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Biomedical subjects

G Ribes

Publications and source records attributed to G Ribes.

At least 73 records · Page 4Linked to original sources
PubMed1984

Effects of fenugreek seeds on endocrine pancreatic secretions in dogs.

The components of fenugreek seeds were separated and analyzed to determine which fraction of the seed had hypoglycemic activity. These fractions were administered orally to normal or diabetic dogs for 8 days. The effect on blood glucose and pancreatic hormones was studied in normal dogs. The lipid extract had no effect; the defatted fraction (50.2% fibers: gum 17.7%, hemicellulose 22%, cellulose 8.3%, lignin 2.2%) lowered basal blood glucose level, plasma glucagon and somatostatin levels and reduced the orally induced hyperglycemia. The addition of this fraction to the insulin treatment resulted in a decrease of hyperglycemia and glycosuria in diabetic dogs. The results indicate that the defatted part is responsible for the antidiabetic action. However, the present study does not permit one to know whether the effects are caused by an unknown pharmacological compound or by the gastrointestinal action of fibers.

Animals↗
PubMed1984

[Importance of the cholinergic nervous system in the postprandial secretion of insulin in dogs].

This work was designed to study the evolution of blood glucose and plasma insulin after food intake. The experiments were performed on normal conscious dogs. Blood was sampled from the jugular vein. The animals had a meal consisting of meat (30 g/kg) or received a nutrient undergoing direct resorption, glucose (1 g/kg). 10 minutes before the intake of meal or glucose, some animals received an i.v. injection of atropine (0.2 mg/kg). The ingestion of meat did not change blood glucose level, but induced a biphasic increase in insulin secretion, the second phase persisted at least for 240 minutes. The previous injection of atropine totally suppressed the increase in insulinemia. The oral intake of glucose induced hyperglycemia and a biphasic increase in insulinemia. The injection of atropine suppressed the first phase of hyperinsulinemia; then the increase of insulinemia evolved in parallel to hyperglycemia. These results, observed in the dog, underline the importance of the cholinergic nervous system not only during the early phase of insulin secretion (cephalic phase), but also during a prolonged post-prandial period.

Animals↗
PubMed1984

Effect of LN 5330 on insulin release and calcium uptake by isolated rat islets of Langerhans. Comparison with diazoxide.

The effect of a new benzothiadiazine derivative, LN 5330, was studied on insulin release and 45Ca++ uptake by isolated rat islets of Langerhans. LN 5330 (0.1 mmol/l) significantly inhibited both insulin release and calcium uptake of islets incubated in MEM (glucose 8.3 mmol/l). This effect was comparable to that of diazoxide. The withdrawal of LN 5330 from the medium resulted in a significant increase of insulin release and calcium uptake by the islets during a subsequent incubation in MEM (glucose 8.3 mmol/l). In contrast, after withdrawal of diazoxide, insulin release and calcium uptake by the islets were not different from the controls. These results suggest a dual action of LN 5330: an effect, similar to that of diazoxide, responsible for the inhibition of insulin release in the presence of the drug; and an effect, specific to LN 5330, which would induce cellular changes, the consequence of which appears only upon withdrawal of the drug.

Animals↗
PubMed1983

Differences between the effects of adrenaline and noradrenaline on insulin secretion in the dog.

The effects of adrenaline and noradrenaline infusions on pancreaticoduodenal venous insulin output were studied in anaesthetized normal dogs. Two experimental protocols were used. In the first, the dogs had a normal blood glucose level at the start of the catecholamine infusion (normoglycaemic dogs). In the second, the animals were made hyperglycaemic by a continuous glucose infusion (hyperglycaemic dogs). In the normoglycaemic dogs, adrenaline (0.5 micrograms X kg-1 X min-1) provoked hyperglycaemia accompanied by an increase in insulin output. Noradrenaline (0.5 micrograms X kg-1 X min-1) also caused an increase in insulin output but without any significant change in blood glucose. In hyperglycaemic dogs, adrenaline (2 micrograms X kg-1 X min-1) reduced the insulin response and enhanced the hyperglycaemia; noradrenaline (2 micrograms X kg-1 X min-1) markedly increased the insulin response (+ 2250%) without any significant change in blood glucose. Propranolol (0.3 mg/kg, IV) prevented the increase of insulin induced by noradrenaline. These findings show that, in the normal dog, adrenaline and noradrenaline infusions can produce opposite effects on insulin response depending on the experimental conditions.

