Insulin binding to mouse adipocytes exposed to clenbuterol and ractopamine in vitro and in vivo.

Insulin binding to mouse adipocytes was measured after in vitro (30 min) and in vivo (5 days) exposure to clenbuterol and ractopamine. At 10(-6) M, both agonists decreased insulin binding by 20-30% after a 30 min preincubation at each insulin concentration between 1 and 25 ng/ml. Binding was not decreased if propranolol was present. Scatchard plots suggested that decreased binding was due to a decrease in insulin receptor concentration. Insulin binding was decreased approximately 10% at agonist concentrations as low as 10(-13) M, but binding was not further decreased until concentrations exceeded 10(-9) M. Rate of gain was increased 2-fold by clenbuterol (10 mg/liter of drinking water) and 50% by 500 mg ractopamine/liter, but not by 50 mg ractopamine/liter. Clenbuterol and ractopamine (500 mg/liter) decreased fat pad weight but only clenbuterol increased hind limb muscle mass. Insulin binding following in vivo administration was not influenced by ractopamine at 50 mg/liter, but tended to be increased by clenbuterol and ractopamine at 500 mg/liter. The disparity in results between administering the beta-agonists in vitro or in vivo suggests that counter regulatory factors influenced insulin binding capacity in vivo. Results indicate that ractopamine and clenbuterol can decrease insulin binding to adipocytes but the relevance of this response to decreased fat accretion is not clear.