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 glu cagon binding, by attenuating inhibition of lipolysis, or both. Fat ce lls isolated from abdominal fat were preincubated with T3 for .5 to 24 h before removal of T3 by washing and measurement of lipolysis. Prein cubation of adipocytes with T3 enhanced (P < .05) basal as well as glu cagon-stimulated lipolysis in a dose-response and time-dependent manne r. Enhancement of lipolysis was maximal in the presence of 15 to 150 n M 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 t o enhancement of lipolysis stimulated by a maximal dose of glucagon bu t was greater (P < .05) than its enhancement of basal lipolysis. Pretr eatment of adipocytes with T3 did not alter (P >.05) binding of I-125- glucagon to cell-surface receptors. When fat cells were preincubated w ith 150 nM T3 for 24 h, the ability of somatostatin to inhibit basal a nd glucagon-stimulated lipolysis was reduced (P < .05). Thus, prolonge d 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 li polytic responsiveness to glucagon, and attenuated inhibition of lipol ysis by somatostatin.