Effects of triiodothyronine administration on dietary [14C]triolein partitioning between deposition in adipose tissue and oxidation to [14C]CO2 in ad libitum-fed or food-restricted rats.
Refeeding a chow meal containing [1-14C]triolein to food-restricted rats results in increased accumulation of [14C]lipid in carcass and epididymal adipose tissue and lower oxidation to [14C]CO2 compared to ad libitum-fed rats (Biochem. J. 285, 773-778, 1992). In the present experiments the effects of treatment with triiodothyronine (T3) for three days on lipid accumulation in refed food-restricted rats has been examined. T3 decreased accumulation of [14C]lipid in carcass and epididymal adipose tissue (32 and 77%, respectively) of food-restricted rats on refeeding the chow-[1-14C]triolein meal. This decreased accumulation of [14C]lipid was accompanied by increased [14C]CO2 production (77%) and decreased heparin-elutable lipoprotein lipase activity in the epididymal fat pad (90%) and subcutaneous adipose tissue (80%). Accumulation of [14C]lipid in the latter did not decrease significantly. In contrast, T3 treatment of ad libitum-fed rats increased [14C]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 libitum+T3 rats, however, decreased. Thus, the effects of T3 on [14C]lipid deposition are adipose-tissue-depot-specific and depend on the previous dietary intake (over 14 days) of the rat. T3-treatment increased the lipoprotein lipase activity released from perfused hearts to a similar extent in both food-restricted and ad libitum-fed rats compared to the corresponding untreated groups. The rates of lipogenesis in-vivo in liver, epididymal and subcutaneous adipose tissue of food-restricted rats refed chow were not altered by T3. It is concluded that the increased deposition of dietary lipid in the food-restricted rat can be partially reversed by treatment with T3, suggesting that the low-T3 state associated with this condition may be in part responsible.
Cruz
M L
ML
Metabolic Research Laboratory, Nuffield Department of Clinical Medicine, Radcliffe Infirmary, Oxford, UK.
Williamson
D H
DH
D000273:Adipose Tissue / Q000201:enzymology / Q000378:metabolism*; D000821:Animal Feed; D000818:Animals; D001835:Body Weight; D002245:Carbon Dioxide / Q000032:analysis*; D002250:Carbon Radioisotopes; D004032:Diet; D005227:Fatty Acids / Q000096:biosynthesis; D006980:Hyperthyroidism / Q000378:metabolism; D008071:Lipoprotein Lipase / Q000378:metabolism*; D008297:Male; D009206:Myocardium / Q000201:enzymology; D010084:Oxidation-Reduction; D051381:Rats; D017208:Rats, Wistar; D014018:Tissue Distribution; D014284:Triiodothyronine / Q000097:blood / Q000494:pharmacology*; D014304:Triolein / Q000008:administration & dosage / Q000493:pharmacokinetics*; D014316:Tritium
D002250:Carbon Radioisotopes; D005227:Fatty Acids; D014284:Triiodothyronine; D014316:Tritium; D014304:Triolein; D002245:Carbon Dioxide; D008071:Lipoprotein Lipase