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Nicotine’ actions on energy balance: Friend or foe?
Journal article   Open access   Peer reviewed

Nicotine’ actions on energy balance: Friend or foe?

Patricia Seoane-Collazo, Carlos Diéguez, Rubén Nogueiras, Kamal Rahmouni, José Manuel Fernández-Real and Miguel López
Pharmacology & therapeutics (Oxford), Vol.219, pp.107693-107693
03/2021
DOI: 10.1016/j.pharmthera.2020.107693
PMID: 32987056
url
https://doi.org/10.1016/j.pharmthera.2020.107693View
Published (Version of record) Open Access

Abstract

Obesity has reached pandemic proportions and is associated with severe comorbidities, such as type 2 diabetes mellitus, hepatic and cardiovascular diseases, and certain cancer types. However, the therapeutic options to treat obesity are limited. Extensive epidemiological studies have shown a strong relationship between smoking and body weight, with non-smokers weighing more than smokers at any age. Increased body weight after smoking cessation is a major factor that interferes with their attempts to quit smoking. Numerous controlled studies in both humans and rodents have reported that nicotine, the main bioactive component of tobacco, exerts a marked anorectic action. Furthermore, nicotine is also known to modulate energy expenditure, by regulating the thermogenic activity of brown adipose tissue (BAT) and the browning of white adipose tissue (WAT), as well as glucose homeostasis. Many of these actions occur at central level, by controlling the activity of hypothalamic neuropeptide systems such as proopiomelanocortin (POMC), or energy sensors such as AMP-activated protein kinase (AMPK). However, direct impact of nicotine on metabolic tissues, such as BAT, WAT, liver and pancreas has also been described. Here, we review the actions of nicotine on energy balance. The relevance of this interaction is interesting, because considering the restricted efficiency of obesity treatments, a possible complementary approach may focus on compounds with known pharmacokinetic profile and pharmacological actions, such as nicotine or nicotinic acetylcholine receptors signaling.
Obesity Nicotine Adipose tissue Food intake Glucose homeostasis Nicotinic acetylcholine receptors Energy expenditure Hypothalamus

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