2023, Número 2
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Revista Mexicana de Trastornos Alimentarios 2023; 13 (2)
La alteración hipotalámica en la obesidad: neuroinflamación y disfunción metabólica
Torres GH, Ramírez CRJ, Rodríguez CYM, Chavarría A
Idioma: Español
Referencias bibliográficas: 89
Paginas: 170-186
Archivo PDF: 340.36 Kb.
RESUMEN
La obesidad es considerada actualmente como un problema de salud pública global y se caracteriza
por la hipertrofia e hiperplasia del tejido adiposo debido a la ingesta hipercalórica y la falta de
actividad física, disfunción metabólica, inflamación sistémica crónica de bajo grado y gradualmente
neuroinflamación hipotalámica. El tejido adiposo actúa como un órgano endocrino secretando
adipocinas y citocinas que actúan como reguladores del metabolismo. Sin embargo, la presencia de
niveles elevados de ácidos grasos libres y de moléculas inflamatorias derivadas de los adipocitos,
pueden alterar la respuesta inmunitaria sistémica, generando inflamación crónica, comprometiendo
la integridad de la barrera hematoencefálica y estimulando la respuesta de la glía, especialmente en
regiones específicas del hipotálamo, centro de regulación de la homeostasis energética. Las células
gliales hipotalámicas son importantes en la transmisión de señales inflamatorias relacionadas con
la dieta, pueden modular la actividad neuronal, responder a las señales inmunológicas periféricas e
iniciar una respuesta inflamatoria local y gliosis. Esta revisión se enfoca en la descripción general de
la disfunción metabólica asociada a la obesidad y su participación en la alteración de la regulación
hipotalámica, provocando neuroinflamación y modificaciones en la conducta alimentaria.
REFERENCIAS (EN ESTE ARTÍCULO)
Artemniak-Wojtowicz, D., Kucharska, A. M., & Pyrżak, B.(2020). Obesity and chronic inflammation crosslinking.Central-European Journal of Immunology, 45(4), 461-468. Recuperado enero 6, 2023, a partir de https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7882402/
Baufeld, C., Osterloh, A., Prokop, S., Miller, K. R., &Heppner, F. L. (2016). High-fat diet-induced brain region-specific phenotypic spectrum of CNS resident microglia.Acta Neuropathologica, 132, 361-375.
Buckman, L. B., Thompson, M. M., Lippert, R. N., Blackwell,T. S., Yull, F. E., & Ellacott, K. L. J. (2015). Evidence fora novel functional role of astrocytes in the acute homeostaticresponse to high-fat diet intake in mice. Molecular Metabolism, 4(1), 58-63.
Buttini, M., Limonta, S., & Boddeke, H. W. (1996). Peripheraladministration of lipopolysaccharide induces activation ofmicroglial cells in rat brain. Neurochemistry International,29(1), 25-35.
Cintra, D. E., Ropelle, E. R., Moraes, J. C., Pauli, J. R., Morari,J., Souza, C. T. de, Grimaldi, R., et al. (2012). Unsaturatedfatty acids revert diet-induced hypothalamic inflammation inobesity. PloS One, 7(1), e30571.
Colonna, M., & Butovsky, O. (2017). Microglia Function in theCentral Nervous System During Health and Neurodegeneration.Annual Review of Immunology, 35, 441-468.
Cuspidi, C., Tadic, M., & Grassi, G. (2014). Diastolic dysfunction,blood pressure and obesity: New insights from a generalpopulation. Journal of Hypertension, 32(12), 2359-2361.
Czech, M. P. (2020). Mechanisms of insulin resistance relatedto white, beige, and brown adipocytes. Molecular Metabolism,34, 27-42.
De Souza, C. T., Araujo, E. P., Bordin, S., Ashimine, R., Zollner,R. L., Boschero, A. C., Saad, M. J. A., et al. (2005).Consumption of a fat-rich diet activates a proinflammatoryresponse and induces insulin resistance in the hypothalamus.Endocrinology, 146(10), 4192-4199.
Dhingra, R., Sullivan, L., Jacques, P. F., Wang, T. J., Fox, C.S., Meigs, J. B., D’Agostino, R. B., et al. (2007). Soft drinkconsumption and risk of developing cardiometabolic risk factorsand the metabolic syndrome in middle-aged adults in thecommunity. Circulation, 116(5), 480-488.
