Nicotine is one of the many, albeit most famous, alkaloid in cigarettes that naturally occurs in tobacco. Nicotine itself exists in many other plants (those of the Solanaceae family such as eggplant or peppers) but at miniscule doses. When nicotine is isolated from tobacco containing products or cigarettes, it has a significantly different profile of effects in the body and for all intents and purposes should be seen as a different intervention.
Nicotine has a few mechanisms at its roots. The first is that nicotine mimics the neurotransmitter acetylcholine and can directly activate acetylcholine receptors (which can then induce increases of catecholamines such as adrenaline and dopamine; this mechanism underlies both potential addiction and fat burning). Nicotine may also act as an anti-estrogenic compound, inhibiting aromatase and one of the two estrogen receptors directly; this may underlie some of the side-effects associated with chronic usage of nicotine, particularly in women. Finally, nicotine is pro-oxidative in nature but at a level which may be hormetic in nature, that works with the acetylcholine mechanism just mentioned to exert anti-inflammatory effects.
Nicotine appears to have a role as a fat burner due to its mechanisms, which for the most part increase adrenaline and then work through beta-adrenergic receptors (the molecular target of ephedrine); this increase in adrenaline mediates the increase in metabolic rate which is significant but short-lived with moderate usage. The increase in lipolysis (how available fatty acids are to be burnt) appears to be mediated by other, possibly pro-oxidative, mechanisms and not by adrenaline.
In regards to addiction, the risk of nicotine and addiction is a measurement between how much nicotine is taken (with more nicotine being associated with greater risk) and the speed of nicotine reaching the brain (with faster spikes in neural concentration being associated with both greater perceived benefits and greater risk of addiction). Gums and patches have less potential risk for addiction than do cigarettes (with inhalers in the middle) due to speed nicotine reaches the brain.
Acutely, potential side-effects of nicotine are similar to acute side-effects of other stimulants such as ephedrine, yohimbine, or caffeine due to increasing catecholamines. Over the long term, the side-effect profile of nicotine may rival ephedrine as those two retain a degree of catecholamine secretion over time (the other two losing efficacy in 2 weeks or less).