EFFECTS OF TRIIODOTHYRONINE ADMINISTRATION ON DIETARY [C-14] TRIOLEINPARTITIONING BETWEEN DEPOSITION IN ADIPOSE-TISSUE AND OXIDATION TO [C-14] CO2 IN AD LIBITUM-FED OR FOOD-RESTRICTED RATS

Refeeding a chow meal containing [1-C-14]triolein to food-restricted r ats results in increased accumulation of [C-14]lipid in carcass and ep ididymal adipose tissue and lower oxidation to [C-14]CO2 compared to a d libitum-fed rats (Biochem. J. 285, 773-778, 1992). In the present ex periments the effects of treatment with triiodothyronine (T3) for thre e days on lipid accumulation in refed food-restricted rats has been ex amined. T3 decreased accumulation of [C-14]lipid in carcass and epidid ymal adipose tissue (32 and 77%, respectively) of food-restricted rats on refeeding the chow-[1-C-14]triolein meal. This decreased accumulat ion of [C-14]lipid was accompanied by increased [C-14]CO2 production ( 77%) and decreased heparin-elutable lipoprotein lipase activity in the epididymal fat pad (90%) and subCUtaneous adipose tissue (80%). ACCum ulation of [C-14]lipid in the latter did not decrease significantly. I n contrast, T3 treatment of ad libitum-fed rats increased [C-14]lipid deposition in carcass (44%) and in subcutaneous adipose tissue (240%) on refeeding, when compared to untreated ad libitum rats. Lipoprotein lipase activity in the two adipose tissue depots of the refed ad libit um + T3 rats, however, decreased. Thus, the effects of T3 on [C-14]lip id deposition are adipose-tissue-depot-specific and depend on the prev ious dietary intake (over 14 days) of the rat. T3-treatment increased the lipoprotein lipase activity released from perfused hearts to a sim ilar extent in both food-restricted and ad libitum-fed rats compared t o the corresponding untreated groups. The rates of lipogenesis in-vivo in liver, epididymal and subcutaneous adipose tissue of food-restrict ed rats refed chow were not altered by T3. It is concluded that the in creased deposition of dietary lipid in the food-restricted rat can be partially reversed by treatment with T3, suggesting that the low-T3 st ate associated with this condition may be in part responsible.