In vitro and in vivo impairment of alpha2-adrenergic receptor-dependent antilipolysis by fatty acids in human adipose tissue.

Stéphane Gesta (1) , Jindra Hejnová (2) , Michel Berlan (1, 3) , Danièle Daviaud (1) , François Crampes (1, 4) , Vladimir Stich (2) , Philippe Valet (1) , Jean Sébastien Saulnier-Blache (1)

1 Unité de recherche sur les obésités
2 Department of Sport Medicine
3 Laboratoire Pharmacocinétique et de Toxicologie [CHU Toulouse]
4 Laboratoire des Adaptations de l'Organisme à l'Exercice Musculaire

The aim of the present study was to study the influence of fatty acids on the adrenergic control of lipolysis both in vitro and in vivo. Human subcutaneous adipose tissue explants were cultured for 48 h in the presence of 100 microM bromopalmitate (BrPal), and lipolysis was measured in isolated adipocytes. In control conditions, beta-AR-dependent activation of lipolysis by epinephrine was almost undetectable, and could be fully restored by pharmacological blockade of alpha2-AR-dependent antilipolysis. After BrPal treatment, epinephrine became fully lipolytic and was no longer influenced by alpha2-AR-blockade. Radioligand binding analysis revealed that BrPal treatment led to a significant reduction in the coupling of alpha2-AR to G proteins. In parallel, a chronic and significant increase in plasma fatty acids resulting from a 4-day high-fat diet (HFD) was accompanied by an impairment of the amplifying effect of the alpha2-AR antagonist phentolamine on exercise-induced lipolysis (measured in the subcutaneous adipose tissue with the use of a microdialysis probe) normally observed after a low-fat diet. In conclusion, in vitro and in vivo studies showed that fatty acids impair alpha2-AR-dependent antilipolysis.

Domaines: Biologie cellulaire

Stéphane Gesta, Jindra Hejnová, Michel Berlan, Danièle Daviaud, François Crampes, et al.. In vitro and in vivo impairment of alpha2-adrenergic receptor-dependent antilipolysis by fatty acids in human adipose tissue.. Horm Metab Res, 2001, 33 (12), pp.701-7. ⟨10.1055/s-2001-19140⟩. ⟨inserm-00110155⟩