Disease relevance of nicotine

• The metabolic effects of nicotine have been implicated in the relation between smoking and lower body weight [1].
• Transdermal nicotine for active ulcerative colitis [2].
• Our data also suggest that the weight gain that often follows smoking cessation may be influenced not only by nicotine intake but also by the level of physical activity a smoker typically engages in while smoking [1].
• The patients in the nicotine group had greater improvement in the global clinical grade of colitis (P < 0.001) and the histologic grade (P = 0.03), lower stool frequency (a difference of 1.6 stools daily; P = 0.008), less abdominal pain (P = 0.05), and less fecal urgency (P = 0.009) [2].
• The safety of transdermal nicotine as an aid to smoking cessation in patients with cardiac disease [3].

Psychiatry related information on nicotine

• In the future, people who continue to smoke will be individuals with severe nicotine dependence or psychiatric symptoms; thus, clinicians will increasingly be called on to provide pharmacotherapy for smoking cessation [4].
• Pharmacotherapies for tobacco dependence include nicotine replacement medications in the form of gum, transdermal patch, lozenge, sublingual tablet, nasal spray, and vapor inhaler formulations [5].
• Five medications--bupropion, nicotine gum, nicotine inhaler, nicotine nasal spray, and nicotine patch--and one proven psychosocial therapy (behavior therapy) appear equally effective and safe; i.e., they all double quit rates and are associated with a less than 5% dropout rate due to adverse events [4].
• This study examined whether the nicotine-induced increase in the metabolic rate observed at rest is also present during physical activity [1].
• This AChBP structure is relevant for the development of drugs against, for example, Alzheimer's disease and nicotine addiction [6].

High impact information on nicotine

• A new study identifies 'quantitative trait transcripts' for nicotine resistance in large populations of wild strains of Drosophila melanogaster by comparing global gene expression patterns, survival time and metabolite levels in the presence or absence of nicotine [7].
• Nicotine patches for aphthous ulcers due to Behçet's syndrome [8].
• Transdermal nicotine as maintenance therapy for ulcerative colitis [9].
• Side effects were reported by 35 patients--21 in the nicotine group and 14 in the placebo group--the most common of which were nausea, lightheadedness, and itching [9].
• The effect of nicotine on energy expenditure during light physical activity [1].

Chemical compound and disease context of nicotine

• A controlled trial of sustained-release bupropion, a nicotine patch, or both for smoking cessation [10].
• If higher cotinine levels among blacks indicate higher nicotine intake or differential pharmacokinetics and possibly serve as a marker of higher exposure to cigarette carcinogenic components, they may help explain why blacks find it harder to quit and are more likely to experience higher rates of lung cancer than white smokers [11].
• In choriocarcinoma cell cultures, nicotine, cotinine (a major metabolite of nicotine), and anabasine (a minor component of cigarette tobacco) all inhibited androstenedione conversion to estrogen in a dose-dependent fashion [12].
• Tachygastria (> 4.5 cycle/min) increased from 2% +/- 2% to 16% +/- 3% of recording time, and arrhythmias (frequency instability index) increased from 0.5 +/- 0.1 to 1.1 +/- 0.2 cycle/min with nicotine in nonsmokers (P < 0.05), which normalized with indomethacin [13].
• METHODS: Twenty subjects (9 smokers and 11 nonsmokers) participated in 4 laboratory sessions during which they were challenged with 0, 0.8, 1.6, or 3.2 mg/70 kg of naloxone and then monitored for 1 hour for subjective signs and symptoms of opiate-like withdrawal, nicotine craving, and alterations in cortisol levels [14].

