K. Andersson et P. Arner, Systemic nicotine stimulates human adipose tissue lipolysis through local cholinergic and catecholaminergic receptors, INT J OBES, 25(8), 2001, pp. 1225-1232
OBJECTIVE: To evaluate whether the lipolytic effects of systemic nicotine a
re not only attributed to indirect adrenergic mechanisms, but also to a dir
ect action of nicotine on fat cells.
DESIGN: The effect of a systemic nicotine infusion (0.5 mug/kg/min for 30 m
in) 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 infusi
on. Nicotine induced a mean (+/- s.e.) percentage peak increase in adrenali
ne 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 adipo
se glycerol levels was inhibited by similar to 45% (P = 0.02). A correspond
ing local beta-adrenoceptor blockade with propranolol (10(-4) M), inhibited
the increase in adipose glycerol levels by similar to 60% (P = 0.02). Infu
sion of saline (ie placebo) had no effect on the parameters mentioned above
.
CONCLUSION: Systemically administered nicotine induces lipolysis, in part b
y activating the classical adrenergic mechanism (mediated by a nicotine-ind
uced release of catecholamines stimulating beta-adrenoceptors), and in part
by directly activating a nicotinic cholinergic lipolytic receptor located
in adipose tissue.