A number of the metabolic effects of nicotine (or tobacco smoke) reported in mammals are reviewed, and attention is drawn to the relative deficiency in this area of investigation. The suggestion is made that, concomitant with the advance of newer and more sophisticated biochemical and biophysical techniques, the effects of nicotine be more systematically studied using concentrations that include those encountered in man.
In general, nicotine appears capable of increasing heat production, oxygen consumption, metabolic rate, and blood sugar. Studies of tissue metabolism show that nicotine can inhibit pyruvate oxidation by inhibiting specifically pyruvic dehydrogenase. Nicotine has been shown to possess anticholinesterase activity and to suppress acetylcholine synthesis. These observations may all be of importance in finally elucidating the mechanism of the neurotropic action of nicotine and deserve to be extended.
The uncomplicated effect of nicotine on serum cholesterol and lipoprotein levels is not yet clearly apparent. Generally, the levels appear to be higher in smokers than in nonsmokers; the reason for the difference is obscure. Effects of nicotine on nitrogen metabolism are virtually unknown; effects on mineral metabolism, when demonstrable, appear indirect and to lack both consistency and significance. Vitamin metabolism is largely unaffected, except for ascorbic acid, which reportedly may be depleted to a perhaps significant extent.
It is interesting and significant to note that there are few clinical reports which implicate nicotine (or tobacco smoke) etiologically or otherwise in deficiency or metabolic disorders.