Central nicotine induces browning through hypothalamic κ opioid receptor

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2019_natcommun_seoane_central_nicotine.pdf (6.43 MB)
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URI: http://hdl.handle.net/10347/21557
E-ISSN: 2041-1723
DOI: 10.1038/s41467-019-12004-z

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2019

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Nature Publishing Group
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[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 obesity

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Fat metabolism| Metabolic diseases| Neuroendocrinology

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Seoane-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)

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The research leading to these results has received funding from the Xunta de Galicia (J.L.L.-G.: ED431C 2018/10; R.N.: 2015-CP080 and 2016-PG057; M.L.: 2015-CP079 and 2016-PG068); Ministerio de Economía y Competitividad (MINECO) co-funded by the FEDER Program of EU (J.L.L.-G.: BFU2015–70523; R.N.: BFU2015–70664R; C.D.: BFU2017–87721-P; M.L.: RTI2018-101840-B100; BFU2015–70454-REDT/Adipoplast and RTI2018–101840-B-I00); Instituto de Salud Carlos III (J.L.L.-G.: RD16/0011/0016; J.M.F.-R.: PI15–01934); European Molecular Biology Organization (A.D.: EMBO-Installation Grant 3037); Human Frontier Science Program (A.D.: HFSP-RGY0070/2016); Howard Hughes Medical Institute (A.D.: HHMI-208576/Z/17/Z); US National Institutes of Health (K.R.: HL084207); American Heart Association (K.R.: EIA#14EIA18860041); the University of Iowa Fraternal Order of Eagles Diabetes Research Center (K.R.); Atresmedia Corporación (R.N. and M.L.: 2017-PO004); Fundación BBVA (R.N.), European Foundation for the Study of Diabetes (R.N.); and ERC Synergy Grant-2019-WATCH-810331 (R.N.). P.S.-C. is recipient of a fellowship from Xunta de Galicia (ED481B 2018/050). L.L.-P. is recipient of a fellowship from Xunta de Galicia (ED481A-2016/094); E.R.-P. is recipient of a fellowship from MINECO (BES-2015–072743). N.M.-S. is recipient of a fellowship from Xunta de Galicia (ED481B 2016/168–0) and from the European Union’s Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie actions. The CiMUS is supported by the Xunta de Galicia (2016–2019, ED431G/05). CIBER de Fisiopatología de la Obesidad y Nutrición is an initiative of ISCIII

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© 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/

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Fisioloxía
Centro de Investigación en Medicina Molecular e Enfermidades Crónicas (CiMUS)
Ciencias Morfolóxicas