Browsing by Author "Seibel, M. J."

The in vitro metabolism of glycerol by epididymal fat pads from thyroidectomized rats daily injected with either 0, 0.1 or 1.8 μg of L-thyroxine/100 g body wt. was compared with that from intact controls. The basal as well as the adrenalin- or glucose-enhanced release of glycerol to the medium were similar in the tissues from all the groups. The effect of insulin in decreasing the lipolytic action of adrenalin was greater in the thyroidectomized animals treated with either O or 0.1 μg of thyroxine than in the other two groups. The utilization of p-1 4c]glycerol for the formation of CO2 and glyceride glycerol was increased in the thyroidectomized rats; this effect was smaller when the animals were treated with 0.1 μg of thyroxine and disappeared when they were treated with 1.8 μg. In the presence of glucose the difference in utilization of glycerol between the groups disappeared. The formation of fatty acids from glycerol was greater in the presence than in the absence of glucose and was similar in the hypothyroid animals and the controls. The effect of adrenalin in decreasing the utilization of [1-1 4C]glycerol was less in the tissues from hypothyroid rats than in the controls. The decrease of the action of adrenalin by insulin in the tissues from thyroidectomized rats treated with O or 0.1 μg of thyroxine was greater than in the controls. The increased capacity to form glyceride glycerol from glycerol in tissues from hypothyroid animals contributes to the high re-esterification of fatty acids described for these animals. The effect of glucose is explained in terms of its competition with glycerol for the synthesis of a-glycerophosphate.

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.