Dorfman, M. D., & Thaler, J. P. (2015). Hypothalamic inflammationand gliosis in obesity. Current opinion inendocrinology, diabetes, and obesity, 22(5), 325-330.
Douglass, J. D., Dorfman, M. D., Fasnacht, R., Shaffer, L. D.,& Thaler, J. P. (2017). Astrocyte IKK/NF-B signaling isrequired for diet-induced obesity and hypothalamic inflammation.Molecular Metabolism, 6(4), 366-373.
Freire-Regatillo, A., Argente-Arizón, P., Argente, J.,García-Segura, L. M., & Chowen, J. A. (2017). Non-NeuronalCells in the Hypothalamic Adaptation to MetabolicSignals. Frontiers in Endocrinology, 8, 51.
Fujihara, M., Muroi, M., Tanamoto, K., Suzuki, T., Azuma,H., & Ikeda, H. (2003). Molecular mechanisms of macrophageactivation and deactivation by lipopolysaccharide:Roles of the receptor complex. Pharmacology & Therapeutics,100(2), 171-194.
Gao, Y., Ottaway, N., Schriever, S. C., Legutko, B., García-Cáceres, C., de la Fuente, E., Mergen, C., et al. (2014).Hormones and diet, but not body weight, control hypothalamicmicroglial activity. Glia, 62(1), 17-25.
García-Bueno, B., Serrats, J., & Sawchenko, P. E. (2009).Cerebrovascular Cyclooxygenase-1 Expression, Regulation,and Role in Hypothalamic-Pituitary-Adrenal Axis Activationby Inflammatory Stimuli. The Journal of Neuroscience,29(41), 12970-12981.
García-Cáceres, C., Quarta, C., Varela, L., Gao, Y., Gruber,T., Legutko, B., Jastroch, M., et al. (2016). Astrocytic InsulinSignaling Couples Brain Glucose Uptake with NutrientAvailability. Cell, 166(4), 867-880.
Glass, C. K., Saijo, K., Winner, B., Marchetto, M. C., & Gage,F. H. (2010). Mechanisms underlying inflammation in neurodegeneration.Cell, 140(6), 918-934.
González-García, I., & García-Cáceres, C. (2021). HypothalamicAstrocytes as a Specialized and Responsive CellPopulation in Obesity. International Journal of MolecularSciences, 22(12), 6176.
Guillemot-Legris, O., & Muccioli, G. G. (2017). Obesity-InducedNeuroinflammation: Beyond the Hypothalamus.Trends in Neurosciences, 40(4), 237-253.
Gupta, S., Knight, A. G., Gupta, S., Keller, J. N., & Bruce-Keller, A. J. (2012). Saturated Long Chain Fatty acidsActivate Inflammatory Signaling in Astrocytes. Journal ofNeurochemistry, 120(6), 1060-1071. Recuperado enero6, 2023, a partir de https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3296820/
van der Heijden, R. A., Sheedfar, F., Morrison, M. C., Hommelberg,P. P. H., Kor, D., Kloosterhuis, N. J., Gruben,N., et al. (2015). High-fat diet induced obesity primes inflammationin adipose tissue prior to liver in C57BL/6j mice.Aging, 7(4), 256-268.
Holland, W. L., Bikman, B. T., Wang, L.-P., Yuguang, G.,Sargent, K. M., Bulchand, S., Knotts, T. A., et al. (2011).Lipid-induced insulin resistance mediated by the proinflammatoryreceptor TLR4 requires saturated fatty acid-inducedceramide biosynthesis in mice. The Journal of Clinical Investigation,121(5), 1858-1870.
Hotamisligil, G. S. (2006). Inflammation and metabolic disorders.Nature, 444(7121), 860-867. Nature PublishingGroup.
Huang, S., Rutkowsky, J. M., Snodgrass, R. G., Ono-Moore,K. D., Schneider, D. A., Newman, J. W., Adams, S. H.,et al. (2012). Saturated fatty acids activate TLR-mediatedproinflammatory signaling pathways. Journal of Lipid Research,53(9), 2002-2013.
Hyvärinen, T., Hagman, S., Ristola, M., Sukki, L., Veijula,K., Kreutzer, J., Kallio, P., et al. (2019). Co-stimulationwith IL-1 and TNF- induces an inflammatory reactiveastrocyte phenotype with neurosupportive characteristicsin a human pluripotent stem cell model system. ScientificReports, 9(1), 16944. Nature Publishing Group. Recuperadoenero 6, 2023, a partir de https://www.nature.com/articles/s41598-019-53414-9
Jäkel, S., & Dimou, L. (2017). Glial Cells and Their Function inthe Adult Brain: A Journey through the History of Their Ablation.Frontiers in Cellular Neuroscience, 11, 24.