Biological context of nicotine

• The excess energy expenditure attributable to nicotine was more than twice as great during exercise (difference between groups, 0.51 kJ per kilogram per hour, or 12.1 percent of the metabolic rate at rest; P less than 0.001) than during rest (0.23 kJ per kilogram per hour, or 5.3 percent of the metabolic rate at rest; P less than 0.05) [1].
• We conclude that the relatively small metabolic effect of nicotine when the subject is at rest is enhanced during light exercise [1].
• We report here that high-affinity binding sites for nicotine are absent from the brains of mice homozygous for the beta 2-subunit mutation [15].
• Hippocampal synaptic transmission enhanced by low concentrations of nicotine [16].
• Neurobiology: memories of nicotine [17].

Anatomical context of nicotine

• To test the hypothesis that the reduction in tar and nicotine content of cigarette smoke that began in the 1950s should be reflected by the histologic changes in the bronchial epithelium of cigarette smokers, 20, 424 sections taken at autopsy from the bronchial tubes of 445 men (non-lung-cancer deaths) were examined microscopically in random order [18].
• Nicotine is known to act on presynaptic nAChRs within the habenula of chick to enhance glutamatergic transmission; here we report that a similar mechanism operates in the hippocampus [16].
• Effects of nicotine on the nucleus accumbens and similarity to those of addictive drugs [19].
• We now show that enkephalin and catecholamines are released together from primary cultures of bovine adrenal medullary chromaffin cells by nicotine in a Ca2+-dependent manner [20].
• Nicotine increased endothelial-cell growth and tube formation in vitro, and accelerated fibrovascular growth in vivo [21].

Associations of nicotine with other chemical compounds

• Exposure of the fetus, neonate, and nursed infant to nicotine and cotinine from maternal smoking [22].
• Here we report that intravenous nicotine in the rat, at doses known to maintain self-administration, stimulates local energy metabolism, as measured by 2-deoxyglucose autoradiography, and dopamine transmission, as estimated by brain microdialysis, in the shell of the nucleus accumbens [19].
• These receptors do not bind alpha-bungarotoxin but have a high affinity for nicotine and antibodies raised against them block the function of acetylcholine receptors in ciliary ganglia [23].
• That the SCN contains a cholinergic marker like ChAT and is responsive to cholinergic agents but does not bind nicotine or ACh reflects a general problem in reconciling functional, physiological, and anatomical markers of neurotransmission [24].
• Tolbutamide and other sulfonylureas inhibited spontaneous and nicotine-induced release of catecholamines from the perfused cat adrenal gland and nicotine-induced release of [3-H]norepinephrine from isolated guinea pig hearts [25].

Gene context of nicotine

• The mitogenic effects of nicotine were mediated via the alpha7-nAChR subunit and resulted in enhanced recruitment of E2F1 and Raf-1 on proliferative promoters in NSCLC cell lines and human lung tumors [26].
• Expression of GRPR mRNA in lung fibroblasts was elevated following exposure to nicotine [27].
• Corticotropin-releasing factor-binding protein ligand inhibitor blunts excessive weight gain in genetically obese Zucker rats and rats during nicotine withdrawal [28].
• Our findings provide strong evidence suggesting a common CHRNA4 haplotype might be protective against vulnerability to nicotine addiction in men [29].
• We studied six single-nucleotide polymorphisms (SNPs) in the CHRNA4 gene and four SNPs in the CHRNB2 gene with respect to nicotine dependence in a collection of 901 subjects (815 siblings and 86 parents) from 222 nuclear families with multiple nicotine-addicted siblings [29].

Analytical, diagnostic and therapeutic context of nicotine

• Pharmacotherapy for nicotine dependence [5].
• Information about the potential health hazards of nicotine, as well as oral pathology, may be incorporated into educational programs to help discourage the use of smokeless tobacco, with a resultant decrease in the associated cancer risk [30].
• We treated 80 patients with ulcerative colitis in remission with either transdermal nicotine or placebo patches for six months in a randomized, double-blind study [9].
• Nicotine is the primary component of tobacco that drives use, and like other addictive drugs, nicotine reinforces self-administration and place preference in animal studies [31].
• In a mouse model of hind-limb ischemia, nicotine increased capillary and collateral growth, and enhanced tissue perfusion [21].

References