Animals↗
PubMed1983

Stimulation of pancreatic polypeptide secretion in the dog by hypoglycemic agent HB 699.

HB 699 is a hypoglycemic agent that has a structural similarity to glibenclamid but does not contain the sulfonylurea group. We have studied the effects of HB 699 and the sulfonylurea glipizide on pancreatic polypeptide (PP) and insulin secretion in the dog. Both HB 699 and glipizide stimulated insulin release and caused hypoglycemia in normal dogs. The secretion of PP was stimulated by HB 699 before the onset of hypoglycemia, whereas, following glipizide administration, PP secretion increased only after the onset of hypoglycemia. As expected, in alloxan-diabetic dogs neither substance affected plasma insulin or blood glucose levels. There was, however, a stimulation of PP secretion by HB 699 that was not observed with glipizide. It appears therefore that HB 699, in contrast to glipizide, stimulates PP secretion in the absence of any changes in circulating glucose and insulin concentrations. The direct action of HB 699 on the pancreas was shown by stimulation of insulin and PP secretion in the in vitro perfused uncinate process. In view of its direct pancreatic actions, HB 699 may prove a useful tool for further study of PP secretory mechanisms.

Animals↗
PubMed1983

Involvement of Ca2+ in the impaired glucose-induced insulin release from islets cultured at low glucose.

Islet culture at a low glucose concentration results in a progressive impairment of glucose-induced insulin release. The role of Ca2+ in this defect was studied by comparing rat islets cultured for 6 days either at 8.3 mM (control) or 2.8 mM glucose. For measurement of 45Ca content and 45Ca2+ efflux, islets were kept in the presence of 45Ca2+ throughout. In islets cultured at 8.3 mM glucose, stimulation with 16.7 mM glucose during perifusion caused a typical biphasic pattern of insulin release paralleled by an increase in the rate of 45Ca2+ efflux. Both effects of glucose were markedly reduced in islets kept at 2.8 mM glucose, despite a similar insulin content. Islet 45Ca content was reduced. Both 45Ca content and insulin release were restored when islets were kept for an additional 24 h at 8.3 mM glucose. Insulin release induced by 3-isobutyl-1-methylxanthine (IBMX) or alpha-ketoisocaproic acid was not impaired, demonstrating that there is no generalized release defect. In contrast, glyceraldehyde- or K+-induced release was decreased. In islets maintained at 2.8 mM glucose, the stimulatory effect of glucose on Ca2+ uptake and the inhibitory effect on Ca2+ efflux (in the absence of Ca2+) were found to be operative. A defect may therefore lie distal to the Ca2+ uptake step involving either the mechanism by which glucose uses cellular Ca or another step yet to be identified.

Animals↗
PubMed1983

[Effects of clonidine on the insulin secretion from the isolated, perfused pancreas of rats and newborn dogs].

The effects of clonidine were studied on insulin secretion from the isolated pancreas of the rat and newborn dog perfused in presence of 8.3 mmol/l glucose. The effects were compared to those induced by adrenalin. In the rat, clonidine and adrenalin infused for 30 minutes at 0.01 mumol/l caused an immediate and marked inhibition of insulin release (-- 79.1 +/- 2.6% for clonidine and -- 75.7 +/- 4.7% for adrenaline at the 15th minute of infusion). The inhibition due to clonidine has not completely disappeared 15 minutes after stopping the infusion. In the dog, both substances also induced an immediate and marked inhibition; but the effect of adrenalin disappeared before the end of the infusion. It follows that the inhibitory effect of clonidine on insulin secretion is more durable than that of adrenalin.

Animals↗
PubMed1982

Effects of chronic administration of sodium 2 chloropropionate in normal and diabetic dogs.