Jessen, K. R. (2004). Glial cells. The International Journal ofBiochemistry & Cell Biology, 36(10), 1861-1867.
Jurga, A. M., Paleczna, M., & Kuter, K. Z. (2020). Overview ofGeneral and Discriminating Markers of Differential MicrogliaPhenotypes. Frontiers in Cellular Neuroscience, 14.Recuperado agosto 18, 2022, a partir de https://www.frontiersin.org/articles/10.3389/fncel.2020.00198.
Kasim-Karakas, S. E., Tsodikov, A., Singh, U., & Jialal,I. (2006). Responses of inflammatory markers to a lowfat,high-carbohydrate diet: Effects of energy intake. TheAmerican Journal of Clinical Nutrition, 83(4), 774-779. Recuperado enero 5, 2023, a partir de https://doi.org/10.1093/ajcn/83.4.774.
Kawai, T., Autieri, M. V., & Scalia, R. (2021). Adipose tissueinflammation and metabolic dysfunction in obesity. AmericanJournal of Physiology. Cell Physiology, 320(3),C375-C391.
Kigerl, K. A., de Rivero Vaccari, J. P., Dietrich, W. D., Popovich,P. G., & Keane, R. W. (2014). Pattern recognitionreceptors and central nervous system repair. ExperimentalNeurology, 258, 5-16.
Kim, D. W., Glendining, K. A., Grattan, D. R., & Jasoni, C.L. (2016). Maternal Obesity in the Mouse Compromises theBlood-Brain Barrier in the Arcuate Nucleus of Offspring. Endocrinology,157(6), 2229-2242.
Lawson, L. J., Perry, V. H., & Gordon, S. (1992). Turnover ofresident microglia in the normal adult mouse brain. Neuroscience,48(2), 405-415.
Liddelow, S. A., Guttenplan, K. A., Clarke, L. E., Bennett,F. C., Bohlen, C. J., Schirmer, L., Bennett, M. L., et al.(2017). Neurotoxic reactive astrocytes are induced by activatedmicroglia. Nature, 541(7638), 481-487.
Liu, L.-R., Liu, J.-C., Bao, J.-S., Bai, Q.-Q., & Wang, G.-Q.(2020). Interaction of Microglia and Astrocytes in the NeurovascularUnit. Frontiers in Immunology, 11, 1024.
Lumeng, C. N., Bodzin, J. L., & Saltiel, A. R. (2007). Obesityinduces a phenotypic switch in adipose tissue macrophage polarization.The Journal of Clinical Investigation, 117(1),175-184.
Lumeng, C. N., & Saltiel, A. R. (2011). Inflammatory linksbetween obesity and metabolic disease. The Journal of ClinicalInvestigation, 121(6), 2111-2117. American Societyfor Clinical Investigation.
Maldonado-Ruiz, R., Montalvo-Martínez, L., Fuentes-Mera, L., & Camacho, A. (2017). Microglia activationdue to obesity programs metabolic failure leading to type twodiabetes. Nutrition & Diabetes, 7(3), e254-e254. NaturePublishing Group. Recuperado enero 6, 2023, a partirde https://www.nature.com/articles/nutd201710
Marques, B. G., Hausman, D. B., & Martin, R. J. (1998).Association of fat cell size and paracrine growth factors indevelopment of hyperplastic obesity. American Journal ofPhysiology-Regulatory, Integrative and ComparativePhysiology, 275(6), R1898-R1908. American PhysiologicalSociety. Recuperado diciembre 20, 2022, apartir de https://journals.physiology.org/doi/full/10.1152/ajpregu.1998.275.6.R1898
Milanski, M., Degasperi, G., Coope, A., Morari, J., Denis, R.,Cintra, D. E., Tsukumo, D. M. L., et al. (2009). Saturatedfatty acids produce an inflammatory response predominantlythrough the activation of TLR4 signaling in hypothalamus:Implications for the pathogenesis of obesity. The Journal ofNeuroscience: The Official Journal of the Society forNeuroscience, 29(2), 359-370.
