Submitted on May 31, 2007
Revised on July 3, 2007
Accepted on July 11, 2007
Acute exposure to long-chain fatty acids impairs alpha2-adrenergic receptor-mediated antilipolysis in human adipose tissue
Jan Polak, Cédric Moro, David Bessière, Jindra Hejnova, Marie A. Marquès, Magda Bajzova, Max Lafontan, François Crampes, Michel Berlan, and Vladimir Stich
Inserm Unit 858, Institut de Médecine Moléculaire de Rangueil (I2MR), Toulouse Cedex 4 31432
Corresponding Author: Max.Lafontan{at}toulouse.inserm.fr
The acute in vitro and in vivo effects of long-chain fatty acids (LCFA) on the regulation of adrenergic lipolysis were investigated in human adipose tissue. The effect of a 2-hour incubation, without or with LCFA (200 
mol/l), on basal and hormonally-induced lipolysis was tested in vitro on isolated fat cells. The lipolytic response to epinephrine was enhanced by suppression of the antilipolytic alpha2-adrenergic effect. Then, healthy lean and obese male subjects performed a 45 min exercise bout at 50% of their heart rate reserve either after an overnight fast or 3 hours after a high fat meal (HFM: 95 % fat, 5 % carbohydrates). Subcutaneous adipose tissue lipolysis was measured by microdialysis in the presence or absence of an alpha-antagonist (phentolamine). In vivo, a HFM increased plasma levels of non-esterified fatty acids in lean and obese subjects. In both groups, the HFM did not alter hormonal responses to exercise. Under fasting condition, the alpha2-adrenergic antilipolytic effect was more pronounced in obese than in lean subjects. The HFM totally suppressed the alpha2-adrenergic antilipolytic effect in lean and obese subjects during exercise. LCFA per se, in vitro as well as in vivo, suppress alpha2-adrenergic mediated antilipolysis in adipose tissue. LCFA-mediated suppression of antilipolytic pathways represents another mechanism whereby a high fat content in the diet might increase adipose tissue lipolysis.
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