was associated with normalized mRNA levels of AgRP, NPY, and POMC in the ARC, as well as reduced or restored levels of thermogenic markers in BAT increased previously by nicotine treatment. Overall, our results indicate that nicotine impairs AMPK function in the hypothalamus and that this effect is essential for the weight loss, hypophagia, and increased BAT-mediated energy dissipation. The mechanism connecting the nicotine-induced changes in the hypothalamus that stimulates the thermogenic program in the BAT is likely mediated via activation of the α3β4-nicotinic acetylcholine receptors (3) and through the SNS. This is supported by recent evidence showing that AMPK inhibition stimulates thermogenic program in the BAT through the SNS (7,8,41) and that nicotine increases BAT thermogenesis and UCP1 expression in rats through SNS activation (7,8,23,24,38,41).
