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Biomedical subjects

G Ribes

Publications and source records attributed to G Ribes.

At least 91 records · Page 5Linked to original sources
PubMed1979

Evidence for a role of exogenous or endogenous hyperlactatemia in insulin secretion in the dog.

Various types of experimental hyperlactatemia were induced in the normal anesthetized dog, and the changes in insulin secretion were measured in the pancreatico-duodenal vein. Hyperlactatemia was induced in the absence or in the presence of an infusion of sodium dichloroacetate (DCA), which activates pyruvate dehydrogenase. 1. Exogenous hyperlactatemia: The infusion of sodium L(+)lactate resulted in a strong increase in blood lactate level which was accompanied by a significant increase in the insulin output from the pancreatico-duodenal vein. The administration of DCA did not counteract the increase in lactate level and did not modify insulin output either. 2. Endogenous hyperlactatemia: This was induced either by pharmacological means: the subcutaneous injection of an antidiabetic biguanide, phenformin (20 mg/kg), or by physiological means: intense muscular work. In both cases an increase in the lactate level and in insulin output was recorded. The administration of DCA suppressed the hyperlactatemia and counteracted the increase in insulin output. These results show that there is a relationship between lactate level and insulin secretion, and give evidence for a role of endogenous lactate in the regulation of insulin secretion.

Animals↗
PubMed1978

[Endogenous hyperlactatemia and insulin secretion].

In the normal anesthetized dog, the endogenous hyperlactatemia induced either by intense muscular work or by a high dose of phenformin (20 mg/kg subtucaneously) is followed by an increase in the pancreaticoduodenal insulin output. A previous perfusion of sodium dichloroacetate (50 mg/kg. h) opposes the hyperlactatemia, and reduces or suppresses the increase in insulin output.

Animals↗
PubMed1978

[Sodium dichloracetate: its application to the therapeutics of experimental hyperiactatemia (author's transl)].

Different types of experimental hyperlactatemia and hyperpyruvicemia with or without lowering of blood pH were induced in anesthetized dogs. The initially studied experimental model was the hyperlactatemia and hyperpyruvicemia with lowering of blood pH induced by the intraduodenal administration of high doses of phenformin. Intravenous perfusion of sodium dichloroacetate (150 mg/kg infused during 20 minutes), which acts on the enzymatic complex of pyruvate dehydrogenase, reduced the hyperiactatemia and hyperpyruvicemia with or without acidosis provoked by phenformin injected intraduodenally (30 mg/kg), by intense muscular work, by hypoxia or by continous perfusion or adrenaline. Exogenous or endogenous insulin combined with sodium dichloracetate reduced the hyperlactatemia and hyperpyruvicemia as well as the changes in blood pH provoked by phenformin, more strongly than did sodium dichloroacetate alone. These findings have been confirmed in the conscious dog.

Acetates↗
PubMed1977

[Lack of concordance in the effect of large doses of phenformin on insulin secretion and glycemia. Tentative analysis].

In the anesthetized dog normal or pretreated with phenformin (20 mg/kg per os) for 7 days, a subcutaneous injection of this biguanide (20 mg/kg) triggers a considerable hyperinsulinemia without concomitant hypoglycemia. The insulin secreted by these animals is biologically active on rat epididymal fat pads. On the other hand, epididymal fat pads of rats pretreated with phenformin display a lower response to insulin than that of non treated rats. The hypoglycemic effect of the same dose of insulin is less important in the normal dog after chronic pretreatment with phenformin.

Adipose Tissue↗
PubMed1977

[Actions of sodium dichloroacetate in combination with insulin on hyperlactatemia and hyperpyruvicemia induced in dogs by phenformin].

In the normal anesthetized dog the combination of insulin, whether of exogenous or endogenous origin, with sodium dichloroacetate provoke a rapid and important reduction of the hyperlactatemia and hyperpyruvicemia induced by the intraduodenal injection of high doses of phenformin. Furthermore this combination prevents the progressive and important lowering of the arterial pH provoked by phenformin.

Acetates↗
PubMed1977

Phospholipases A1 and A2 in subcellular fractions and plasma membranes of Krebs II ascites cells.

