Anti-inflammatory effects of nicotine in obesity and ulcerative colitis

Abstract

Cigarette smoke is a major risk factor for a number of diseases including lung cancer and respiratory infections. Paradoxically, it also contains nicotine, an anti-inflammatory alkaloid. There is increasing evidence that smokers have a lower incidence of some inflammatory diseases, including ulcerative colitis, and the protective effect involves the activation of a cholinergic anti-inflammatory pathway that requires the α7 nicotinic acetylcholine receptor (α7nAChR) on immune cells. Obesity is characterized by chronic low-grade inflammation, which contributes to insulin resistance. Nicotine significantly improves glucose homeostasis and insulin sensitivity in genetically obese and diet-induced obese mice, which is associated with suppressed adipose tissue inflammation. Inflammation that results in disruption of the epithelial barrier is a hallmark of inflammatory bowel disease, and nicotine is protective in ulcerative colitis. This article summarizes current evidence for the anti-inflammatory effects of nicotine in obesity and ulcerative colitis. Selective agonists for the α7nAChR could represent a promising pharmacological strategy for the treatment of inflammation in obesity and ulcerative colitis. Nevertheless, we should keep in mind that the anti-inflammatory effects of nicotine could be mediated via the expression of several nAChRs on a particular target cell.

Review article: ulcerative colitis, smoking and nicotine therapy

“…4 Intermittent smokers have often been reported to experience symptomatic exacerbation during periods of nonsmoking and alleviation of symptoms on recommencement of smoking. 2,5,6,15,20 The observation that heavier smokers who quit smoking are more susceptible to the rebound effect of developing UC, compared to lighter smokers, also corroborates the notion of a dose-dependent relationship. 6,9,10,16 Current smokers with UC have been found to have less relapses, 33 require fewer hospitalisations 1,6,24,34,35 and demonstrate a reduced need for oral corticosteroid and immunosuppressant therapy for their disease, compared to ex-smokers and nonsmokers with UC.…”

Enhanced vulnerability to tobacco use in persons with diabetes: A behavioral and neurobiological framework

“…Smoking significantly worsens insulin resistance to a greater extent in persons with diabetes as compared to healthy controls (Axelsson et al, 2001;Targher et al, 1997). The latter findings appear to be related to a direct effect of nicotine given that administration of this drug reduces insulin sensitivity via activation of alpha-7 subunit containing nicotinic acetylcholine receptors (Lakhan and Kirchgessner, 2011;Wang et al, 2011;Xu et al, 2012).…”

Nicotinic Regulation of Energy Homeostasis

“…Moreover, this may be of pathophysiological relevance in obesity. Accordingly, nicotine acting on α7 receptors decreases WAT inflammation and improves glucose homeostasis and insulin sensitivity in genetic or diet-induced obese mice (Lakhan & Kirchgessner, 2011;Wang, Yang, Xue, & Shi, 2011).…”