Central nicotine induces browning through hypothalamic κ opioid receptor.
Patricia Seoane-CollazoLaura Liñares-PoseEva Rial-PensadoAmparo Romero-PicóJosé María Moreno-NavarreteNoelia Martinez-SanchezPablo Garrido-GilRamón Iglesias-ReyDonald A MorganNaoki TomasiniSamuel Andrew MaloneAna SenraCintia FolgueiraGema Medina-GomezTomás SobrinoJosé L Labandeira-GarcíaRuben NogueirasAna I DomingosJosé-Manuel Fernández-RealKamal RahmouniCarlos DiéguezMiguel LópezPublished in: Nature communications (2019)
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.
Keyphrases
- smoking cessation
- body weight
- adipose tissue
- replacement therapy
- insulin resistance
- high fat diet induced
- chronic pain
- binding protein
- endothelial cells
- metabolic syndrome
- high fat diet
- pain management
- poor prognosis
- machine learning
- weight loss
- long non coding rna
- small molecule
- high glucose
- working memory
- minimally invasive