Adipoplast research teams identify TAGLN2 as a protein expressed in adipose tissue and associated with obesity and inflammation, being normalized upon weight loss

Seoane-Collazo P, Liñares-Pose L, Rial-Pensado E, Romero-Picó A, Moreno-Navarrete JM,
Martínez-Sánchez N, Garrido-Gil P, Iglesias-Rey R, Morgan DA, Tomasini N, Malone SA, Senra A, Folgueira C, Medina-Gomez G, Sobrino T, Labandeira-García JL, Nogueiras R, Domingos AI, Fernández-Real JM, Rahmouni K, Diéguez C, López M.

Central nicotine induces browning through hypothalamic κ opioid receptor.

Nat Commun. 2019 Sep 6;10(1):4037. doi: 10.1038/s41467-019-12004-z.

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.