Mills, C. D. (2012). M1 and M2 Macrophages: Oracles of Healthand Disease. Critical Reviews in Immunology, 32(6),463-488.
Morari, J., Anhe, G. F., Nascimento, L. F., de Moura, R.F., Razolli, D., Solon, C., Guadagnini, D., et al. (2014).Fractalkine (CX3CL1) is involved in the early activation ofhypothalamic inflammation in experimental obesity. Diabetes,63(11), 3770-3784.
Moreno-Navarrete, J. M., Blasco, G., Puig, J., Biarnés, C.,Rivero, M., Gich, J., Fernández-Aranda, F., et al. (2017).Neuroinflammation in obesity: Circulating lipopolysaccharide-binding protein associates with brain structure andcognitive performance. International Journal of Obesity,41(11), 1627-1635. Nature Publishing Group. Recuperadoagosto 20, 2022, a partir de https://www.nature.com/articles/ijo2017162
Morton, G. J., Meek, T. H., & Schwartz, M. W. (2014). Neurobiologyof food intake in health and disease. Nature Reviews.Neuroscience, 15(6), 367-378.
Ndisang, J. F., Vannacci, A., & Rastogi, S. (2014). Oxidativestress and inflammation in obesity, diabetes, hypertension,and related cardiometabolic complications. Oxidative Medicineand Cellular Longevity, 2014, 506948.
Nishimura, S., Manabe, I., & Nagai, R. (2009). Adipose tissueinflammation in obesity and metabolic syndrome. DiscoveryMedicine, 8(41), 55-60.
Panee, J. (2012). Monocyte Chemoattractant Protein 1 (MCP-1)in Obesity and Diabetes. Cytokine, 60(1), 1-12. Recuperadodiciembre 20, 2022, a partir de https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3437929/
Posey, K. A., Clegg, D. J., Printz, R. L., Byun, J., Morton, G.J., Vivekanandan-Giri, A., Pennathur, S., et al. (2009).Hypothalamic proinflammatory lipid accumulation, inflammation,and insulin resistance in rats fed a high-fat diet.American Journal of Physiology. Endocrinology andMetabolism, 296(5), E1003-1012.
Ransohoff, R. M., & Cardona, A. E. (2010). The myeloid cells ofthe central nervous system parenchyma. Nature, 468(7321),253-262.
Reilly, S. M., & Saltiel, A. R. (2017). Adapting to obesity withadipose tissue inflammation. Nature Reviews. Endocrinology,13(11), 633-643.
Rodríguez, E. M., Blázquez, J. L., & Guerra, M. (2010). Thedesign of barriers in the hypothalamus allows the median eminenceand the arcuate nucleus to enjoy private milieus: Theformer opens to the portal blood and the latter to the cerebrospinalfluid. Peptides, 31(4), 757-776.
Schenk, S., Saberi, M., & Olefsky, J. M. (2008). Insulin sensitivity:Modulation by nutrients and inflammation. TheJournal of Clinical Investigation, 118(9), 2992-3002.
Secretaría de Salud, Instituto Nacional de Salud Pública,& Instituto Nacional de Estadística y Geografía.(2019). Encuesta Nacional de Salud y Nutrición México 2018| CODAJIC. Encuesta Nacional de Salud y Nutrición.Recuperado agosto 11, 2022, a partir de http://www.codajic.org/node/4182.
Seong, J., Kang, J. Y., Sun, J. S., & Kim, K. W. (2019). Hypothalamicinflammation and obesity: A mechanistic review.Archives of Pharmacal Research, 42(5), 383-392.
Shapouri-Moghaddam, A., Mohammadian, S., Vazini, H.,Taghadosi, M., Esmaeili, S.-A., Mardani, F., Seifi, B.,et al. (2018). Macrophage plasticity, polarization, and functionin health and disease. Journal of Cellular Physiology,233(9), 6425-6440.
Shoelson, S. E., Lee, J., & Goldfine, A. B. (2006). Inflammationand insulin resistance. Journal of Clinical Investigation,116(7), 1793-1801.
Sopasakis, V. R., Sandqvist, M., Gustafson, B., Hammarstedt,A., Schmelz, M., Yang, X., Jansson,P.-A., et al. (2004). High local concentrations and effects ondifferentiation implicate interleukin-6 as a paracrine regulator.Obesity Research, 12(3), 454-460.
