Modulation of porcine adipocyte β-adrenergic receptors by a β-adrenergic agonist
Journal
Journal of Animal Science
Journal Volume
78
Journal Issue
4
Pages
919-926
Date Issued
2000
Author(s)
Abstract
Mammalian cells have several mechanisms to decrease the response to β-adrenergic agonists. Agonists are metabolized or taken up by nerve endings. The β-adrenergic receptors (βAR) are inactivated by phosphorylation and removed from the cell membrane, and synthesis is decreased or degradation is increased. Knowledge about adipocyte βAR desensitization is mostly from rodent adipocytes with > 90% β3AR. Porcine adipocyte βAR have functional and ligand-binding properties that are quite different from those in many other species. Furthermore, the predominant βAR sub-type in the porcine adipocyte is the β1AR (70 to 80%). Given these species differences, it might be expected that desensitization in porcine adipocytes would not be totally concordant with the rodent-derived model. Isolated porcine adipocytes were incubated without or with a βAR agonist, isoproterenol. The total βAR number, measured by ligand-binding in a crude membrane fraction, tended to be lower after 6 h of incubation without isoproterenol. The addition of 10-5 M isoproterenol during the incubation caused the βAR number to decrease 43% compared to cells incubated without isoproterenol. The β1AR and β2AR transcript concentrations both decreased 45% after 6 h of incubation without isoproterenol. There was no decrease in mRNA when cells were incubated with isoproterenol. The results suggest the βAR were desensitized by incubation with isoproterenol, perhaps by phosphorylation and removal from the membrane, but this was not accompanied by modulation of the concentration of transcripts for β1AR or β2AR.
Type
journal article