Modulation of porcine adipocyte beta-adrenergic receptors by hormones and butyrate.
The beta-adrenergic receptors (betaAR) on the surface of mammalian cells are desensitized when the cell is stimulated by betaAR agonists to eliminate excessive response by the cell. Investigations with adipocytes, primarily rodent-derived cells, indicate other hormones and substrates also can modulate the individual betaAR subtypes. For example, glucocorticoids decrease the beta1AR and the beta3AR but increase the beta2AR. Insulin decreases the beta3AR. Thyroid hormones increase the beta3AR and butyrate increases beta1AR and beta2AR but dramatically decreases beta3AR. Because porcine adipocytes have unique functional and ligand-binding properties compared to rodent adipocytes and because porcine adipocytes contain predominantly beta1AR, compared to rodent adipocytes with predominantly beta3AR, we expect the regulation of porcine adipocyte betaAR by hormones and substrates to be different from that in rodent adipocytes. Isolated porcine adipocytes were incubated for 6 and 21 h without and with dexamethasone, insulin, triiodothyronine, or butyrate. Cells incubated without hormone or butyrate had a decreased betaAR number at 21 h. The beta1AR and beta2AR transcript concentrations were decreased after 6 h and tended to rebound after 21 h of incubation. Dexamethasone did not change the total betaAR number but tended to increase the beta1AR and beta2AR transcript concentrations. Insulin increased the betaAR number and decreased both transcript concentrations at 21 h. Triiodothyronine and butyrate did not change the receptor number or transcript concentrations. The results indicate that betaAR transcript concentrations do not accurately predict the betaAR protein concentration (estimated by ligand binding). Results also indicate that betaAR in porcine adipocytes are relatively unresponsive to hormones and butyrate compared to rodent-derived adipocytes described in the literature.
Ding
S T
ST
USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030-2600, USA. sding@bcm.tmc.edu
Smith
E O
EO
McNeel
R L
RL
Mersmann
H J
HJ
D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D002087:Butyrates / Q000494:pharmacology*; D002478:Cells, Cultured; D003907:Dexamethasone / Q000494:pharmacology*; D005260:Female; D007328:Insulin / Q000494:pharmacology*; D008297:Male; D012333:RNA, Messenger / Q000378:metabolism; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D013552:Swine; D014284:Triiodothyronine / Q000494:pharmacology*
D002087:Butyrates; D007328:Insulin; D012333:RNA, Messenger; D011943:Receptors, Adrenergic, beta; D014284:Triiodothyronine; D003907:Dexamethasone