2001; Lupien & Bray, 1988; Yoshida, Yoshioka, Hiraoka, & Kondo, 1990; Yoshida et al., 1999) systemic nicotine as well as chronic cigarette exposure (Chen et nevertheless al., 2008) increases sympathetic activity, noradrenaline release, and UCP1 expression in BAT, thus increasing thermogenesis. The target nAChRs for this effect are not known. Whereas there is no evidence for nAChRs in BAT (but see below the discussion of resident macrophages), both sympathetic ganglia and central sympathetic control circuits are possible candidates for nicotine effects on BAT. Systemic nicotine-elicited release of noradrenaline in BAT can be blocked by antagonists of the corticotropin-releasing hormone type 1 receptors (Mano-Otagiri et al., 2009), suggesting the involvement of hypothalamic control circuits of the sympathetic system (Usui et al.
, 2009). White Adipose Tissue As discussed above, a consistent effect of nicotine treatment is decreased body weight with reduction of WAT mass. Decrease in WAT mass may be due to a direct lipolytic effect. Both in vivo (Andersson & Arner, 2001; Mjos, 1988) and ex vivo (Sztalryd et al., 1996) nicotine, as well as smoking, (Laudon Meyer, Waldenlind, & Marcus, 2005) induces lipolysis in WAT. In addition, nicotine increases lipoprotein lipase activity in several tissues (Ashakumary & Vijayammal, 1997). These effects of nicotine lead to increased plasma levels of free fatty acids and other lipids (Ashakumary & Vijayammal, 1997). In parallel, nicotine increases free fatty acid utilization in muscle contributing to decreased adiposity (Sztalryd et al., 1996).
Aside from nicotine��s primary and secondary (e.g. drug cues) reinforcing effects (Caggiula et al., 2001; Corrigall, 1999; Fowler & Kenny, 2011), animal research indicates that nicotine may enhance the reinforcing value of rewards, especially sensory stimuli, that are independent of nicotine intake (Caggiula et al., 2009; Donny et al., 2003; Olausson, Jentsch, & Taylor, 2004; Raiff & Dallery, 2008). Support in humans for this reinforcement enhancing effect of nicotine is suggestive but perhaps specific to reward type, dependence level, measure of reinforcement, or other procedural factors (e.g. Attwood, Penton-Voak, & Munafo, 2009; Barr, Pizzagalli, Culhane, Goff, & Evins, 2008; Dawkins, Powell, West, Powell, & Pickering, 2006; McGrath, Barrett, Stewart, & Schmid, 2012; Perkins, Grottenthaler, & Wilson, 2009). A key implication of these findings is that quitting smoking would result in removal of these reinforcement enhancing effects of nicotine, decreasing Dacomitinib the reinforcing value of rewarding stimuli in an ex-smoker��s environment, as indicated in rodent research (e.g. Weaver et al., 2012).
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