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T Torlińska

Publications and source records attributed to T Torlińska.

30 records · Page 2Linked to original sources

Triiodothyronine effect on some parameters of carbohydrate metabolism in rat blood and liver. I. In vivo effect of triiodothyronine on liver glycogen content, blood metabolites and serum glycogenolytic activity.

Short (7 days) T3-treatment has no influence on the plasma glucose and FFA concentration and blood lactate level, as well as on the hepatic glycogen content in the rats. The rise in T3 levels, observed in our study, was accompanied by a fall in T4 concentrations, indicating suppression of the endogenous T4 production. On the other hand, glycogenolytic activity of rat serum in vitro is the highest in the system: control liver slices-serum of rats pretreated with T3 as compared to the system: control liver slices-control serum. These observations may lead to conclusions, that serum of rats pretreated with T3 contains factors exhibiting the greater ability to mobilize glucose from liver slices than the control serum (euthyroid). The possibility, that pretreatment with T3 may cause a decrease in the number and/or affinity of beta-adrenergic receptors in the rat liver, is discussed.

Animals↗

Hyperthermia effect on lipolytic processes in rat blood and adipose tissue.

Rats anaesthetized with Brevinarcon were placed in a high-temperature chamber (air temperature 50 degrees C, relative humidity 50%) for induction of hyperthermia (rectal temperature 41.0 +/- +/- 0.5 degrees C). The control group comprised rats anaesthetized in the same way but kept at room temperature. In the serum in both groups glucose, free fatty acids, immunoreactive insulin, lipolytic activity and ability to mobilize lipids in vitro were determined. It was shown that the glucose and free fatty acid levels and the activity mobilizing serum lipids in vitro in the rats subjected to hyperthermia were lower than in the control group by 12%, 23% and 150% respectively. The lipolytic activity of the serum of rats subjected to hyperthermia was 42% higher, and the level of immunoreactive insulin rose by about 224% in relation to the control group. These results point to inhibition of lipolysis in the adipose tissue with simultaneous activation of intravascular lipolysis during hyperthermia in rats.

Adipose Tissue↗

Effect of 2-deoxy-D-glucose on lipolytic processes in blood and adipose tissue of rat.

The effect of 2-deoxy-D-glucose on lipolytic processes in the blood and adipose tissue was studied. Rats treated with this antimetabolite showed a significant increase in serum glucose, FFA and glycerol level, as well as in the lipid mobilizing activity. On the other hand, the lipolytic activity of rat serum decreased when compared to control group. From these results it may be concluded that during hypothermia induced by administration of 2-deoxy-D-glucose intracellular, but not intravascular, lipolysis is enhanced.

Adipose Tissue↗

Effects of insulin and beta-adrenergic blockade on certain indicators of carbohydrate metabolism in the blood and tissues of rats during short-lasting hypothermia.

Administration of insulin 1 i.u./100 g of body weight to hypothermic rats causes a fall of glucose and lactate levels in the serum and a rise in myocardial glycogen level in relation to the group of control rats kept at room temperature and to the group of rats subjected only to hypothermia. Beta-adrenergic blockade (propranolol 0.6-1 mg/kg) caused no changes in the levels of carbohydrate metabolites in the serum of hypothermic rats but raised the myocardial glycogen level by 42% in relation to the animals subjected only to hypothermia. Simultaneous administration of both these agents during hypothermia produces a fall of the serum levels of glucose and pyruvate with a rise in the level of lactate, and raises the glycogen level in the myocardium (by about 161%) and in the skeletal muscle (by 54%) in relation to the rats subjected to hypothermia alone. Insulin and/or propranolol fail to prevent glycogen reserve exhaustion in the liver of hypothermic rats which could be due to activation of non-blocked alpha-adrenergic receptors or to the action of yet another glycogenolytic agent, e.g. glucagon, during hypothermia.

Acute Disease↗

Somatostatin effect on the level of adenyl nucleotides in the blood and tissues of rats during short-lasting hypothermia.

Short-lasting hypothermia during thiobutabarbital general anaesthesia causes no decrease of the absolute ATP level in the blood and liver of rats. The adenylate energy charge in the tissues is relatively high - 0.86 in the liver and 0.85 in the muscles, which might be an evidence of a significant "energy sparing" during moderate hypothermia (26 +/- 1 degree C). Somatostatin in a dose of 20 micrograms/kg of body weight given to the rats during hypothermia decreased the ATP level, the ATP/ADP ratio and the adenylate energy charge in the studied tissues, especially in the liver, evidencing increased intensity of catabolic processes caused by the inhibitory action of somatostatin on the release of insulin and glucagon, among other hormones, and on the change of the insulin/glucagon ratio.

Adenosine Diphosphate↗

Effect of certain factors modifying the lipid-mobilizing activity in vitro in the serum of rats during hypothermia.

The serum of hypothermic animals shows in vitro the ability of mobilizing fatty acids from the adipose tissue. This ability is quantitatively comparable to the lipolytic activity of glucagon but is lower than that of adrenaline. Propranolol decreases the lipid-mobilizing activity in the serum of hypothermic animals in vitro. Similarly insulin added to the medium with the serum of hypothermic animals decreased the lipid-mobilizing activity.

Adipose Tissue↗

In vitro serum glycogenolytic activity in rats during hypothermia induced with 2-deoxy-D-glucose.

During hypothermia induced by intraperitoneal administration of 2-deoxy-D-glucose (600 mg/kg of body weight) the serum levels of glucose and FFA rise and the hepatic glycogen content falls in relation to rats in control group. The glycogenolytic activity of the serum in vitro determined against liver slices is also higher in the group of rats receiving 2-DG. The obtained results point to an activation of the glycogenolysis process and glycolysis in the organism of rats after administration of hypothermia-inducing doses of 2-DG.

Animals↗

Effect of hyperthermia on blood levels of corticosterone and certain metabolites in rats during thiobutabarbital anaesthesia.

No changes were found in the serum levels of corticosterone, pyruvate and lactate in rats during general anaesthesia with thiobutabarbital (Brevinarcon) subjected to short-lasting hyperthermia in a high-temperature chamber (air temperature 50 degrees C, relative humidity 50%) in relation to a control group of rats during similar general anaesthesia at room temperature. However, in the serum of rats during hyperthermia (rectal temperature 40-41 degrees C) the glucose level was about 52% lower and FFA were about 39% lower than in rats kept under normothermic conditions (rectal temperature 36.5-37.5 degrees C) which may point to an increased requirement of tissues for energy-yielding substrates at higher body temperatures and/or increased insulin secretion.

Anesthesia↗

Activity of certain enzymes in the mitochondrial and cytoplasmic fractions of liver cells, myocardium and skeletal muscle of the rat during short-lasting hypothermia.

During short-lasting hypothermia in rats the activity of isocitrate dehydrogenase (E.C.1.1.1.42) and malic dehydrogenase (E.C.1.1.1.37) was determined in the mitochondrial fraction of liver cells, myocardial cells and skeletal muscle fibres of the femoral muscle and no statistically significant differences were found between the obtained values and those in a control group. On the other hand, the activity of glucose-6-phosphate dehydrogenase (E.C.1.1.1.49) in the cytoplasmic fraction of these tissues was decreased in the hypothermic rats by 46% in the liver, by 50% in the myocardium and by 59% in the skeletal muscle of the thigh. A possible cause of this reduced activity of this enzyme in hypothermia could be changes in the structure of the enzymatic protein, deficiency of the hormone activating the enzyme, that is insulin, and/or inhibition of the pentose-phosphate cycle by fatty acids released in excess.

Animals↗