Pancreatic hormonal and metabolic responses to chronic administration of sodium 2 chloropropionate (2 CP) were investigated in conscious dogs. We subcutaneously administered 2 CP daily for 7 days at the dose of 0.58 mmol/kg (62.5 mg/kg) in normal dogs and those rendered diabetic by injection of alloxan (0.24 mmol/kg, i.v.). In the normal dogs, the chronic administration of 2 CP provoked a decrease in blood lactate and pyruvate but not in blood glucose concentrations. Urinary oxalate was not increased by the daily injection of 2 CP. Blood ketone body concentrations progressively increased after the third day of treatment. At the same time, plasma cholesterol slowly decreased. The 2 CP chronic administration did not change the plasma somatostatin, glucagon, and insulin levels. In the alloxan-diabetic dogs, treated with insulin alone, blood glucose, ketone body concentrations, and plasma somatostatin and glucagon levels were elevated. The adjunction of 2 CP with insulin injections resulted in a fall in blood lactate and pyruvate levels and a progressive decrease of blood glucose concentrations. Blood ketone bodies, which were already high at the start, were not affected when 2 CP was combined with insulin. The hypersomatostatinemia was not decreased, whereas the hyperglucagonemia was considerably reduced. So, I/G ratio, which was strongly decreased with insulin alone, progressively returned to normal values. As to urinary compounds, 2 CP induced a marked decrease in glucosuria and did not change the elevated urinary beta hydroxybutyrate levels. In conclusion, these findings show that the adjunction of sodium 2 chloropropionate to insulin in diabetic dogs results in a reduction of hyperglycemia and hyperglucagonemia.

Animals↗
PubMed1982

[Effect of chronic administration of an acylamino alcoyl derivative of benzoic acid, HB 699, on the pancreatic polypeptide secretion in the dog].

HB 699, a hypoglycemic and insulin stimulating agent, which does not belong to the sulphonylurea group, was administered per os to the dog at the dose of 15 mg/kg, daily for 14 days. This agent induced an increase in fasting plasma levels of pancreatic polypeptide, without modifying blood glucose, insulin, glucagon and somatostatin levels.

Administration, Oral↗
PubMed1981

Effect of a new hypoglycaemic agent (HB 699) on the in vivo secretion of pancreatic hormones in the dog.

The effects of HB 699, a non-sulphonyl urea acyl-amino-alcyl benzoic acid derivative, were studied in unanesthetized dogs. Changes in blood glucose and plasma insulin, glucagon, pancreatic polypeptide and somatostatin were measured after a single intravenous injection. HB 699 caused hypoglycaemia and stimulated insulin secretion in a dose-dependent manner. The effects of HB 699 (40 mg/kg) on pancreatic hormone secretion were compared to those of tolbutamide give at a dose (12 mg/kg) which induced a similar maximal hypoglycaemia. Both drugs caused a similar increase in insulin release (180 +/- 32% for tolbutamide and 240 +/- 41% for HB 699) lasting for approximately 1 hour. Despite hypoglycaemia, plasma glucagon concentrations were unaltered by either substance. HB 699 caused a marked increase in the secretion of pancreatic polypeptide (220 +/- 60% at 30 min) for up to 2 hours, whereas tolbutamide caused no significant change in plasma pancreatic polypeptide levels. In contrast, while tolbutamide caused a significant (45 +/- 12%) but short-lived increase in plasma somatostatin concentrations, HB 699 had no significant effect.

Animals↗
PubMed1981

Rapid changes in calcium content of rat pancreatic islets in response to glucose.

To study whether glucose affects total islet Ca content, 45Ca content was measured in isolated pancreatic islets, loaded with 45Ca++, during up to 48 h in tissue culture conditions. In islets maintained in 2.8 mM or 8.3 mM glucose the 45Ca content did not increase further after the 24 h, indicating that, at this time point, islets are in isotopic equilibrium. Islets maintained in 8.3 mM glucose had a significantly higher Ca content of 9 pmol/islet than the 5 pmol of islets maintained in 2.8 mM glucose. An increase in the glucose concentration from 2.8 mM to 8.3 mM after 24 h, in the continued presence of 45Ca++, caused a significant and rapid augmentation of the Ca content (+2.5 pmol/islet/5 min). Conversely, a decrease of the glucose concentration from 8.3 mM to 2.8 mM resulted in a rapid loss of cellular Ca. Thus, glucose rapidly affects the total Ca content of islets, the turnover of Ca amounting to approximately 10% of the total content per minute. Islets maintained in 8.3 mM glucose for 24 h exhibited a greater insulin release in response to 16.7 mM glucose than islets maintained for 24 h in 2.8 mM glucose. The increased response, however, was not correlative with the difference in Ca content.

