Systemic nicotine stimulates human adipose tissue lipolysis through local cholinergic and catecholaminergic receptors.

OBJECTIVE: To evaluate whether the lipolytic effects of systemic nicotine are not only attributed to indirect adrenergic mechanisms, but also to a direct action of nicotine on fat cells.
DESIGN: The effect of a systemic nicotine infusion (0.5 microg/kg/min for 30 min) on lipolysis in subcutaneous adipose tissue was investigated in situ in 11 non-obese, non-smoking, healthy male subjects under placebo-controlled conditions. MEASUREMENTS: By using microdialysis probes the glycerol levels (lipolysis index) and blood flow were monitored locally in subcutaneous adipose tissue.
RESULTS: Plasma nicotine levels peaked (7.2 ng/ml) at the end of the infusion. Nicotine induced a mean (+/-s.e.) percentage peak increase in adrenaline and noradrenaline plasma levels of 213+/-30% (P<0.01) and 118+/-5% (P<0.05), respectively. Nicotine increased venous plasma glycerol levels by 144+/-9% (P<0.001), arterialized plasma glycerol levels by 148+/-12% (P<0.001) and adipose glycerol levels by 148+/-16% (P<0.001), but did not alter blood flow. By inducing a local cholinoceptor blockade with mecamylamine (10(-5) M) via the microdialysis system, the increase in adipose glycerol levels was inhibited by approximately 45% (P=0.02). A corresponding local beta-adrenoceptor blockade with propranolol (10(-4) M), inhibited the increase in adipose glycerol levels by approximately 60% (P=0.02). Infusion of saline (ie placebo) had no effect on the parameters mentioned above.
CONCLUSION: Systemically administered nicotine induces lipolysis, in part by activating the classical adrenergic mechanism (mediated by a nicotine-induced release of catecholamines stimulating beta-adrenoceptors), and in part by directly activating a nicotinic cholinergic lipolytic receptor located in adipose tissue.

RCT Entities:   Population Interventions Outcomes