1. Investigación

1.8 or 25 µg of L-thyroxine/100 g body wt. were compared with intact controls (C). The appearance of radioacitvity in fatty acids 30 min after the i.p. injection•of (3-14C)pyruvate was reduced in adipose tissue and enhanced in liver of T+25, being no differences between the other groups and C. ( 14C)- Fatty acids are reduced with 3 h of fasting only in the adipose tissue of T+ 1.8 and C, while 24 h produces a reduction in liver in the T+ 1.8, T+25 and C, and in adipose tissue in the T+l.8 and C animals. The highest percentage of radioactivity was observed in the liver glyceride glycerol fraction, being greater in T+25 than in the other groups. Fasting produces an increment in the ( 14C)-glyceride glycerol fraction. being significant only in the hypothyroid animals in both liver and adipose tissue. The most sensitive parameter to fasting was the formation of ( 14C)-non-saponifiable lipid in both the C and T+ 1.8 animals, while it does not change in T+0 or T+0.I, but is enhanced within 24 h in the adipose tissue of T + 25. It is proposed that most of the observed changes are due to the other endocrine disfunction s which appear in hypo- and hyperthyroidism, as the in vivo results do not comply with in vitro effects of thyroxine on lipogenesis of others.

To determine adipose tissue cellularity in hypo- and hyperthyroidism, male rats were thyroidectomized after weaning (T) and injected daily with either 0, 0.1, 1. 8, or 25 µg of L-thyroxine/100 g body weight for 40 days. They were compared with intact controls (C). Both epididymal fat-pad weight and adipocyte diameter were reduced in T+0, T+0.1 and T+25 animals. When corrected per unit of body weight, the diameters of adipocytes from T+0 and T+0. l animals were larger than in the other groups. Those same animals have reduced absolute adipocyte number but not when corrected per unit of body weight. The fat-pad protein concentration varied conversely with the fat cell diameter. These findings indicate that thyroid hormone deficiency reduces thf proliferation of fat cells in parallel with body growth while hyperthyroidism causes reduction in the size, but not the number, of fat cells which corresponds to its depletion of fat storage.

1) Thyoridectomized rats were fed with a low iodine diet, injected daily with 0, 0.1, 1.8 or 25 µg of L-thyroxine/100 g body wt., and compared with intact controls. 2) Plasma protein-bound iodine was decreased in the rats given the 0 and 0.1 µg doses, unchanged in those given the 1.8 µg doses, unchanged in those given the 1.8 µg dose increased in those given the 25 µg one. 3) The liver content of DNA-P, phospholipid-P, proteins and fatty acids was decreased in the rats that did not receive thyr.oxine, practically recuperated in those receiving 0.1 µg and normal in those given 1.8 or 25 µg of thyroxine. 4) 3 h of starvation produced a reduction in the liver content of total fatty acids that disappeared after 24 h. 5) When fod, liver glycogen concentration was low in the rats given 25 µg of thyroxine. 6) With starvation, the fall in liver glycogen and blood glucose, and the rise in liver acetylCoA and citrate and blood glycerol concentrations were faster in the thyroidectomized rats that did not receive thyroxine than in the other groups. 7) The rise in plasma free fatty acid and blood ketone bodies concentrations were similar in all the groups, the greater level of the first parameter being observed after 6 h of starvation in the rats given 25 µg of thyroxine and in the second one after 24 h in the rats given either 0.1, 1.8 or 25 µg of thyroxine. 8) The rapid decrease in the availability of carbohydrate stores with starvation in the thyroidcctomized rats could be responsible for their fast call for lipid utilization. The slower response to fasting in the hyperthyroid animals is probably a consequence of their reduced amount of endogenous substrates to be mobilized.