Department of Physiology, CiMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, 15782, Santiago de Compostela, Spain.
CIBER Fisiopatología de la Obesidad y Nutrición (CIBEROBN), 28029, Santiago de Compostela, Spain.
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.
体重增加是干扰戒烟的一个主要因素。尼古丁是烟草中的主要生物活性化合物，已被证明会影响能量平衡，因为它会影响中枢神经系统的摄食和能量消耗。在尼古丁对体重的中枢作用中，人们非常关注其对棕色脂肪组织（BAT）产热的影响，尽管其对白色脂肪组织（WAT）的褐变作用尚不清楚。在这里，我们表明，尼古丁通过中枢机制诱导 WAT 褐变，并且这种作用依赖于κ阿片受体（KOR），特别是在下丘脑外侧区（LHA）。与这些发现一致的是，吸烟者的 WAT 中解偶联蛋白 1（UCP1）的表达水平更高，这与吸烟状况相关。这些数据表明，中枢尼古丁诱导的 WAT 褐变的调节可能是对抗人类肥胖的一个靶点。
