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M Llobera

Publications and source records attributed to M Llobera.

63 records · Page 4Linked to original sources
PubMed1980

Effects of starvation on in vivo gluconeogenesis in hypo- and hyperthyroid rats.

Studies were performed on rats in vivo to determine whether starvation disrupts glucose metabolic balance after removal of the thyroid gland. Intact controls and thyroidectomized rats were injected daily with 0, 0.1, 1.8, or 25 microgram L-T4/100 g BW. Glucose spaces were similar in all groups. The disappearance of labeled glucose from blood was faster in the thyroidectomized rats injected with 25 microgram L-T4 than in the other groups. Starvation enhanced the production of [14C]glucose from [3-14C]pyruvate in all groups, but this effect occurred earlier in control rats and thyroidectomized rats given 1.8 or 25 microgram L-T4 than in thyroidectomized rats given either 0 or 0.1 microgram L-T4. Starvation also enhanced the appearance of radioactivity in liver glycogen 30 min after the injection of [3-14C]pyruvate in all groups, but this effect was lesser in thyroidectomized rats given 0, 0.1, or 25 microgram L-T4 than in other groups. The normal net production of glucose in fed thyroidectomized rats may be the result of a balanced equilibrium between reduced gluconeogenesis and glycolysis. Results obtained in thyroidectomized rats given 25 microgram L-T4 are discussed in terms of the augmented utilization of the newly formed glucose which compensates for their enhanced gluconeogenesis.

Animals↗
PubMed1979

Effects of hypo- and hyper-thyroidism on in vivo lipogenesis in fed and fasted rats.

Thyroidectomized rats (T) daily injected with either 0, 0.1, 1.8 or 25 microgram of L-thyroxine/100 g body wt. were compared with intact controls (C). The appearance of radioactivity 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+1.8 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 thehypothyroid 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+0.1, 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 onlipogenesis of others.

Animals↗
PubMed1979

Adipose tissue cellularity in hypo-and hyperthyroid rats.

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 microgram 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+0.1 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 the 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.

Adipose Tissue↗
PubMed1978

Metabolic response to short periods of starvation in hypo- and hyper-thyroid male rats.

1) Thyroidectomized rats were fed with a low iodine diet, injected daily with 0, 0.1, 1.8 or 25 microgram 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 microgram doses, unchanged in those given the 1.8 microgram doses, unchanged in those given the 1.8 microgram dose increased in those given the 25 microgram one. 3) The liver content of DNA-P, phospholipid-P, proteins and fatty acids was decreased in the rats that did not receive thyroxine, practically recuperated in those receiving 0.1 microgram and normal in those given 1.8 or 25 microgram 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 fed, liver glycogen concentration was low in the rats given 25 microgram of thyroxine. 6) With starvation, the fall in liver glycogen and blood glucose, and the rise in liver acetyl-CoA 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 microgram of thyroxine and in the second one after 24 h in the rats given either 0.1, 1.8 or 25 microgram of thyroxine. 8) The rapid decrease in the availability of carbohydrate stores with starvation in the thyroidectomized 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.

Acetyl Coenzyme A↗
PubMed1977

Effects of hypo and hyperthyroidism on the response to glucose loading of blood glucose, ketones and insulin and liver glycogen as studied in the fasted rat.

After receiving an i.p. glucose load, 24 h fasted thyroidectomized rats showed a progressive increase in blood glucose and a slow decrease in blood ketone bodies. Both liver glycogen and plasma insulin levels showed no differences within 60 min of the glucose administration. It is suggested that the glucose intolerance in these animals is partly due to an insulin deficiency. Thyroidectomized rats treated daily with 25 microgram of L-thyroxine/100 g body weight for 40 days responded to the glucose test with a supranormal and more persistent elevation of blood glucose but with a faster and a greater fall in blood ketone bodies, as compared to controls. Sixty min after the glucose loading, liver glucogen levels were lower and plasma insulin were slightly higher than controls. It is suggested that a diminished extraction of glucose during transhepatic passage can be responsible for the impaired glucose tolerance observed in the hyperthyroid animals.

Animals↗
PubMedDate not supplied

Permanent abnormal response to a glucose load after prenatal ethanol exposure in rats.

Postnatal development of the glucose and insulin balance in offspring of ethanol-treated and control rats has been studied. Newborn rats were separated from their mothers and placed with normal lactating, nonethanol-treated dams. Prenatal exposure to ethanol led to hypoglycemia on the first day of extrauterine life and a general tendency to hyperinsulinemia during the entire postnatal period studied. The glucose-tolerance test in weaned rats (30 days old) gave a greater and faster increase than controls in levels of both glucose and plasma insulin. At adult age (90 days) the response of blood glucose to an oral glucose load in offspring from ethanol-treated mothers was not different from that in offspring from controls, but the insulin response was higher. This abnormal insulin response, such a long time after the end of ethanol exposure, suggests either a permanent alteration in the pancreatic response, or a peripheral insulin resistance and/or differences in the rate of insulin degradation in these animals.

Animals↗