It is well known that nicotine, the main addictive constituent of tobacco, is the major component linking smoking to negative energy balance. Nicotine exerts anorectic actions and elicits weight loss in humans and rodents (1,2,4,35,36). Several hypotheses have been put forward. Data showing that the peripheral nicotine administration leads to increased expression of UCP1 in BAT (and white adipose tissue) were interpreted as a mechanism by which nicotine influences body weight homeostasis by acting at peripheral level in nonneural tissues (23,38). However, it is generally accepted that despite the many effects exerted by nicotine at peripheral level, the main effect of nicotine on feeding homeostasis is exerted at a central level. Data gleaned in this regard have led to the assumption that the main hypothalamic effects of nicotine are exerted on NPY (19–21,39,40) and POMC neurons (3,22) in the ARC. In light of the aforementioned findings we decided to focus our attention in the VMH, since data have involved this nucleus in the context of AMPK-driven biological effects (7,8,18).
