Triiodothyronine attenuates somatostatin inhibition of broiler adipocyte lipolysis.

A study with broiler adipocytes in culture was undertaken to determine whether triiodothyronine (T3) potentiates lipolysis by increasing glucagon binding, by attenuating inhibition of lipolysis, or both. Fat cells isolated from abdominal fat were preincubated with T3 for .5 to 24 h before removal of T3 by washing and measurement of lipolysis. Preincubation of adipocytes with T3 enhanced (P < .05) basal as well as glucagon-stimulated lipolysis in a dose-response and time-dependent manner. Enhancement of lipolysis was maximal in the presence of 15 to 150 nM T3. Potentiation of lipolysis by 150 nM T3 was evident at 4 and 24 h but not at .5 h of pretreatment. Overall, T3 enhancement of lipolysis stimulated by submaximal doses of glucagon was similar in magnitude to enhancement of lipolysis stimulated by a maximal dose of glucagon but was greater (P < .05) than its enhancement of basal lipolysis. Pretreatment of adipocytes with T3 did not alter (P > .05) binding of 125I-glucagon to cell-surface receptors. When fat cells were preincubated with 150 nM T3 for 24 h, the ability of somatostatin to inhibit basal and glucagon-stimulated lipolysis was reduced (P < .05). Thus, prolonged exposure of adipocytes to T3 did not increase lipolytic sensitivity to glucagon or binding of glucagon to cell-surface receptors. However, T3-treated adipocytes exhibited enhanced basal lipolysis, enhanced lipolytic responsiveness to glucagon, and attenuated inhibition of lipolysis by somatostatin.