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Review
. 2012 Nov;14(11):1270-90.
doi: 10.1093/ntr/nts159. Epub 2012 Sep 18.

Nicotinic regulation of energy homeostasis

Affiliations
Review

Nicotinic regulation of energy homeostasis

Michele Zoli et al. Nicotine Tob Res. 2012 Nov.

Abstract

Introduction: The ability of nicotine, the primary psychoactive substance in tobacco smoke, to regulate appetite and body weight is one of the factors cited by smokers that prevents them from quitting and is the primary reason for smoking initiation in teenage girls. The regulation of feeding and metabolism by nicotine is complex, and recent studies have begun to identify nicotinic acetylcholine receptor (nAChR) subtypes and circuits or cell types involved in this regulation.

Discussion: We will briefly describe the primary anatomical and functional features of the input, output, and central integration structures of the neuroendocrine systems that regulate energy homeostasis. Then, we will describe the nAChR subtypes expressed in these structures in mammals to identify the possible molecular targets for nicotine. Finally, we will review the effects of nicotine and its withdrawal on feeding and energy metabolism and attribute them to potential central and peripheral cellular targets.

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Figures

Figure 1.
Figure 1.
Schematic representation of the principal structures of the systems that regulate energy metabolism. AMY = amygdala; ARC = arcuate nucleus; DMH = dorsomedial hypothalamic nucleus; GI = gastrointestinal; INS = insula; LH = lateral hypothalamus; nAc = nucleus accumbens; NTS = nucleus of the solitary tract; OFC = orbitofrontal cortex; PFC = prefrontal cortex; PVH = paraventricular hypothalamic nucleus; VMH = ventromedial hypothalamic nucleus; VTA = ventral tegmental area.
Figure 2.
Figure 2.
Expression of nicotinic acetylcholine receptors in systems that regulate energy metabolism. For abbreviations, see legend to figure 1. ANS = autonomic nervous system; BAT = brown adipose tissue; ENS = enteric nervous system; WAT = white adipose tissue.

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