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ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #101688
Title: MODULATION OF PORCINE ADIPOCYTE BETA-ADRENERGIC RECEPTORS BY HORMONES AND BUTYRATE

Author
item DING, SHIH-TORNG - BAYLOR COLLEGE OF MED.
item SMITH, E. - BAYLOR COLLEGE OF MED.
item MCNEEL, RONALD - BAYLOR COLLEGE OF MED.
item Mersmann, Harry

Submitted to: Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/19/1999
Publication Date: N/A
Citation: N/A

Interpretive Summary: Beta-adrenergic receptors (BARs) are cell membrane sites that control fat cell metabolism and fat cell tissue growth. Certain substances can interact with these receptors and affect fat metabolism. We wanted to know the effects of certain hormones (dexamethasone, insulin, triiodothyronine) and a substrate called butyrate on pig fat cell BARs. Previous studies have shown that all these substances modify BARs in rat and mouse cells. Our results indicated that the BARs in pig fat cells responded marginally to these substances; they are relatively unresponsive to hormones and butyrate compared to rodent fat cells described in prior reports. Porcine BARs are different than classical BAR described in rodent tissues. Our findings indicate that BARs in pig fat cells are regulated by hormones and substrates differently than classical fat cell BARs. Part of the species differences may be associated with the different distribution of BAR subtypes in their fat cells. Ultimately, these findings suggest that the pig may be an appropriate model for studies of fat metabolism and endocrine influences in the human.

Technical Abstract: The beta-adrenergic receptors (BAR) on the surface of mammalian cells are desensitized when the cell is stimulated by BAR agonists to eliminate excessive response by the cell. Investigations with adipocytes indicate other hormones and substrates also can modulate the individual BAR subtypes. For example, glucocorticoids decrease the B1AR and the B3AR, but increase the B2AR. Insulin decreases B3AR. Thyroid hormones increase the B3AR and butyrate increases B1AR and B2AR, and decreases B3AR. Because porcine adipocytes have unique properties compared to rodent adipocytes, and because porcine adipocytes contain predominantly B1AR compared to the B3AR in rodent adipocytes, we expect the regulation of porcine adipocyte BAR by hormones and substrates to be different than in rodent adipocytes. Isolated porcine adipocytes were incubated for 6 and 21 h without and with dexamethasone, insulin, triiodothyronine, or butyrate. Dexamethasone did not change the total BAR number, but tended to increase the B1AR and B2AR transcript concentrations. Insulin increased the BAR 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 BAR transcript concentrations do not accurately predict the BAR protein concentration (estimated by ligand binding). Results also indicate the BAR in porcine adipocytes are relatively unresponsive to hormones and butyrate compared to rodent-derived adipocytes, described in the literature.