A method is described for the localization and characterization of phospholipases A1 and A2 (EC3.1.1.4) in Krebs II ascites cells, particularly in the plasma membranes. Cells were lysed with a Dounce homogenizer in an isotonic sucrose medium. Plasma membranes sediment with mitochondria and lysosomes during subcellular fractionation and are finally isolated on a continuous sucrose gradient. The membranes are localized at two levels in the gradient, at densities of 1.06 and 1.15, in which 5'-nucleotidase (EC 3.1.3.5) activity exhibits a 9- and 21-fold purification, respectively. Total contamination by endoplasmic reticulum, lysosomes, and mitochondria is 17 percent for the low-density membrane fraction and 25 percent for the high-density fraction. The phospholipases A present in Krebs II cells are active at pH 4.0 and pH 7.5. At the 2 pH values, they have A1 and A2 specificities. The intracellular distribution of acidic forms is comparable to that of acid phosphatase (EC 3.1.3.1), while neutral forms are localized like lactate dehydrogenase (EC 1.1.1.27). A small proportion of neutral phospholipase A2 has the same repartition on the sucrose gradient as nicotinamide adenine dinucleotide diaphorase (EF 1.6.4.3), an endoplasmic reticulum marker, and as 5'-nucleotidase, a plasma membrane marker.

Animals↗
PubMed1976

[Effect of sodium dichloroacetate on hyperlactatemia and hyperpyruvicemia induced by phenformin in the dog].

In the normal anesthetized dog a continuous perfusion of sodium dichloroacetate (30 mg/kg.h) prevents the increase in blood lactates and pyruvates as well as the lowering of the arterial pH induced by the intraduodenal administration of phenformin (30 mg/kg). Furthermore a perfusion of sodium dichloroacetate (7.5 mg/kg.mn) during 20 minutes, three hours after the administration of phenformin, tends to improve the utilization of blood lactates and pyruvates.

Acetates↗
PubMed1975

[Consequences of the chronic administration of phenformine on the blood thiamine level in the dog].

The chronic oral administration of phenformin (20 mg/kg daily during 8 days) to the normal concious dog provokes a decrease in the fasting thiamine levels of plasma and erythrocytes. During intragastric loading tests with thiamine hydrochloride (30 mg/kg), carried out during the chronic treatment with the biguanide, the curve of plasma hyperthiaminemia is increased. The authors suggest an explanation for these apparently contradictory results.

Animals↗
PubMed1975

[Experimental study of glipizide. A comparison with other hypoglycemic sulfonamides (author's transl)].

Glipizide is a new hypoglycaemic sulphonylurea. In this work we have studied experimentally the hypoglycaemic activity of this drug, its insulin secretory effect and its action on the development of the islets of Langerhans. Studies in the dog: In the normal conscious dog the hypoglycaemic effect of the drug was studied when increasing doses (0,03 mg/kg, 0,05 mg/kg, 0,07 mg/kg and 0,09 mg/kg) were injected intravenously. The hypoglycaemic effect of the drug occurred rapidly, reaching a maximum in about 30 minutes. The relative potency of glipizide was determined in comparison with tolbutamide. Under our experimental conditions, glipizide proved to be on average 99 times more active than tolbutamide when the doses were evaruated by weight; when the doses were expressed in moles it was 163 times more active. Plasma insulin levels manifested an increase at the first minute. This rose rapidly to a maximum at 5 to 15 minutes after the injection. Following this, insulinemia decreased and the values recorded at 60 minutes were about the same as the starting values. There is a linear relation between the logarithm of the dose and the area under the insulin curve measured for the first sixty minutes. After oral administration to the normal dog, glipizide (081 mg/kg and 1mg/kg) provoked a hypoglycemia manifested after a 30 to 60 minutes latent period. With the dose of 1 mg/kg the maximal effect on blood glucose level was reached between 1,30 and 3 hours, depending on the animal. Plasma insulin levels also increased after a latent period which varied from one animal to another. The dogs presenting the earliest increase in insulinemia were those in which glycemia drops most rapidly. Comparison with other sulfonamides (glibenclamide, glisoxepide and tolbutamide) showed that the hypoglycemic action of glipzide was very similar to that of glisoxepide and that it occurred much earlier than with glibenclamide. The insulin secretory effect of glipizide also occurred much earlier than that of glibenclamide, manifesting itself as early as that of glisoxepide and tolbutamide. Studies on the isolated rat pancreas: On the isolated rat pancreas perfused with Krebs-Ringer solution containing glucose (1,5 g/l), glipizide (10 mug/I) considerably increased the amount of secreted insulin. The stimulation of insulin secretion occurred rapidly and persisted powerfully during the entire duration of the infusion. It faded out progressively after stopping the infusion and the secretion remained higher than the control secretion during the following 45 minutes of the experiment. A concentration as low as 0,5 mug/I provoked a distinct increase of insulin secretion. Studies on the development of the islets of langerhans in the mouse: The prolonged administration of glipizide (100 mg/kg daily for 35 days) increased the "insular index", which is directly proportional to the islet weight, by 27%. Therefore this product possesses betacytotrophic activity...

Administration, Oral↗