In vivo evidence for alpha 2-adrenergic-dependent inhibition of lipid mobilization in the rabbit.
Both alpha- and beta-agonists were infused i.v. in unanesthetized rabbits. The alpha-adrenergic effect on lipid mobilization was investigated by comparing the modifications of blood glycerol levels induced by clonidine (alpha 2-agonist) and amidephrine (alpha 1-agonist) alone or in combination with isoprenaline (beta-agonist). Clonidine (2 micrograms X kg-1 X min-1) was found to significantly reduce the basal or isoprenaline-stimulated glycerol levels whereas amidephrine (10 micrograms X kg-1 X min-1) was without any effect. Plasma IRI levels were also reduced by clonidine. The results suggest that the reduction of lipid mobilization produced by clonidine could have been the consequence of the stimulation of the alpha 2-adrenergic antilipolytic receptors previously shown to be present in isolated fat cell membranes.
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D003000:Clonidine / Q000494:pharmacology; D005990:Glycerol / Q000097:blood; D007328:Insulin / Q000097:blood; D007545:Isoproterenol / Q000494:pharmacology; D008053:Lipid Mobilization / Q000187:drug effects*; D008297:Male; D011817:Rabbits
D000316:Adrenergic alpha-Agonists; D000318:Adrenergic beta-Agonists; D007328:Insulin; D007545:Isoproterenol; D003000:Clonidine; D005990:Glycerol