Animals↗
PubMed1981

Effects of a new benzothiadiazine derivative, LN 5330, on insulin secretion.

The effect of a new benzothiadiazine derivative, LN 5330, was studied on insulin secretion from isolated perfused rat pancreas. LN 5330 (1 mg/l to 125mg/l) induced an inhibition of insulin secretion evoked by glucose 1.5 g/l. In all cases the inhibition recorded during the infusion was followed by an increase in insulin secretion after stopping the infusion. This increase was biphasic with LN 5330 at 1, 3, 5 and 15 mg/l. The insulin increase as well as the insulin decrease were dose-related but the additional amount of insulin released after stopping LN 5330 was higher than the amount of insulin which was not released during the infusion of LN 5330. Diazoxide and somatostatin were infused at concentrations which induced an inhibitory effect similar to that obtained with LN 5330 (15 mg/l). When diazoxide infusion was stopped, only a very transient overshoot appeared and after somatostatin infusion insulin secretion progressively returned to reference value. It is concluded that LN 5330 by inducing inhibition and secondary increase of insulin output might be a valuable tool for studying the mechanisms involved in insulin secretion.

Animals↗
PubMed1981

[Toxic effect of the combination of propranolol and phenformin combination in anesthetized dogs].

Phenformin (20 mg/kg subcutaneously) as well as propranolol (0.3 mg/kg. i.v.) induced an increase in blood lactate level in the normal anesthetized log; with phenformin a slight decrease in the arterial pH was noted. The combined administration of phenformin (20 mg/kg subcutaneously) and propranolol (0.3 mg/kg. i.v.) induced a more rapid increase in lactate level, a slight reduction of arterial pH and led to the death of the animals in all cases. After a chronic treatment by phenformin (20 mg/kg daily orally during 7 days, the administration of phenformin (20 mg/kg subcutaneously) induced lactic acidosis in 3 out of the 8 animals and death within 150 minutes. In the animals pretreated by phenformin, the combined administration of phenformin (20 mg/kg subcutaneously) and propranolol (0.3 mg/kg i.v.) caused the death of all the animals without the occurrence of lactic acidosis. These results point to the possible toxicity of the propranolol-phenformin combination.

Anesthesia↗
PubMed1981

Sodium 2-chloropropionate: its effects on experimental hyperlactatemia in the dog.

The effects of sodium 2-chloropropionate (2-CP), an activator of pyruvate dehydrogenase were studied on normal dogs. Two sets of experiments were performed: 1) 2-CP was administered to conscious dogs by gastric intubation at 1.16 mmol/kg b.wt. The drug induced a decrease in blood lactate and pyruvate levels but did not produce any significant change in blood glucose, blood beta-hydroxybutyrate or acetoacetate levels. 2) 2-CP given i.v. (1.16 mmol/kg b.wt. during 20 min) rapidly reduced the experimental hyperlactatemia induced by continuous infusion of epinephrine (1.5 microgram/kg . min) or fructose (0.5 g/kg . hr). Considering the metabolic side effects induced by dichloroacetate, another activator of pyruvate dehydrogenase, we suggest that use of 2-CP rather than dichloroacetate might be of interest, particularly in the treatment of hyperlactatemia or lactic acidosis.

Anesthesia↗
PubMed1980

[Hypolactatemic effect of sodium difluoroacetate].

In the anesthetized rat, the intraperitoneal injection of 40 mg/kg sodium difluoroacetate (DFA), an activator of the pyruvate dehydrogenase, counteracted the hyperlactatemia induced by a high dose of phenformin (40 mg/kg) injected concomitantly. In the normal conscious dog, the administration of 150 mg/kg by gastric intubation decreased the blood lactate and pyruvate levels; however, this effect was less marked than that produced by the same dose of sodium dichloroacetate (DCA).

Animals↗