justin Cross, and Marcel R. M. van den Brink. "Expression of the Butyrate/Niacin Receptor, GPR109a on T Cells Plays an Important Role in a Mouse Model of Graft Versus Host Disease." Blood 132, Supplement 1 (2018): 61. http://dx.doi.org/10.1182/blood-2018-99-118783.

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Abstract INTRODUCTION: The intestinal microbiota is essential for the fermentation of fibers into the short-chain fatty acids (SCFA) butyrate, acetate and propionate. SCFA can bind to G-protein-coupled receptors GPR41, GPR43 and GPR109a to activate downstream anti-inflammatory signaling pathways. In colitis or graft versus host disease (GVHD), GPR43 signaling has been reported as an important regulator of intestinal homeostasis by increasing the pool of regulatory T cells. In contrast to GPR43, which binds preferentially propionate and acetate, GPR109a is the major receptor for butyrate. We an
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Geisler, Caroline E., Kendra E. Miller, Susma Ghimire, and Benjamin J. Renquist. "The Role of GPR109a Signaling in Niacin Induced Effects on Fed and Fasted Hepatic Metabolism." International Journal of Molecular Sciences 22, no. 8 (2021): 4001. http://dx.doi.org/10.3390/ijms22084001.

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Signaling through GPR109a, the putative receptor for the endogenous ligand β-OH butyrate, inhibits adipose tissue lipolysis. Niacin, an anti-atherosclerotic drug that can induce insulin resistance, activates GPR109a at nM concentrations. GPR109a is not essential for niacin to improve serum lipid profiles. To better understand the involvement of GPR109a signaling in regulating glucose and lipid metabolism, we treated GPR109a wild-type (+/+) and knockout (−/−) mice with repeated overnight injections of saline or niacin in physiological states characterized by low (ad libitum fed) or high (16 h f
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Zellner, Christian, Clive R. Pullinger, Bradley E. Aouizerat, et al. "Variations in human HM74 (GPR109B) and HM74A (GPR109A) niacin receptors." Human Mutation 25, no. 1 (2004): 18–21. http://dx.doi.org/10.1002/humu.20121.

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Snelson, Matthew, Sih Min Tan, Gavin C. Higgins, Runa S. J. Lindblom, and Melinda T. Coughlan. "Exploring the role of the metabolite-sensing receptor GPR109a in diabetic nephropathy." American Journal of Physiology-Renal Physiology 318, no. 3 (2020): F835—F842. http://dx.doi.org/10.1152/ajprenal.00505.2019.

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Alterations in gut homeostasis may contribute to the progression of diabetic nephropathy. There has been recent attention on the renoprotective effects of metabolite-sensing receptors in chronic renal injury, including the G protein-coupled receptor (GPR)109a, which ligates the short-chain fatty acid butyrate. However, the role of GPR109a in the development of diabetic nephropathy, a milieu of diminished microbiome-derived metabolites, has not yet been determined. The present study aimed to assess the effects of insufficient GPR109a signaling, via genetic deletion of GPR109a, on the developmen
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Ahmed, Kashan, Sorin Tunaru, and Stefan Offermanns. "GPR109A, GPR109B and GPR81, a family of hydroxy-carboxylic acid receptors." Trends in Pharmacological Sciences 30, no. 11 (2009): 557–62. http://dx.doi.org/10.1016/j.tips.2009.09.001.

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Plaisance, Eric P., Martina Lukasova, Stefan Offermanns, Youyan Zhang, Guoqing Cao, and Robert L. Judd. "Niacin stimulates adiponectin secretion through the GPR109A receptor." American Journal of Physiology-Endocrinology and Metabolism 296, no. 3 (2009): E549—E558. http://dx.doi.org/10.1152/ajpendo.91004.2008.

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Niacin (nicotinic acid) has recently been shown to increase serum adiponectin concentrations in men with the metabolic syndrome. However, little is known about the mechanism(s) by which niacin regulates the intracellular trafficking and secretion of adiponectin. Since niacin appears to exert its effects on lipolysis through receptor (GPR109A)-dependent and -independent pathways, the purpose of this investigation was to examine the role of the recently identified GPR109A receptor in adiponectin secretion. Initial in vivo studies in rats demonstrated that niacin (30 mg/kg po) acutely increases s
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Giri, Banabihari, Kasey Belanger, Marissa Seamon, et al. "Niacin Ameliorates Neuro-Inflammation in Parkinson’s Disease via GPR109A." International Journal of Molecular Sciences 20, no. 18 (2019): 4559. http://dx.doi.org/10.3390/ijms20184559.

