RT Journal Article
T1 Central nicotine induces browning through hypothalamic κ opioid receptor
A1 Seoane Collazo, Patricia
A1 Liñares Pose, Laura
A1 Rial Pensado, Eva
A1 Romero Picó, Amparo
A1 Moreno Navarrete, José María
A1 Martínez Sánchez, Noelia
A1 Garrido Gil, Pablo
A1 Iglesias Rey, Ramón
A1 Morgan, Donald A.
A1 Tomasini, Naoki
A1 Malone, Samuel Andrew
A1 Senra, Ana
A1 Folgueira Cobos, Cintia
A1 Medina Gómez, Gema
A1 Sobrino Moreiras, Tomás
A1 Labandeira García, José Luis
A1 Nogueiras Pozo, Rubén
A1 Domingos, Ana I.
A1 Fernández Real, José Manuel
A1 Rahmouni, Kamal
A1 Diéguez González, Carlos
A1 López Pérez, Miguel A.
K1 Fat metabolism
K1 Metabolic diseases
K1 Neuroendocrinology
AB [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
PB Nature Publishing Group
YR 2019
FD 2019
LK http://hdl.handle.net/10347/21557
UL http://hdl.handle.net/10347/21557
LA eng
NO 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)
NO 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
DS Minerva
RD 27 abr 2026