Academic literature on the topic 'Leptin signaling'
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Journal articles on the topic "Leptin signaling"
Panić, Anastasija, Sanja Soskić, and Esma Isenović. "Leptin and its mechanism of action." Medicinska istrazivanja 49, no. 3 (2015): 36–41. http://dx.doi.org/10.5937/medist1502036p.
Full textAhima, Rexford S., and Suzette Y. Osei. "Leptin signaling." Physiology & Behavior 81, no. 2 (April 2004): 223–41. http://dx.doi.org/10.1016/j.physbeh.2004.02.014.
Full textZhou, Yingjiang, and Liangyou Rui. "Leptin signaling and leptin resistance." Frontiers of Medicine 7, no. 2 (April 12, 2013): 207–22. http://dx.doi.org/10.1007/s11684-013-0263-5.
Full textWauman, Joris. "Leptin receptor signaling: pathways to leptin resistance." Frontiers in Bioscience 16, no. 1 (2011): 2771. http://dx.doi.org/10.2741/3885.
Full textYang, Ronghua, and Lili A. Barouch. "Leptin Signaling and Obesity." Circulation Research 101, no. 6 (September 14, 2007): 545–59. http://dx.doi.org/10.1161/circresaha.107.156596.
Full textFoley, J. F. "ROCK Mediates Leptin Signaling." Science Signaling 5, no. 244 (October 2, 2012): ec254-ec254. http://dx.doi.org/10.1126/scisignal.2003656.
Full textTian, Hai-feng, Qiao-mu Hu, Yan Meng, and Han-bing Xiao. "Molecular cloning, characterization and evolutionary analysis of leptin gene in Chinese giant salamander, Andrias davidianus." Open Life Sciences 12, no. 1 (November 23, 2017): 406–17. http://dx.doi.org/10.1515/biol-2017-0048.
Full textSaranac, Ljiljana, Bojko Bjelakovic, Hristina Stamenkovic, and Borislav Kamenov. "Orexitropic Signaling Proteins in Obese Children." Scientific World JOURNAL 7 (2007): 1263–71. http://dx.doi.org/10.1100/tsw.2007.218.
Full textMetlakunta, Anantha S., Maitrayee Sahu, Hideo Yasukawa, Sandeep S. Dhillon, Denise D. Belsham, Akihiko Yoshimura, and Abhiram Sahu. "Neuronal suppressor of cytokine signaling-3 deficiency enhances hypothalamic leptin-dependent phosphatidylinositol 3-kinase signaling." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 300, no. 5 (May 2011): R1185—R1193. http://dx.doi.org/10.1152/ajpregu.00794.2010.
Full textGroba, Claudia, Steffen Mayerl, Alies A. van Mullem, Theo J. Visser, Veerle M. Darras, Andreas J. Habenicht, and Heike Heuer. "Hypothyroidism Compromises Hypothalamic Leptin Signaling in Mice." Molecular Endocrinology 27, no. 4 (April 1, 2013): 586–97. http://dx.doi.org/10.1210/me.2012-1311.
Full textDissertations / Theses on the topic "Leptin signaling"
Buo, Carrie L. "ON LEPTIN AND LEARNING: INVESTIGATING THE INTERACTION OF LEPTINA SIGNALING AND LEARNING IN ZEBRAFISH." University of Akron / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=akron162428966535721.
Full textVauthier, Virginie. "Etude des Endospanines, une nouvelle famille de protéines régulatrices des fonctions du récepteur de la leptine." Thesis, Paris 11, 2011. http://www.theses.fr/2011PA11T097.
Full textObesity is one of the greatest current public health challenges, not only in industrialized countries but also in developing countries. The hypothalamic arcuate nucleus (ARC) is a major integration centre for energy and glucose homeostasis that responds to peripheral hormones such as leptin. Resistance to leptin in the ARC is an important component of obesity development and its prevention or reversal represents a major therapeutic goal. Our laboratory recently described endospanin 1 as a negative regulator of the leptin receptor (OB-R) that by interacting with OB-R retains the receptor inside the cell. Interestingly, both proteins are expressed from the same promoter. Silencing of endospanin 1 in the ARC prevented the development of diet-induced obesity demonstrating the importance of this protein on OB-R in vivo function.Based on these encouraging findings the first aim of this thesis was to extend our understanding of the in vitro and in vivo role of endospanin 1 and its homologue, endospanin 2, on OB-R function. The second aim consisted in the identification of chemical compounds able to sensitize the leptin response in obese patients. We show here that endospanin 1 is up-regulated in the ARC of obese mice suggesting a potential contribution of this protein to the development of leptin resistance. Its silencing in the ARC of naïve and obese mice reverses obesity development and impairs pancreatic insulin secretion. This dual effect correlates with the differential effect of endospanin 1 on OB-R signaling, inhibition of the STAT3 pathway and activation of the AKT pathway. Intriguingly, endospanin 2, the second member of the endospanin family, promotes efficient STAT3 activation suggesting differential roles of both endospanins on OB-R function.We characterized an obese patient carrying a homozygous deletion in the chromosomal 1p31.3 region coding for endospanin 1. This is the first report defining the consequences of endospanin 1-deficiency in humans. Our data suggest that endospanin 1 has no major OB-R-independent functions thus defining endospanin 1 as an attractive and highly specific therapeutic target for the improvement of impaired leptin signaling.In the last part of the thesis two screening assays were developed to identify compounds that either activate OB-R or promote its cell surface expression. Primary screens were successfully performed for both assays and positive hits identified. Validated hits might be useful to resensitize the impaired leptin response in obese patients
Dupuis, Lisa. "Molecular mechanisms of leptin receptor signaling in ovarian granulosa cells." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114600.