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In this study, we used macrophage RAW264.7 cells to elucidate the molecular mechanism underlying the anti-inflammatory actions of niacin. Anti-inflammatory actions of niacin and a possible role of its receptor GPR109A have been studied previously. However, the precise molecular mechanism of niacin’s action in reducing inflammation through GPR109A is unknown. Here we observed that niacin reduced the translocation of phosphorylated nuclear kappa B (p-NF-κB) induced by lipopolysaccharide (LPS) in the nucleus of RAW264.7 cells. The reduction in the nuclear translocation in turn decreased the expre
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Horimatsu, Tetsuo, Andra L. Blomkalns, Mourad Ogbi, et al. "Niacin protects against abdominal aortic aneurysm formation via GPR109A independent mechanisms: role of NAD+/nicotinamide." Cardiovascular Research 116, no. 14 (2019): 2226–38. http://dx.doi.org/10.1093/cvr/cvz303.

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Abstract Aims Chronic adventitial and medial infiltration of immune cells play an important role in the pathogenesis of abdominal aortic aneurysms (AAAs). Nicotinic acid (niacin) was shown to inhibit atherosclerosis by activating the anti-inflammatory G protein-coupled receptor GPR109A [also known as hydroxycarboxylic acid receptor 2 (HCA2)] expressed on immune cells, blunting immune activation and adventitial inflammatory cell infiltration. Here, we investigated the role of niacin and GPR109A in regulating AAA formation. Methods and results Mice were supplemented with niacin or nicotinamide,
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Karunaratne, Tennekoon B., Chijioke Okereke, Marissa Seamon, Sharad Purohit, Chandramohan Wakade, and Amol Sharma. "Niacin and Butyrate: Nutraceuticals Targeting Dysbiosis and Intestinal Permeability in Parkinson’s Disease." Nutrients 13, no. 1 (2020): 28. http://dx.doi.org/10.3390/nu13010028.

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Dysbiosis is implicated by many studies in the pathogenesis of Parkinson’s disease (PD). Advances in sequencing technology and computing have resulted in confounding data regarding pathogenic bacterial profiles in conditions such as PD. Changes in the microbiome with reductions in short-chain fatty acid (SCFA)-producing bacteria and increases in endotoxin-producing bacteria likely contribute to the pathogenesis of PD. GPR109A, a G-protein coupled receptor found on the surface of the intestinal epithelium and immune cells, plays a key role in controlling intestinal permeability and the inflamma
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Ye, Lingyan, Zheng Cao, Xiangru Lai, Ying Shi, and Naiming Zhou. "Niacin Ameliorates Hepatic Steatosis by Inhibiting De Novo Lipogenesis Via a GPR109A-Mediated PKC–ERK1/2–AMPK Signaling Pathway in C57BL/6 Mice Fed a High-Fat Diet." Journal of Nutrition 150, no. 4 (2019): 672–84. http://dx.doi.org/10.1093/jn/nxz303.

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ABSTRACT Background Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease in the world. Hepatic de novo lipogenesis (DNL) has been suggested to contribute to the pathogenesis of NAFLD. Recent studies have demonstrated that niacin (NA) modulates hepatic DNL through GPR109A. However, the underlying mechanism remains largely unknown. Objectives This study aims to elucidate the potential molecular mechanism by which GPR109A inhibits hepatic DNL. Methods C57BL/6 wild-type (WT) and Gpr109a knockout (KO) mice (male, 5 wk old) were fed a high-fat diet (60% energy from fat) firstly
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Dissertations / Theses on the topic "GPR109a"

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Foy, Caroline, and Caroline Foy. "The Role of Ketone Signaling in the Hepatic Response to Fasting." Thesis, The University of Arizona, 2016. http://hdl.handle.net/10150/621472.

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Ketosis is a metabolic condition that occurs during heat stress, prolonged exercise, fasting, and in obese and diabetic individuals. The major ketone body, β-OH butyrate, affects cellular signaling pathways in a hormone-like manner through its receptor GPR109a. While physiological ketosis is often adaptive, chronic hyperketonemia may contribute to the metabolic dysfunction of diabetes. To understand how β-OH butyrate signaling affects hepatic metabolism we compared the fasting response in control and 3-hydroxy-3-methylglutaryl-CoA Synthase II (HMGCS2) knockdown mice that are unable to elevate
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Kawan, Mohamed. "The role of QRFP & GPR103 in human prostate cancer." Thesis, University of Warwick, 2016. http://wrap.warwick.ac.uk/88011/.

