Plasma neuropeptide Y levels relate cigarette smoking and smoking cessation to body weight regulation

Hussain, Tajamul; Al-Daghri, Nasser M.; Al‐Attas, Omar S.; Draz, Hossam M.; Al-Rahman, Sherif H. Abd; Yakout, Sobhy M.

doi:10.1016/j.regpep.2012.02.005

Cited by 25 publications

(15 citation statements)

References 60 publications

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“…Smoking had no effect on the levels of adiponectin and resistin. These findings are in agreement with previous reports that smokers have low serum levels of leptin, which is restored shortly after the cessation of smoking [36, 54, 55]. …”

Section: Resultssupporting

confidence: 93%

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Smoking is Associated with Reduced Leptin and Neuropeptide Y Levels and Higher Pain Experience in Patients with Fibromyalgia

Bokarewa

Erlandsson

Bjersing

et al. 2014

Mediators of Inflammation

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Smoking deregulates neuroendocrine responses to pain supporting production of neuropeptide Y (NpY) by direct stimulation of nicotinic receptors or by inhibiting adipokine leptin. Present study addressed the effect of cigarette smoking on adipokines and pain parameters, in 62 women with fibromyalgia (FM) pain syndrome with unknown etiology. Pain was characterized by a visual analogue scale, tender point (TP) counts, pressure pain threshold, and neuroendocrine markers NpY and substance P (sP). Levels of IGF-1, leptin, resistin, visfatin, and adiponectin were measured in blood and cerebrospinal fluid. Current smokers (n = 18) had lower levels of leptin compared to ex-smokers (n = 25, P = 0.002), while the expected NpY increase was absent in FM patients. In smokers, this was transcribed in higher VAS-pain (P = 0.04) and TP count (P = 0.03), lower pain threshold (P = 0.01), since NpY levels were directly related to the pain threshold (rho = 0.414) and inversely related to TP counts (rho = −0.375). This study shows that patients with FM have no increase of NpY levels in response to smoking despite the low levels of leptin. Deregulation of the balance between leptin and neuropeptide Y may be one of the essential mechanisms of chronic pain in FM.

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Section: Resultssupporting

confidence: 93%

“…Interestingly, a negative effect of smoking on leptin is transitory in nature. It decreased shortly after smoking [51] and was restored after the cessation of smoking [54, 55]. Smoking had no effect on the levels of adiponectin and resistin.…”

Section: Resultsmentioning

confidence: 99%

Smoking is Associated with Reduced Leptin and Neuropeptide Y Levels and Higher Pain Experience in Patients with Fibromyalgia

Bokarewa

Erlandsson

Bjersing

et al. 2014

Mediators of Inflammation

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“…Thus, POMC and NPY have opposing effects on food intake. Smokers show reduced NPY levels compared to non-smokers, and smoking cessation is associated with increased NPY (Hussain et al, 2012), suggesting NPY inhibition as a mechanism for appetite suppression. However, nicotine effects on NPY are complex.…”

Section: α7nachr Effects On Hypothalamic Neuropeptidesmentioning

confidence: 99%

The role of alpha-7 nicotinic receptors in food intake behaviors

2014

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Nicotine alters appetite and energy expenditure, leading to changes in body weight. While the exact mechanisms underlying these effects are not fully established, both central and peripheral involvement of the alpha-7 nicotinic acetylcholine receptor (α7nAChR) has been suggested. Centrally, the α7nAChR modulates activity of hypothalamic neurons involved in food intake regulation, including proopiomelanocortin and neuropeptide Y. α7nAChRs also modulate glutamatergic and dopaminergic systems controlling reward processes that affect food intake. Additionally, α7nAChRs are important peripheral mediators of chronic inflammation, a key contributor to health problems in obesity. This review focuses on nicotinic cholinergic effects on eating behaviors, specifically those involving the α7nAChR, with the hypothesis that α7nAChR agonism leads to appetite suppression. Recent studies are highlighted that identify links between α7nAChR expression and obesity, insulin resistance, and diabetes and describe early findings showing an α7nAChR agonist to be associated with reduced weight gain in a mouse model of diabetes. Given these effects, the α7nAChR may be a useful therapeutic target for strategies to treat and manage obesity.

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“…Smokers are reported to have reduced level of NPY, whereas smoking cessation is linked with increased levels of NPY (Hussain, Al-Daghri et al 2012). In animal studies, mice chronically exposed to low dose nicotine showed decreased NPY levels in the PVN (Chen, Hansen et al 2007) and ARC (Frankish, Dryden et al 1995), as well as reduced NPY receptor density in the hypothalamus (Kane, Parker et al 2001), together with a nicotine-dependent increase in the activity of POMC neurons (Huang, Xu et al 2011).…”

Section: Introductionmentioning

confidence: 99%

“…For example, an in vitro study showed that the effect of nicotine was reduced in isolated POMC neurons through the application of the α7 nAChR non-selective antagonist methyllycaconitine (MLA) (Huang, Xu et al 2011). On the other hand, levels of NPY were shown to be lower in smokers and also to be increased during nicotine cessation, suggesting that NPY has important role in control of food intake and body weight gain following smoking cessation (Hussain, Al-Daghri et al 2012). In similar fashion, α7 nAChR antagonist MLA reduced the excitation of NPY by nicotine (Huang, Xu et al 2011).…”

Section: Introductionmentioning

confidence: 99%

Effects of nicotine on homeostatic and hedonic components of food intake

Stojakovic

Espinosa

Farhad

et al. 2017

Journal of Endocrinology

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Chronic tobacco use leads to nicotine addiction, characterized by exaggerated urges to use the drug despite the accompanying negative health and socioeconomic burdens. Interestingly, nicotine users are found to be leaner than the general population. Review of the existing literature revealed that nicotine affects energy homeostasis and food consumption via altering the activity of neurons containing orexigenic and anorexigenic peptides in the brain. Hypothalamus is one the critical brain areas that regulates energy balance via the action of these neuropeptides. The equilibrium between these two groups of peptides can be shifted by nicotine leading to decreased food intake and weight loss. The aim of this article is to review the existing literature on the effect of nicotine on food intake and energy homeostasis and report on the changes that nicotine brings about in the level of these peptides and their receptors that may explain changes in food intake and body weight induced by nicotine. Furthermore, we review the effect of nicotine on the hedonic aspect of food intake. Finally, we discuss the involvement of different subtypes of nicotinic acetylcholine receptors in the regulatory action of nicotine on food intake and energy homeostasis.

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Plasma neuropeptide Y levels relate cigarette smoking and smoking cessation to body weight regulation

Cited by 25 publications

References 60 publications

Smoking is Associated with Reduced Leptin and Neuropeptide Y Levels and Higher Pain Experience in Patients with Fibromyalgia

Smoking is Associated with Reduced Leptin and Neuropeptide Y Levels and Higher Pain Experience in Patients with Fibromyalgia

The role of alpha-7 nicotinic receptors in food intake behaviors

Effects of nicotine on homeostatic and hedonic components of food intake

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