Full textLes écarts extrêmes de poids par rapport à ce qui est considéré comme un poids normal, telles que l'anorexie et l'obésité, sont liées à des problèmes de la fonction reproductrice chez la femme. Découverte en 1994, la leptine est une hormone sécrétée par le tissu adipeux dans le but d'informer l'hypothalamus sur l'état de satiété de l'organisme. La libération de leptine est directement proportionnelle à la quantité de tissu adipeux et la présence de l'hormone et de son récepteur (Lepr) a été montrée dans différents tissus incluant les cellules de la granulosa des ovaires. Par conséquent, la leptine, via son récepteur, joue un rôle dans la fonction reproductrice de la femme. De nombreuses études ont étudié les effets de Lepr dans les cellules de la granulosa et dans l'ovaire, mais elles ont toutes été réalisées in vitro et les résultats sont contradictoires. Nous présentons ici la première étude in vivo dans le but d'examiner le rôle de Lepr dans les cellules de la granulosa pendant le développement folliculaire et l'ovulation. Des souris immature produisant un grand nombre d'ovocytes ont été utilisées dans toutes nos expériences et les cellules de la granulosa ont été collectées par ponction folliculaire. Les profils d'expression des isoformes de Lepr (LeprA et LeprB) durant les développements folliculaire et lutéal ont été d'abord déterminés, ainsi que ceux des molécules de la voie de signalisation de la leptine et leurs cibles. Les facteurs de transcription régulant potentiellement l'expression de Lepr dans les cellules de la granulosa ont aussi été analysés. Pour évaluer la réponse des cellules de la granulosa à la leptine in vivo, l'hormone leptine a été administrée à différents moments des développements folliculaire et lutéal. Enfin, le récepteur Lepr a été bloqué grâce à l'utilisation d'un antagoniste de Lepr (SMLA) et les effets de ce blocage sur l'ovulation ont été analysés. L'expression de LeprA et LeprB ont augmenté 4h après administration d'hCG, LeprA étant l'isoforme la plus abondante et présentant une expression 23 fois plus importante de 0 à 4h post-hCG. L'expression de la leptine a augmenté durant le même temps ainsi que celle des molécules de la voie de signalisation de Lepr, Stat3 et Socs3, juste après l'induction de Lepr, respectivement 7h et 12h post-hCG. Cebpb, qui a été induit 1h post-hCG, a été identifié comme étant associé au promoteur de Lepr et donc comme étant un régulateur de l'expression de Lepr. Les données concernant la protéine Egr1 et ses ARNm suggèrent qu'il peut s'agir d'un autre potentiel facteur de transcription régulant l'expression de Lepr, notamment en raison d'une augmentation de son expression 1h post-hCG, juste avant l'augmentation de l'expression de Lepr. Les profils d'ARNm des gènes examinés ont donc fourni la preuve du rôle de Lepr durant la période périovulatoire. Ceci a été ensuite confirmé par l'augmentation de la réponse des cellules de la granulosa in vivo suite à une dose physiologique de leptine 6h post-hCG , mise en évidence par la phosphorylation des protéines Mapk et Stat3. Le traitement avec la leptine a aussi accru l'expression des gènes impliqués dans l'ovulation Adamts1, Pdcd1 et Egr1. Le blocage de l'action de Lepr a réduit le taux d'ovulation de 60% chez les animaux traités avec SMLA. Cette réduction apparaît être due, au moins en partie, à la dérégulation de l'expression des gènes de Adamts10, Adamts19, Has2, Areg, Ptx3, et Foxo1. En conclusion, les résultats de cette étude éclairent les mécanismes moléculaires de l'induction du récepteur Lepr ainsi que de la voie de signalisation qui lui est associée dans les cellules de la granulosa. Pour finir, cette étude fournit des preuves concernant le rôle positif joué par la leptine et Lepr durant l'ovulation, ce qui est essentiel pour optimiser la fertilité de la femme.