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Prostate cancer is the leading cause of non-cutaneous malignancy and is the second most commonly diagnosed cancer among men after lung cancer. QRFP is a secreted protein that is extensively expressed in the brain with highest expression levels in the medulla, pituitary gland, cerebellum, retina, and vestibular nucleus; in the periphery it is expressed in the adipose tissue prostate gland, bladder, colon, testis and in the parathyroid and thyroid gland. QRFP is a member of the RF amide neuropeptide family. This family might be implicated in extensive array of biological activities for instance,
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Murakami, Takaaki. "Non-invasive evaluation of GPR119 agonist effects on β-cell mass in diabetic male mice using ¹¹¹In-exendin-4 SPECT/CT". Kyoto University, 2020. http://hdl.handle.net/2433/253194.

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Stone, Virginia May. "Expression and roles of the lipid-responsive receptors GPR119 and GPR120 in pancreatic islets." Thesis, Exeter and Plymouth Peninsula Medical School, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.566051.

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The various endocrine cell types present in mammalian Islets of Langerhans express a range of lipid-responsive G-proteln coupled receptors (GPCRs) including GPR119 and GPR120. These are each reported to be expressed In islet beta-cells and GPR 119 has been Implicated In the augmentation of glucose-stimulated insulin secretion by certain derivatives of long chain unsaturated fatty acids. By contrast GPR 120 does not appear to regulate insulin secretion and its role is unclear In addition to their ability to regulate hormone secretion long-chain fatty acids and their derivatives can also influen
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Moodaley, Runisha. "Free fatty acid receptor (FFA) and lipid receptor (GPR119) signalling mediates nutrient-sensing in mouse intestine." Thesis, King's College London (University of London), 2018. https://kclpure.kcl.ac.uk/portal/en/theses/free-fatty-acid-receptor-ffa-and-lipid-receptor-gpr119-signalling-mediates-nutrientsensing-in-mouse-intestine(6deac195-861b-4967-b005-20ec150df882).html.

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Medium and long chain fatty acids exhibit affinity for free-fatty acid receptor 1 (FFA1) and 4 (FFA4). FFA1 and FFA4 are expressed in the pancreas with a third lipid G-protein coupled receptor, GPR119, and all three GPCRs are also highly expressed by gastrointestinal (GI) enteroendocrine L cells, which release glucagon-like peptide 1 (GLP-1) and peptide YY (PYY). GLP-1 is a stimulant of insulin secretion postprandially, whereas PYY slows GI motility and reduces food intake. The receptor expression patterns raise these receptors’ potential as targets for anti-diabetic and anti-obesity therapeut
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Marotte, Amélie. "Conception rationnelle de nouveaux ligands du GPR103, un récepteur couplé à une protéine G et cible du 26RFa." Rouen, 2013. http://www.theses.fr/2013ROUES039.

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Le 26RFa est un neuropeptide de la famille des RFamides et le ligand du GPR103, un récepteur couplé à une protéine G. Ce système est impliqué dans de nombreux processus biologiques, tels que le contrôle de la prise alimentaire, la reproduction ou la formation des os. Bien que de nombreuses études d'activités aient été menées, seule l'analyse structurale du ligand dans le méthanol a été effectuée. L'objectif de ce travail de thèse a été de déterminer (i) les éléments structuraux du 26RFa nécessaires pour la liaison et l'activation du GPR103; (ii) de concevoir différents analogues du 26RFa et ai
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Ayachi, Safia. "Implication des récepteurs à peptides RF-amide dans la modulation de la douleur et de l'hyperalgésie induite par les opiacés." Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ100.

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La douleur est un problème de santé publique majeur qui réduit la qualité de vie des patients et engendre un coût élevé pour la société. Malgré les efforts fournis pour développer de nouveaux analgésiques, les opiacés restent le moyen le plus efficace pour réduire la douleur moyenne à intense. Cependant, leur utilisation prolongée est responsable du développement d’une tolérance à leurs effets analgésiques et d’une hypersensibilité à la douleur (hyperalgésie). Il a été proposé que ces phénomènes pourraient résulter de l'activation d’un système anti-opioïde tel que celui des récepteurs RF-amide
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Lectez, Benoît. "Caractérisation du système 26Rfa/GPR103 et recherche du mécanisme d’action du 26Rfa dans le contrôle hypotalamique du comportement alimentaire." Rouen, 2009. http://www.theses.fr/2009ROUES001.