Sorrells, S. F., Caso, J. R., Munhoz, C. D., & Sapolsky, R. M.(2009). The stressed CNS: When glucocorticoids aggravateinflammation. Neuron, 64(1), 33-39.
Sorrells, S. F., Munhoz, C. D., Manley, N. C., Yen, S., &Sapolsky, R. M. (2014). Glucocorticoids increase excitotoxicinjury and inflammation in the hippocampus of adult malerats. Neuroendocrinology, 100(2-3), 129-140.
Sousa, C., Golebiewska, A., Poovathingal, S. K., Kaoma, T.,Pires-Afonso, Y., Martina, S., Coowar, D., et al. (2018).Single-cell transcriptomics reveals distinct inflammation-inducedmicroglia signatures. EMBO reports, 19(11), e46171.
Spalding, K. L., Arner, E., Westermark, P. O., Bernard, S.,Buchholz, B. A., Bergmann, O., Blomqvist, L., et al.(2008). Dynamics of fat cell turnover in humans. Nature,453(7196), 783-787. Nature Publishing Group. Recuperadodiciembre 20, 2022, a partir de https://www.nature.com/articles/nature06902
Stenkula, K. G., & Erlanson-Albertsson, C. (2018). Adiposecell size: Importance in health and disease. AmericanJournal of Physiology. Regulatory, Integrative andComparative Physiology, 315(2), R284-R295.
Stolarczyk, E. (2017). Adipose tissue inflammation in obesity: Ametabolic or immune response? Current Opinion in Pharmacology,37, 35-40.
Stranahan, A. M., Hao, S., Dey, A., Yu, X., & Baban, B. (2016).Blood-brain barrier breakdown promotes macrophage infiltrationand cognitive impairment in leptin receptor-deficientmice. Journal of Cerebral Blood Flow and Metabolism:Official Journal of the International Society of CerebralBlood Flow and Metabolism, 36(12), 2108-2121.
Sun, K., Kusminski, C. M., & Scherer, P. E. (2011). Adiposetissue remodeling and obesity. The Journal of Clinical Investigation,121(6), 2094-2101.
Swierczynska, M. M., Mateska, I., Peitzsch, M., Bornstein,S. R., Chavakis, T., Eisenhofer, G., Lamounier-Zepter,V., et al. (2015). Changes in morphology and function ofadrenal cortex in mice fed a high-fat diet. InternationalJournal of Obesity (2005), 39(2), 321-330.
Tang, C.-H., Lu, D.-Y., Yang, R.-S., Tsai, H.-Y., Kao, M.-C.,Fu, W.-M., & Chen, Y.-F. (2007). Leptin-Induced IL-6Production Is Mediated by Leptin Receptor, Insulin ReceptorSubstrate-1, Phosphatidylinositol 3-Kinase, Akt, NF-B, andp300 Pathway in Microglia. The Journal of Immunology,179(2), 1292-1302. Recuperado enero 6, 2023, a partir dehttps://doi.org/10.4049/jimmunol.179.2.1292
Tarassishin, L., Suh, H.-S., & Lee, S. C. (2014). LPS and IL-1differentially activate mouse and human astrocytes: Roleof CD14. Glia, 62(6), 999-1013. John Wiley & Sons, Ltd.Recuperado enero 6, 2023, a partir de https://onlinelibrary.wiley.com/doi/10.1002/glia.22657.
Thaler, J. P., Yi, C.-X., Schur, E. A., Guyenet, S. J., Hwang, B.H., Dietrich, M. O., Zhao, X., et al. (2012). Obesity is associatedwith hypothalamic injury in rodents and humans. TheJournal of Clinical Investigation, 122(1), 153-162.
Uriarte Huarte, O., Richart, L., Mittelbronn, M., & Michelucci,A. (2021). Microglia in Health and Disease: The Strengthto Be Diverse and Reactive. Frontiers in Cellular Neuroscience,15. Recuperado agosto 19, 2022, a partir de https://www.frontiersin.org/articles/10.3389/fncel.2021.660523
Valdearcos, M., Douglass, J. D., Robblee, M. M., Dorfman,M. D., Stifler, D. R., Bennett, M. L., Gerritse, I., et al.(2017). Microglial Inflammatory Signaling Orchestratesthe Hypothalamic Immune Response to Dietary Excess andMediates Obesity Susceptibility. Cell Metabolism, 26(1),185-197.e3.