Ramirez, Oscar. "Implication for the role leptin-induced signaling as a negative regulator of dendritic cell function." To access this resource online via ProQuest Dissertations and Theses @ UTEP, 2009. http://0-proquest.umi.com.lib.utep.edu/login?COPT=REJTPTU0YmImSU5UPTAmVkVSPTI=&clientId=2515.
Full textVaughan, Tamisha Y. "Novel Mechanisms Underlying the Inflammatory Effects of Leptin and Low Dose Endotoxin." Diss., Virginia Tech, 2010. http://hdl.handle.net/10919/28013.
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Dalman, Mark R. "Characterization of Leptin Signaling in the Developing Zebrafish (Danio rerio) Using Molecular, Physiological, and Bioinformatic Approaches." University of Akron / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=akron1418039468.
Full textKuri, Rodríguez Paola Sofía [Verfasser], and Maria [Akademischer Betreuer] Leptin. "Teleost fish models for the in vivo study of inflammasome signaling / Paola Sofía Kuri Rodríguez ; Betreuer: Maria Leptin." Heidelberg : Universitätsbibliothek Heidelberg, 2017. http://d-nb.info/1178008215/34.
Full textSchumacher, Michael Andrew. "Placental Signaling Mechanisms Linking Maternal Obesity, High-Fat Diet, and Adiponectin Levels During Pregnancy to Fetal Overgrowth." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1243013168.
Full textFaßhauer, Martin [Verfasser], Christoph [Akademischer Betreuer] Buettner, Dirk [Akademischer Betreuer] Raddatz, and Blanche [Akademischer Betreuer] Schwappach. "The role of leptin and insulin signaling in the hypothalamic control of liver metabolism / Martin Faßhauer. Gutachter: Dirk Raddatz ; Blanche Schwappach. Betreuer: Christoph Buettner." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2013. http://d-nb.info/1044870028/34.
Full textRonveaux, Charlotte. "Mécanisme des hormones anorexigènes régulant la prise alimentaire au niveau du nerf vague." Thesis, Paris, AgroParisTech, 2015. http://www.theses.fr/2015AGPT0002/document.
Full textAs the initial interface for nutrient sensing, digestion and absorption, the gastrointestinal (GI) tract plays a critical role in the regulation of energy homeostasis. Information that arises from the GI tract is key to normal physiological responses controlling gut function and regulating food intake. Vagal afferent neurons (VAN) are a major pathway by which information about ingested nutrients reaches the central nervous system to influence GI function and food intake behavior. VAN express receptors for many of the regulatory peptides released from the gut that are involved in regulation of food intake and body weight. This dissertation addresses the role of two gut peptides, leptin and glucagon-like peptide-1, acting at the level of VAN, to inhibit food intake. First, the mechanism of action of glucagon-like peptide-1 (GLP-1) on VAN is addressed. GLP-1-induced satiation requires a postprandial state; the data support that feeding changes the localization of GLP-1Rs from the cytoplasm to the neuronal cell membrane. Further, ghrelin and its receptor GHSR1 expressed by VAN is involved in regulating GLP-1 receptor translocation. Second, the importance of leptin receptor expression by VAN in the development of hyperphagia and obesity was demonstrated by selective knockout of the leptin receptor (LepR) in VAN; mice express an obesogenic phenotype. Obesity and its resultant health consequences are a major worldwide health problem. Effective or preventative treatments for obesity are limited. Our findings have filled the gap in our knowledge of the mechanism of GLP-1 and leptin signaling on VAN. Understanding the physiology regulating feeding behavior is imperative in developing non-invasive anti-obesity treatments
Book chapters on the topic "Leptin signaling"
Zabeau, Lennart, Frank Peelman, and Jan Tavernier. "Leptin and Leptin Receptor." In Encyclopedia of Signaling Molecules, 2839–45. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101679.
Full textZabeau, Lennart, Frank Peelman, and Jan Tavernier. "Leptin and Leptin Receptor." In Encyclopedia of Signaling Molecules, 1–6. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101679-1.
Full textLiu, Jiarui, Xiaoning Yang, Siwang Yu, and Ruimao Zheng. "The Leptin Signaling." In Advances in Experimental Medicine and Biology, 123–44. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1286-1_7.
Full textShimizu, Hiroyuki. "Leptin Signaling Pathway." In Signal Transduction: Pathways, Mechanisms and Diseases, 143–58. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-02112-1_8.
Full textMünzberg, Heike. "Leptin-Signaling Pathways and Leptin Resistance." In Frontiers in Eating and Weight Regulation, 123–32. Basel: KARGER, 2009. http://dx.doi.org/10.1159/000264400.
Full textGouilleux, Fabrice. "Erythropoietin, Thrombopoietin and Leptin Receptors." In Hormone Signaling, 145–78. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-3600-7_8.
