Relevant bibliographies by topics / NPY/AgRP neuron

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Academic literature on the topic 'NPY/AgRP neuron'

Author: Grafiati
Published: 2 November 2024
Last updated: 31 July 2025

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Journal articles on the topic "NPY/AgRP neuron"

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Oh, Youjin, Eun-Seon Yoo, Sang Hyeon Ju, et al. "GIRK2 potassium channels expressed by the AgRP neurons decrease adiposity and body weight in mice." PLOS Biology 21, no. 8 (2023): e3002252. http://dx.doi.org/10.1371/journal.pbio.3002252.

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It is well known that the neuropeptide Y (NPY)/agouti-related peptide (AgRP) neurons increase appetite and decrease thermogenesis. Previous studies demonstrated that optogenetic and/or chemogenetic manipulations of NPY/AgRP neuronal activity alter food intake and/or energy expenditure (EE). However, little is known about intrinsic molecules regulating NPY/AgRP neuronal excitability to affect long-term metabolic function. Here, we found that the G protein-gated inwardly rectifying K+ (GIRK) channels are key to stabilize NPY/AgRP neurons and that NPY/AgRP neuron-selective deletion of the GIRK2 s
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van de Wall, Esther, Rebecca Leshan, Allison W. Xu, et al. "Collective and Individual Functions of Leptin Receptor Modulated Neurons Controlling Metabolism and Ingestion." Endocrinology 149, no. 4 (2007): 1773–85. http://dx.doi.org/10.1210/en.2007-1132.

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Two known types of leptin-responsive neurons reside within the arcuate nucleus: the agouti gene-related peptide (AgRP)/neuropeptide Y (NPY) neuron and the proopiomelanocortin (POMC) neuron. By deleting the leptin receptor gene (Lepr) specifically in AgRP/NPY and/or POMC neurons of mice, we examined the several and combined contributions of these neurons to leptin action. Body weight and adiposity were increased by Lepr deletion from AgRP and POMC neurons individually, and simultaneous deletion in both neurons (A+P LEPR-KO mice) further increased these measures. Young (periweaning) A+P LEPR-KO
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Coutinho, Eulalia A., Melanie Prescott, Sabine Hessler, Christopher J. Marshall, Allan E. Herbison, and Rebecca E. Campbell. "Activation of a Classic Hunger Circuit Slows Luteinizing Hormone Pulsatility." Neuroendocrinology 110, no. 7-8 (2019): 671–87. http://dx.doi.org/10.1159/000504225.

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Introduction: The central regulation of fertility is carefully coordinated with energy homeostasis, and infertility is frequently the outcome of energy imbalance. Neurons in the hypothalamus expressing neuropeptide Y and agouti-related peptide (NPY/AgRP neurons) are strongly implicated in linking metabolic cues with fertility regulation. Objective: We aimed here to determine the impact of selectively activating NPY/AgRP neurons, critical regulators of metabolism, on the activity of luteinizing hormone (LH) pulse generation. Methods: We employed a suite of in vivo optogenetic and chemogenetic a
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Jones, Edward S., Nicolas Nunn, Adam P. Chambers, Søren Østergaard, Birgitte S. Wulff, and Simon M. Luckman. "Modified Peptide YY Molecule Attenuates the Activity of NPY/AgRP Neurons and Reduces Food Intake in Male Mice." Endocrinology 160, no. 11 (2019): 2737–47. http://dx.doi.org/10.1210/en.2019-00100.

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Abstract To study the effects of an analog of the gut-produced hormone peptide YY (PYY3-36), which has increased selectivity for the Y2 receptor; specifically, to record its effects on food intake and on hypothalamic neuropeptide Y/agouti-related peptide (NPY/AgRP) neuron activity. NNC0165-1273, a modified form of the peptide hormone PYY3-36 with potent selectivity at Y2 receptor (>5000-fold over Y1, 1250-fold over Y4, and 650-fold over Y5 receptor), was tested in vivo and in vitro in mouse models. NNC0165-1273 has fivefold lower relative affinity for Y2 compared with PYY3-36, but >250-,
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Morton, GJ, and MW Schwartz. "The NPY/AgRP neuron and energy homeostasis." International Journal of Obesity 25, S5 (2001): S56—S62. http://dx.doi.org/10.1038/sj.ijo.0801915.

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Landry, Taylor, Daniel Shookster, Alec Chaves, Katrina Free, Tony Nguyen, and Hu Huang. "Exercise increases NPY/AgRP and TH neuron activity in the hypothalamus of female mice." Journal of Endocrinology 252, no. 3 (2022): 167–77. http://dx.doi.org/10.1530/joe-21-0250.

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Recent evidence identifies a potent role for aerobic exercise to modulate the activity of hypothalamic neurons related to appetite; however, these studies have been primarily performed in male rodents. Since females have markedly different neuronal mechanisms regulating food intake, the current study aimed to determine the effects of acute treadmill exercise on hypothalamic neuron populations involved in regulating appetite in female mice. Mature, untrained female mice were exposed to acute sedentary, low- (10 m/min), moderate- (14 m/min), and high (18 m/min)-intensity treadmill exercise in a
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Smith, A. W., M. A. Bosch, E. J. Wagner, O. K. Rønnekleiv та M. J. Kelly. "The membrane estrogen receptor ligand STX rapidly enhances GABAergic signaling in NPY/AgRP neurons: role in mediating the anorexigenic effects of 17β-estradiol". American Journal of Physiology-Endocrinology and Metabolism 305, № 5 (2013): E632—E640. http://dx.doi.org/10.1152/ajpendo.00281.2013.

