Central nicotine induces browning through hypothalamic kappa opioid receptor
Seoane-Collazo, P.; Linares-Pose, L.; Rial-Pensado, E.; Romero-Pico, A.; Moreno-Navarrete, J. M.; Martinez-Sanchez, N.; Garrido-Gil, P.; Iglesias Rey, Ramón; Morgan, D. A.; Tomasini, N.; Malone, S. A.; Senra, A.; Folgueira, C.; Medina-Gomez, G.; Sobrino Moreiras, Tomas; Labandeira-Garcia, J. L.; Nogueiras, R.; Domingos, A. I.; Fernandez-Real, J. M.; Rahmouni, K.; Dieguez, C.; Lopez, M.
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Identificadores
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Fecha de publicación
2019Título de revista
Nature Communications
Tipo de contenido
Artigo
DeCS
estimulantes ganglionares | animales | mediana edad | peso corporal | humanos | tejido adiposo | termogénesis | nicotina | hipotálamo | adulto | ratas | ratonesMeSH
Adipose Tissue | Adult | Rats | Middle Aged | Humans | Body Weight | Hypothalamus | Mice | Ganglionic Stimulants | Nicotine | Animals | ThermogenesisResumen
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 kappa 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.