Activation of antilipolytic alpha(2)-adrenergic receptors by epinephrine during exercise in human adipose tissue.
The involvement of the antilipolytic alpha(2)-adrenergic pathway and the specific role of epinephrine in the control of lipolysis during exercise in adipose tissue (AT) were investigated in healthy male subjects (age: 24.1 +/- 2.2 yr; body mass index: 23.0 +/- 1.6). An in vitro study carried out on isolated adipocytes showed that the weak lipolytic effect of epinephrine was potentiated after blockade of alpha(2)-adrenergic receptor (AR) by an alpha(2)-AR antagonist and reached that of isoproterenol, a beta-AR agonist. The effect of the nonselective alpha(2)-AR antagonist phentolamine on the response of the extracellular glycerol concentration (EGC) in AT during two successive bouts of aerobic exercise (50% maximum O(2) uptake, 60 min duration) was evaluated using the microdialysis method. The metabolic responses measured in perfused probes with Ringer solution were compared with those obtained in perfused probes with Ringer plus 0.1 mmol/l phentolamine. Plasma norepinephrine level was not different during the two exercise bouts, whereas that of epinephrine was 2.5-fold higher during the second exercise. EGC in AT was twofold higher in the second compared with the first exercise, and the same response pattern was found for plasma glycerol. The exercise-induced increase in EGC was higher in the probe perfused with phentolamine compared with the control probe in both bouts of exercise. However, the potentiating effect of phentolamine on EGC was significant during the second exercise bout but did not reach a significant level during the first. These results suggest that epinephrine is involved in the control of lipid mobilization through activation of antilipolytic alpha(2)-AR in human subcutaneous AT during exercise.
Stich
V
V
Department of Sport Medicine, Third Faculty of Medicine, Charles University, 100 00 Praha, Czech Republic.
de Glisezinski
I
I
Crampes
F
F
Suljkovicova
H
H
Galitzky
J
J
Riviere
D
D
Hejnova
J
J
Lafontan
M
M
Berlan
M
M
D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism*; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D004837:Epinephrine / Q000097:blood / Q000494:pharmacology / Q000502:physiology*; D015444:Exercise / Q000502:physiology*; D005110:Extracellular Space / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005990:Glycerol / Q000097:blood / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000097:blood; D007545:Isoproterenol / Q000494:pharmacology; D008066:Lipolysis / Q000502:physiology*; D008297:Male; D009638:Norepinephrine / Q000097:blood; D010646:Phentolamine / Q000494:pharmacology; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*
D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D011942:Receptors, Adrenergic, alpha; D007545:Isoproterenol; D005990:Glycerol; D009638:Norepinephrine; D004837:Epinephrine; D010646:Phentolamine