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Besides its quintessential role in reproduction, 17β-estradiol (E2) is a potent anorexigenic hormone. E2 and the selective Gq-coupled membrane estrogen receptor (Gq-mER) ligand STX rapidly increase membrane excitability in proopiomelanocortin (POMC) neurons by desensitizing the coupling of GABAB receptors to G protein-coupled inwardly rectifying K+ channels (GIRKs), which upon activation elicit a hyperpolarizing outward current. However, it is unknown whether E2 and STX can modulate GABAB signaling in neuropeptide Y (NPY)/agouti-related peptide (AgRP) neurons. We used single-cell RT-PCR and wh
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Teaney, Nicole A., and Nicole E. Cyr. "Sirtuin 1 Regulates Synapsin 1 in POMC-Producing N43-5 Neurons via FOXO1." Journal of the Endocrine Society 5, Supplement_1 (2021): A56—A57. http://dx.doi.org/10.1210/jendso/bvab048.114.

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Abstract The nutrient-sensor protein Sirtuin 1 (Sirt1; silent mating type information regulation 2 homolog 1) has been shown to have significant and opposing effects on insulin resistance, leptin resistance, and body weight in the periphery and the brain. In the hypothalamic arcuate nucleus (ARC) of the brain, Sirt1 increases in the obese state and acts to promote weight gain as well as insulin and leptin resistance by increasing the orexigenic neuropeptides Agouti-related protein (AgRP) and neuropeptide Y (NPY), and in a distinct set of ARC neurons, by decreasing POMC and thus its anorexigeni
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Johnson, Miranda D., Sebastien G. Bouret, Ambrose A. Dunn-Meynell, Christina N. Boyle, Thomas A. Lutz, and Barry E. Levin. "Early postnatal amylin treatment enhances hypothalamic leptin signaling and neural development in the selectively bred diet-induced obese rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 311, no. 6 (2016): R1032—R1044. http://dx.doi.org/10.1152/ajpregu.00326.2016.

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Selectively bred diet-induced obese (DIO) rats become obese on a high-fat diet and are leptin resistant before becoming obese. Compared with diet-resistant (DR) neonates, DIO neonates have impaired leptin-dependent arcuate (ARC) neuropeptide Y/agouti-related peptide (NPY/AgRP) and α-melanocyte-stimulating hormone (α-MSH; from proopiomelanocortin (POMC) neurons) axon outgrowth to the paraventricular nucleus (PVN). Using phosphorylation of STAT3 (pSTAT3) as a surrogate, we show that reduced DIO ARC leptin signaling develops by postnatal day 7 (P7) and is reduced within POMC but not NPY/AgRP neur
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Krashes, Michael J., Bhavik P. Shah, Shuichi Koda, and Bradford B. Lowell. "Rapid versus Delayed Stimulation of Feeding by the Endogenously Released AgRP Neuron Mediators GABA, NPY, and AgRP." Cell Metabolism 18, no. 4 (2013): 588–95. http://dx.doi.org/10.1016/j.cmet.2013.09.009.

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Dissertations / Theses on the topic "NPY/AgRP neuron"

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Qu, Mengdi. "Molecular mechanism underlying CaMK1D-dependent function in AgRP neurons." Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ029.

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La perturbation des mécanismes de réponse au stress chez les organismes peut entraîner une dysfonction cellulaire et des maladies telles que le syndrome métabolique. L'équilibre énergétique est principalement régulé par le système nerveux central (SNC), qui intègre des signaux hormonaux, neuronaux et alimentaires provenant de divers tissus. Une dysfonction de ce système est liée à l'obésité et au syndrome métabolique, qui sont tous deux des précurseurs du diabète de type 2 (T2D). Notre laboratoire a découvert que la protéine kinase ID dépendante du calcium/calmoduline (CaMK1D), un gène associé
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Ramírez, Flores Sara. "Hypothalamic Ceramide Levels regulated by CPT1C mediate the Orexigenic effect of Ghrelin." Doctoral thesis, Universitat Internacional de Catalunya, 2014. http://hdl.handle.net/10803/276184.

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Recent data suggest that ghrelin exerts its orexigenic action through regulation of hypothalamic AMP-activated protein kinase pathway, leading to a decline in malonyl-CoA levels and desinhibition of carnitine palmitoyltransferase 1A (CPT1A), which increases mitochondrial fatty acid oxidation and ultimately enhances the expression of the orexigenic neuropeptides agouti-related protein (AgRP) and neuropeptide Y (NPY). However, it is unclear whether the brain-specific isoform CPT1C, which is located in the endoplasmic reticulum of neurons, may play a role in this action. Here, we demonstrate that
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Books on the topic "NPY/AgRP neuron"

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Wójcik-Gładysz, Anna. Ghrelin – hormone with many faces. Central regulation and therapy. The Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences, 2020. http://dx.doi.org/10.22358/mono_awg_2020.

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Discovered in 1999, ghrelin, is one of the peptides co-creating the hypothalamicgastrointestinal axis, otherwise known as the brain-gut axis. Ghrelin participates in many physiological processes and spectrum of its activity is still being discovered. This 28 amino acid peptide ‒ a product of the ghrl gene, was found in all vertebrates and is synthesized and secreted mainly from enteroendocrine X/A cells located in the gastric mucosa of the stomach. Expression of the ghrelin receptor has been found in many nuclei of the hypothalamus involved in appetite regulation. Therefore it’s presumed that
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Journal articles
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