Seoane Collazo, PatriciaLiñares Pose, LauraRial Pensado, EvaRomero Picó, AmparoMoreno Navarrete, José MaríaMartínez Sánchez, NoeliaGarrido Gil, PabloIglesias Rey, RamónMorgan, Donald A.Tomasini, NaokiMalone, Samuel AndrewSenra, AnaFolgueira Cobos, CintiaMedina Gómez, GemaSobrino Moreiras, TomásLabandeira García, José LuisNogueiras Pozo, RubénDomingos, Ana I.Fernández Real, José ManuelRahmouni, KamalDiéguez González, CarlosLópez Pérez, Miguel A.2020-04-202020-04-202019Seoane-Collazo, P., Liñares-Pose, L., Rial-Pensado, E. et al. (2019). Central nicotine induces browning through hypothalamic κ opioid receptor. Nat Commun 10, 4037 (https://doi.org/10.1038/s41467-019-12004-z)http://hdl.handle.net/10347/21557[ENG]Increased body weight is a major factor that interferes with smoking cessation. Nicotine, the main bioactive compound in tobacco, has been demonstrated to have an impact on energy balance, since it affects both feeding and energy expenditure at the central level. Among the central actions of nicotine on body weight, much attention has been focused on its effect on brown adipose tissue (BAT) thermogenesis, though its effect on browning of white adipose tissue (WAT) is unclear. Here, we show that nicotine induces the browning of WAT through a central mechanism and that this effect is dependent on the κ opioid receptor (KOR), specifically in the lateral hypothalamic area (LHA). Consistent with these findings, smokers show higher levels of uncoupling protein 1 (UCP1) expression in WAT, which correlates with smoking status. These data demonstrate that central nicotine-induced modulation of WAT browning may be a target against human obesityeng© The Author(s) 2019. Open Access. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/https://creativecommons.org/licenses/by/4.0/Fat metabolismMetabolic diseasesNeuroendocrinologyjournal article10.1038/s41467-019-12004-z2041-1723open access