Anderson, K., Arner, P. "Systemic nicotine stimulates human adipose tissue lipolysis through local cholinergic and catecholeaminergic receptors." International Journal of Obesity . Aug. 2001, vol. 25 no. 8. pp. 1225-1232.
[ABSTRACT]
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 ug/kg/min for 30 minutes) 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. 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 to the -5 power M) via the microdialysis system, the increase in adipose glycerol levels was inhibited by ~45% (P=0.02). A corresponding local beta-adrenoceptor blockade with propanolol (10 to the -4 power M), inhibited the increase in adipose glycerol levels by ~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.
BMJ
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