Full textKarmazyn, Morris, Daniel M. Purdham, Venkatesh Rajapurohitam, and Asad Zeidan. "Leptin Signaling in the Cardiovascular System." In Signal Transduction in the Cardiovascular System in Health and Disease, 377–95. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-09552-3_20.
Full textBarrios, Vicente, Emma Burgos-Ramos, and Jesús Argente. "Insulin-Leptin Signaling in the Brain." In Metabolic Syndrome and Neurological Disorders, 75–84. Chichester, UK: John Wiley & Sons Ltd, 2013. http://dx.doi.org/10.1002/9781118395318.ch4.
Full textSaxena, Neeraj K., and Dipali Sharma. "Leptin-Signaling Pathways as Therapeutic Targets in Cancer." In Adipocytokines, Energy Balance, and Cancer, 67–87. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-41677-9_4.
Full textGómez, Rodolfo, Javier Conde, Morena Scotece, and Oreste Gualillo. "Chapter 3. One Receptor for Multiple Pathways: Focus on Leptin Signaling." In Extracellular and Intracellular Signaling, 44–56. Cambridge: Royal Society of Chemistry, 2011. http://dx.doi.org/10.1039/9781849733434-00044.
Full textConference papers on the topic "Leptin signaling"
Battle, Monica, Corey Gillespie, Tanisha McGlothen, Marta Torroella-Kouri, and Ruben R. Gonzalez-Perez. "Abstract 1400: Obesity induced leptin-notch signaling axis in breast cancer." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1400.
Full textEndo, Hiroki, Kunihiro Hosono, Takashi Uchiyama, Hirokazu Takahashi, Masahiko Inamori, and Atsushi Nakajima. "Abstract 2479: Leptin signaling regulates colorectal tumor growth through Stat3 signaling: Tumor growth induced by dietary intake." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2479.
Full textMcGlothen, TZ, C. Gillespie, L. Colbert, D. Blaylock-Hogans, S. Guo, and Perez RR Gonzalez-. "P5-06-10: Leptin Signaling Impacts Notch and Wnt Crosstalk in Breast Cancer." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p5-06-10.
Full textLipsey, Crystal C., Adriana Harbuzariu, Courtney Dill, and Ruben R. Gonzalez-Perez. "Abstract B96: Tackling obesity-related cancer health disparity, new inhibitors of leptin signaling." In Abstracts: Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; November 13-16, 2015; Atlanta, Georgia. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7755.disp15-b96.
Full textGuo, Shanchun, Miles Fuller, and Ruben R. Gonzalez-Perez. "Abstract LB-365: Regulation of VEGFR-2 by leptin-Notch signaling crosstalk in mammary cancer cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-365.
Full textSouza Torsoni, Adriana, and Debora Cristina Gustavo VitorÉli. "IMPLICATIONS OF MATERNAL HIGH-FAT DIET ON CENTRAL LEPTIN SIGNALING IN NEWLY WEANED OFFSPRING OF MICE." In XXIII Congresso de Iniciação Científica da Unicamp. Campinas - SP, Brazil: Galoá, 2015. http://dx.doi.org/10.19146/pibic-2015-37181.
Full textChang, MC, M. Ennis, RJO Dowling, V. Stambolic, and PJ Goodwin. "Abstract P6-02-03: Leptin receptor (OB-R) in breast carcinoma tissue: Ubiquitous expression and correlation with leptin-mediated signaling, but not with systemic markers of obesity." In Abstracts: 2016 San Antonio Breast Cancer Symposium; December 6-10, 2016; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-p6-02-03.
Full textTalati, M., N. Fortune, E. Hornsby, J. D. West, and A. Hemnes. "Leptin Modulates Insulin Signaling Protein Intermediates Involved in Fatty Acid Metabolism in Cultured Cardiomyocytes with BMPR2 Mutation." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2798.
Full textGillespie, Corey, Shanchun Guo, Weiqiang Zhou, and Ruben Rene Gonzalez-Perez. "Abstract 825: Leptin signaling disruption prevents DMBA-induced mammary tumors in lean and diet-induced-obesity (DIO) mice." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-825.
Full textWatanabe, K., M. Suzukawa, K. Kobayashi, H. Tashimo, A. Hebisawa, S. Tohma, T. Nagase, and K. Ohta. "Leptin Enhances Inflammatory Mediator Production by Normal Human Lung Fibroblasts Via the Leptin Receptor, P38 MAPK and JAK2/STAT3 Signaling Pathway and May Contribute to Worsening of Asthma in Obesity." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4425.
Full textReports on the topic "Leptin signaling"
Boisclair, Yves R., and Arieh Gertler. Development and Use of Leptin Receptor Antagonists to Increase Appetite and Adaptive Metabolism in Ruminants. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7697120.bard.
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