Nicotine’ actions on energy balance: Friend or foe?

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...

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Bibliographic Details
Published in:Pharmacology & therapeutics (Oxford) 2021-03, Vol.219, p.107693-107693, Article 107693
Main Authors: Seoane-Collazo, Patricia, Diéguez, Carlos, Nogueiras, Rubén, Rahmouni, Kamal, Fernández-Real, José Manuel, López, Miguel
Format: Article
Language:English
Subjects:
Adipose tissue
Adipose Tissue, Brown - metabolism
Adipose Tissue, White - metabolism
Body Weight
Diabetes Mellitus, Type 2 - metabolism
Energy expenditure
Energy Metabolism
Food intake
Glucose homeostasis
Humans
Hypothalamus
Nicotine
Nicotine - metabolism
Nicotinic acetylcholine receptors
Obesity
Obesity - drug therapy
Obesity - metabolism
Thermogenesis
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Summary: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.
ISSN:0163-7258
1879-016X
DOI:10.1016/j.pharmthera.2020.107693