LAUSR

Beyond promoting smoking initiation and preventing smokers from quitting, nicotine can reduce food intake and body weight and thus is viewed as desirable by some smokers, especially many women. During the last several decades, the molecular mechanisms underlying the inverse correlation between smoking and body weight have been investigated extensively in both animals and humans. Nicotine’s weight effects appear to result especially from the drug’s stimulation of α3β4 nicotine acetylcholine receptors (nAChRs), which are located on pro-opiomelanocortin (POMC) neurons in the arcuate nucleus (ARC), leading to activation of the melanocortin circuit, which is associated with body weight. Further, α7- and α4β2-containing nAChRs have been implicated in weight control by nicotine. This review summarizes current understanding of the regulatory effects of nicotine on food intake and body weight according to the findings from pharmacological, molecular genetic, electrophysiological, and feeding studies on these appetite-regulating molecules, such as α3β4, α7, and α4β2 nAChRs; neuropeptide Y (NPY); POMC; melanocortin 4 receptor (MC4R); agouti-related peptide (AgRP); leptin, ghrelin, and protein YY (PYY).