Valdearcos, M., Robblee, M. M., Benjamin, D. I., Nomura,D. K., Xu, A. W., & Koliwad, S. K. (2014). Microglia dictatethe impact of saturated fat consumption on hypothalamicinflammation and neuronal function. Cell Reports, 9(6),2124-2138.
Varela, L., Stutz, B., Song, J. E., Kim, J. G., Liu, Z.-W., Gao,X.-B., & Horvath, T. L. (2021). Hunger-promoting AgRPneurons trigger an astrocyte-mediated feed-forward autoactivationloop in mice. The Journal of Clinical Investigation,131(10), 144239.
Vasile, F., Dossi, E., & Rouach, N. (2017). Human astrocytes:Structure and functions in the healthy brain. Brain Structure& Function, 222(5), 2017-2029.
Vessby, B. (2003). Dietary fat, fatty acid composition in plasmaand the metabolic syndrome. Current Opinion in Lipidology,14(1), 15-19.
Villarroya, F., Cereijo, R., Gavaldà-Navarro, A., Villarroya,J., & Giralt, M. (2018). Inflammation of brown/beige adiposetissues in obesity and metabolic disease. Journal ofInternal Medicine, 284(5), 492-504.
Vinuesa, A., Bentivegna, M., Calfa, G., Filipello, F., Pomilio,C., Bonaventura, M. M., Lux-Lantos, V., et al. (2019).Early Exposure to a High-Fat Diet Impacts on HippocampalPlasticity: Implication of Microglia-Derived Exosome-likeExtracellular Vesicles. Molecular Neurobiology, 56(7),5075-5094.
Wang, T., & He, C. (2018). Pro-inflammatory cytokines: Thelink between obesity and osteoarthritis. Cytokine & GrowthFactor Reviews, 44, 38-50. Recuperado diciembre 20,2022, a partir de https://www.sciencedirect.com/science/article/pii/S1359610118301199
Wang, Z., Liu, D., Wang, F., Liu, S., Zhao, S., Ling, E.-A., &Hao, A. (2012). Saturated fatty acids activate microglia viaToll-like receptor 4/NF-B signalling. The British Journalof Nutrition, 107(2), 229-241.
Wärnberg, J., Moreno, L. A., Mesana, M. I., Marcos, A., &AVENA group. (2004). Inflammatory mediators in overweightand obese Spanish adolescents. The AVENA Study.International Journal of Obesity and Related MetabolicDisorders: Journal of the International Association forthe Study of Obesity, 28 Suppl 3, S59-63.
Waterson, M. J., & Horvath, T. L. (2015). Neuronal Regulationof Energy Homeostasis: Beyond the Hypothalamus and Feeding.Cell Metabolism, 22(6), 962-970.
Weisberg, S. P., McCann, D., Desai, M., Rosenbaum, M.,Leibel, R. L., & Ferrante, A. W. (2003). Obesity is associatedwith macrophage accumulation in adipose tissue. Journalof Clinical Investigation, 112(12), 1796-1808.
Wendeln, A.-C., Degenhardt, K., Kaurani, L., Gertig, M.,Ulas, T., Jain, G., Wagner, J., et al. (2018). Innate immunememory in the brain shapes neurological disease hallmarks.Nature, 556(7701), 332-338. Nature Publishing Group.Recuperado enero 6, 2023, a partir de https://www.nature.com/articles/s41586-018-0023-4
World Health Organization. (2022). Controlling the globalobesity epidemic. Nutrition and Food Safety. Organization, .Recuperado a partir de https://www.who.int/activities/controlling-the-global-obesity-epidemic
Wu, H., & Ballantyne, C. M. (2020). Metabolic Inflammationand Insulin Resistance in Obesity. Circulation Research,126(11), 1549-1564.
Xu, S., Lu, J., Shao, A., Zhang, J. H., & Zhang, J. (2020). GlialCells: Role of the Immune Response in Ischemic Stroke. Frontiersin Immunology, 11, 294.
Yang, L., Qi, Y., & Yang, Y. (2015). Astrocytes control food intakeby inhibiting AGRP neuron activity via adenosine A1 receptors.Cell Reports, 11(5), 798-807.
Zhang, Y., Reichel, J. M., Han, C., Zuniga-Hertz, J. P., & Cai,D. (2017). Astrocytic Process Plasticity and IKK/NF-B inCentral Control of Blood Glucose, Blood Pressure, and BodyWeight. Cell Metabolism, 25(5), 1091-1102.e4.