Literatura científica selecionada sobre o tema "Neurones NPY/AgRP"
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Artigos de revistas sobre o assunto "Neurones NPY/AgRP"
Williams, Gareth, Joanne A. Harrold e David J. Cutler. "The hypothalamus and the regulation of energy homeostasis: lifting the lid on a black box". Proceedings of the Nutrition Society 59, n.º 3 (agosto de 2000): 385–96. http://dx.doi.org/10.1017/s0029665100000434.
Texto completo da fonteDenis, R. G. P., C. Bing, S. Brocklehurst, J. A. Harrold, R. G. Vernon e G. Williams. "Diurnal changes in hypothalamic neuropeptide and SOCS-3 expression: effects of lactation and relationship with serum leptin and food intake". Journal of Endocrinology 183, n.º 1 (outubro de 2004): 173–81. http://dx.doi.org/10.1677/joe.1.05659.
Texto completo da fonteJoly, A., R. Denis, J. Castel, R. Palmiter, C. Magnan e S. Luquet. "O35 Rôle des Neurones NPY/AgRP dans le contrôle de la balance énergétique". Diabetes & Metabolism 36 (março de 2010): A10. http://dx.doi.org/10.1016/s1262-3636(10)70039-2.
Texto completo da fonteJoly, A., R. Denis, J. Castel, C. Cansell, C. Magnan e S. Luquet. "035 Implication des neurones NPY/AgRP dans le contrôle de la partition des flux énergétiques en périphérie". Diabetes & Metabolism 37, n.º 1 (março de 2011): A9. http://dx.doi.org/10.1016/s1262-3636(11)70523-7.
Texto completo da fonteFeng, Bing, Frank Greenway, Jerney Harms, Hesong Liu, Chunmei Wang, Pingwen Xu e Yanlin He. "OR23-3 Hunger Hormone Asprosin Activates Orexigenic Neurons via SK Currents". Journal of the Endocrine Society 6, Supplement_1 (1 de novembro de 2022): A19. http://dx.doi.org/10.1210/jendso/bvac150.039.
Texto completo da fonteOh, Youjin, Eun-Seon Yoo, Sang Hyeon Ju, Eunha Kim, Seulgi Lee, Seyun Kim, Kevin Wickman e Jong-Woo Sohn. "GIRK2 potassium channels expressed by the AgRP neurons decrease adiposity and body weight in mice". PLOS Biology 21, n.º 8 (18 de agosto de 2023): e3002252. http://dx.doi.org/10.1371/journal.pbio.3002252.
Texto completo da fonteGoldstone, Anthony P., Unga A. Unmehopa, Stephen R. Bloom e Dick F. Swaab. "Hypothalamic NPY and Agouti-Related Protein Are Increased in Human Illness But Not in Prader-Willi Syndrome and Other Obese Subjects". Journal of Clinical Endocrinology & Metabolism 87, n.º 2 (1 de fevereiro de 2002): 927–37. http://dx.doi.org/10.1210/jcem.87.2.8230.
Texto completo da fonteBugarith, Kishor, Thu T. Dinh, Ai-Jun Li, Robert C. Speth e Sue Ritter. "Basomedial Hypothalamic Injections of Neuropeptide Y Conjugated to Saporin Selectively Disrupt Hypothalamic Controls of Food Intake". Endocrinology 146, n.º 3 (1 de março de 2005): 1179–91. http://dx.doi.org/10.1210/en.2004-1166.
Texto completo da fonteFraley, G. S., e S. Ritter. "Immunolesion of Norepinephrine and Epinephrine Afferents to Medial Hypothalamus Alters Basal and 2-Deoxy-d-Glucose-Induced Neuropeptide Y and Agouti Gene-Related Protein Messenger Ribonucleic Acid Expression in the Arcuate Nucleus". Endocrinology 144, n.º 1 (1 de janeiro de 2003): 75–83. http://dx.doi.org/10.1210/en.2002-220659.
Texto completo da fontePhillips, Colin T., e Richard D. Palmiter. "Role of Agouti-Related Protein-Expressing Neurons in Lactation". Endocrinology 149, n.º 2 (1 de novembro de 2007): 544–50. http://dx.doi.org/10.1210/en.2007-1153.
Texto completo da fonteTeses / dissertações sobre o assunto "Neurones NPY/AgRP"
Qu, Mengdi. "Molecular mechanism underlying CaMK1D-dependent function in AgRP neurons". Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ029.
Texto completo da fonteDisruption of stress response mechanisms in organisms can lead to cellular dysfunction and diseases like metabolic syndrome. Energy balance is mainly regulated by the central nervous system (CNS), which integrates hormonal, neuronal, and dietary signals from various tissues. Dysfunction in this system is linked to obesity and metabolic syndrome, both precursors to type 2 diabetes (T2D). Our laboratory discovered that calcium/calmodulin-dependent protein kinase ID (CaMK1D), a gene associated with T2D, promotes ghrelin-mediated food intake in mice. However, CaMK1D signaling in NPY/AgRP neurons still remains questions. In this work, we proformed RNA sequencing using the GT1-7 hypothalamic cell line. To this end, we found that CalHM6 is a downstream target of CaMK1D signaling. CalHM6 mRNA levels were significantly upregulated in CaMK1D-/- cells and downregulated when CaMK1D was re-expressed. This was confirmed in vivo in the hypothalamus of CaMK1D-/- mice. CalHM6, likely a voltage-gated calcium channel, showed increased intracellular Ca2+ levels in response to ghrelin in CaMK1D-/- cells compared to CaMK1D+/+ cells using jGCamps method. Altogether, our work showed CalHM6 is a novel target of CaMK1D. High CaMK1D, leading to low CalHM6 expression, may enhance food intake and obesity by modulating calcium-dependent signaling in NPY/AgRP neuron
Joly, Aurélie. "Rôle du système nerveux dans le développement du syndrôme métabolique : étude de l'effet du glucose portal sur la sensibilité à l'insuline chez le rat : implication des neurones NPY/AgRP dans le contrôle de la balance énergétique chez la souris". Paris 7, 2011. http://www.theses.fr/2011PA077091.
Texto completo da fonteSeveral neuronal populations are involved in the regulation of energy balance. Among these, the hypothalamic agouti-related protein neurons (AgRP-neurons) are well characterized for their ability to promote food intake. Using cell-specific ablation we investigated a possible role of AgRP neurons in nutrient partitioning independent from food intake. We show that mice lacking AgRP neuron developed a non-hyperphagic obesity due to increased feed efficiency (weight gain/kcal consumed) on regular chow. At a time that preceded obesity catecholamine turnover rate was selectively decreased in the pancreas, liver, and glycolytic muscle, while it was increased in oxidative muscle. Respiratory quotient measurements revealed a change in substrate utilization towards lipid oxidation enhanced by synergistic increase in liver triglyceride synthesis and lipid substrate preference in oxidative muscle mitochondria. On high fat diet, mice lacking AgRP neurons displayed reduced body weight gain and paradoxical improvement in glucose tolerance. Finally we evidenced that Gamma Aminobutyric Acid (GABA) made by AgRP neurons is important in the central control of peripheral substrate utilization. This study reveals a new function for AgRP neurons in the coordination, via the sympathetic nervous System, of inter-organs communication and nutrient partitioning. These results offer a new conceptual framework for the understanding of obesity-related disorders
Livros sobre o assunto "Neurones NPY/AgRP"
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.
Texto completo da fonte