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Le 26RFa est un nouveau membre de la famille des peptides RFamides qui a été initialement isolé dans le cerveau de la grenouille et ensuite caractérisé chez les mammifères. Parallèlement, le 26RFa a été identifié comme le ligand endogène d’un récepteur jusqu’alors orphelin, le GPR103. Chez les rongeurs, les ARNm du 26RFa sont essentiellement exprimés dans le noyau hypothalamique ventromédian (VMH) et l’aire hypothalamique latérale (LH), deux structures bien connues pour être impliquées dans le contrôle du comportement alimentaire, et il a été montré que l’injection intracérébroventriculaire (i
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Hurst, Katrina M. "Modulation of Synaptic Plasticity: Endocannabinoids and Novel G-protein Coupled Receptors Expression and Translational Effects in Interneurons." BYU ScholarsArchive, 2017. https://scholarsarchive.byu.edu/etd/6940.

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Learning and memory are important processes that occur in the brain. The brain is comprised of neurons that make connections with each other known as synapses. Synaptic plasticity is widely believed to be the physiologic mechanism by which learning and memory occur. Synapses can either be strengthened through a process known as long-term potentiation (LTP) or weakened through long-term depression (LTD). The area of the brain that is most studied for its role in learning and memory is the hippocampus, which has been shown to be involved in memory consolidation. The detection of endocannabi
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Botteselle, Lorenzo [Verfasser], and Martin [Akademischer Betreuer] Storr. "Interaktion zwischen GPR119 und CB1-Rezeptoren bei der Modulation der gastrointestinalen Motilität im Maus- und Humangewebe / Lorenzo Botteselle ; Betreuer: Martin Storr." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/115438604X/34.

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Book chapters on the topic "GPR109a"

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Meigs, Thomas E., Alex Lyakhovich, Hoon Shim, et al. "GPR100." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100563.

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Meigs, Thomas E., Alex Lyakhovich, Hoon Shim, et al. "GPR105." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100564.

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Shah*, Unmesh, Scott Edmondson, and Jason W. Szewczyk. "Chapter 7. Recent Advances in the Discovery of GPR119 Agonists." In Drug Discovery. Royal Society of Chemistry, 2012. http://dx.doi.org/10.1039/9781849735322-00177.

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Shen, Hong C., and Steven L. Colletti. "High-Affinity Niacin Receptor GPR109A Agonists." In Annual Reports in Medicinal Chemistry. Elsevier, 2010. http://dx.doi.org/10.1016/s0065-7743(10)45005-8.

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Bridges, Allison, Pragya Rajpurohit, Puttur D. Prasad, and Muthusamy Thangaraju. "Vitamin B3: niacin and transcriptome analysis in relation to the GPR109A receptor." In Molecular Nutrition. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-811907-5.00031-2.

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"GPR105." In Encyclopedia of Signaling Molecules. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101520.

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"(GPR100)." In Encyclopedia of Signaling Molecules. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_100067.

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"GPR129." In Encyclopedia of Signaling Molecules. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_105031.

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Reynet, CR. "GPR119 agonists (revision number 23)." In Diapedia. Diapedia.org, 2014. http://dx.doi.org/10.14496/dia.8105219819.23.

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Zhu, Xiaoyun, Wenglong Huang, and Hai Qi. "GPR119 Agonists: A Novel Strategy for Type 2 Diabetes Treatment." In Diabetes Mellitus - Insights and Perspectives. InTech, 2013. http://dx.doi.org/10.5772/48444.

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Conference papers on the topic "GPR109a"

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Kump, Annie, Daniel Herrera, and Leah T. Stiemsma. "Abstract A12: Expression of GPR41, GPR43, and GPR109A in breast tissue in relation to breast cancer development." In Abstracts: AACR Special Conference on the Microbiome, Viruses, and Cancer; February 21-24, 2020; Orlando, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.mvc2020-a12.

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Bardhan, Kankana, Vadivel Ganapathy та Kebin Liu. "Abstract 3140: Constitutive and regulated expression of GPR109A by DNA methylation and IFN-γ in human colon carcinoma cells". У Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3140.

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Chandra Kaushik, Aman, and Shakti Sahi. "3D structure prediction and molecular dynamics simulation studies of GPR139." In 2016 International Conference on Bioinformatics and Systems Biology (BSB). IEEE, 2016. http://dx.doi.org/10.1109/bsb.2016.7552143.

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