PubMed Health⌕ Search

Biomedical subjects

J C Basabe

Publications and source records attributed to J C Basabe.

At least 55 records · Page 3Linked to original sources
PubMed1976

Evidence for a hypophyseal factor that stimulates insulin secretion by the pancreas (insulotrophine?)

The continuous infusion of glucose (1 mg/kg/min) via the carotid artery in anesthetized dogs produced a biphasic pattern of insulin secretion. The first peak reached a maximum 3 min after glucose infusion and decreased to basal level at 7 min. As long as glucose infusion persisted a slow and maintained increase in insulin level in the pancreatico-duodenal vein was observed. The same amount of glucose infused in to the carotid arteries of hypophysectomized dogs, failed to induce any change in plasma insulin level. Plasma sample obtained from the jugular vein of dogs receiving glucose via the carotid arteries were infused into a second dog via the pancreatico-duodenal artery. One minute after the onset of infusion a rise in insulin was observed in the pancreatico-duodenal vein. The stimulating effect was not due to the high blood glucose level present in the jugular vein of dogs undergoing the cephalic glucose infusion. Infusion through the pancreatico-duodenal artery of a glucose solution at a concentration equal to the highest blood glucose level observed in the jugular vein did not evoke insulin secretion. Plasma samples obtained from the jugular vein of dogs receiving saline via the carotid arteries did not evoke insulin secretion when receiving into the pancreatico-duodenal arteries of dogs. Pancreatic infusion of plasma obtained from the jugular vein of hypophysectomized dogs infused glucose through the carotid arteries did not evoke any pancreatic response. These findings are demonstrative of the presence of a hypophyseal humoral insulin stimulating factor in the jugular vein of dogs receiving a cephalic glucose load.

Animals↗
PubMed1975

Effect of cephalic glucose infusion on insulin secretion.

The continuous infusion of glucose (1 mg/kg/min) via the carotid artery in anesthetized dogs produces a biphasic pattern of insulin secretion. The first peak reaches a maximum 3 min after glucose infusion and drops to basal level at 7 min. As long as the glucose infusion persists a slow and mantained increase in insulin level in the pancreaticoduodenal vein can be observed. The same amount of glucose infused in the general circulation via the jugular vein provoked a different pattern of insulin secretion. Cerebral glucose infusion to vagotomized dogs also produced a two phase response to insulin secretion, but the levels reached in the first phase were lower that those observed in the normal dogs. The infusion of glucose, via the jugular vein, in vagotomized dogs, failed to induce any change in plasma insulin levels. Our data suggest that a glucose load to the brain induces pancreatic insulin secretion mediated partially by the vagus nerves. These results are also compatible with the hypothesis that a humoral factor could be involved in the pancreatic response.

Animals↗
PubMedDate not supplied

The influence of pentoxyfylline [1-(5-oxohexyl-) 3,7-dimethylxanthine] (BL 191) on the insulin secretion induced by glibenclamide and by arginine/glucose in the perfused pancreas.

Pharmacodynamic characteristics of pentoxyfylline (BL 191) related to insulin secretion by the isolated perfused rat pancreas are studied. The results obtained show that: 1) BL 191 (5 mM) is capable of stimulating insulin secretion, even in the presence of another stimulator; 2) BL 191 increases both phases of the secretion produced by constant arginine 20 mM/glucose 5 mM perfusion; 3) BL 191 significantly increases and turns biphasic the monophasic insulin secretion pattern produced by 1 microgram/ml glibenclamide; 4) the effects mentioned in points 2) and 3) are inhibited if the phosphodiesterase activator imidazole (300 mg/100 ml) is present in the perfusion medium; 5) the phosphodiesterase inhibitor theophylline has the same effects as BL 191, except for its inability to stimulate insulin release in the absence of another stimulator; 6) somatostatin (100 ng/ml) significantly inhibits insulin secretion produced by arginine/glucose or glibenclamide, as well as by arginine, glucose plus theophylline or BL 191, and by glibenclamide plus theophylline or BL 191, in both cases the inhibitory effect of somatostatin is reduced by the presence of BL 191 or theophylline.

Animals↗
PubMedDate not supplied

Effect of salicylate poisoning on insulin secretion. Studies on its mechanism of action.

Sodium salicylate poisoning increased glucose-induced insulin secretion by slices of rat pancreas. The alpha adrenergic blocker phentolamine, but not salicylate poisoning, overcame the inhibitory effect of epinephrine on insulin secretion. Theophylline (5, 10 and 15 mM) significantly increased the insulin secretion induced by 11 mM glucose. The highest insulin response was obtained when theophylline was used at a 10 mM concentration. However, when pancreas slices from salicylate poisoned rats were used, a 5 mM concentration was sufficient to achieve maximal insulin response. Salicylate poisoning diminished the free tubulin pool, an action that was impaired by imidazole; however, imidazole did not modify the effect of the ionophore A23187. The results suggest that: a) sodium salicylate poisoning increases B-cell response to glucose; b) changes in alpha adrenergic activity are not related to the mechanism of action of salicylate; c) an increment in the cAMP concentration may mediate the stimulatory effect of salicylate poisoning on insulin secretion; d) the effect of salicylate on the microtubular system is indirect and probably mediated through an increment in pancreatic cAMP.

Animals↗
PubMedDate not supplied

Internalization and release of insulin from hepatocytes.

Degradation of internalized insulin was studied after binding at 25 degrees C and 37 degrees C to isolated hepatocytes. The cells were washed to avoid extracellular insulin contamination. Degradation of both, intracellular and extracellular 125I-insulin, was measured with TCA and insulin antibody. In these conditions binding at 25 degrees C and 37 degrees C was equal but both intra and extracellular degradation were greater at 37 degrees C than at 25 degrees C. At both temperatures, intracellular degradation was greater than extracellular degradation with accumulation of degraded and non-degraded intracellular insulin. To study in what state hepatocytes release internalized insulin into the medium, 125I-insulin association was performed at an intermediate temperature (30 degrees C). Extracellular insulin contamination (whether associated or not) was avoided by three methods: 1) washing; 2) treatment with insulin degrading enzyme(s) and washing; 3) treatment with insulin degrading enzyme(s) then with trypsin and washing. Kinetics of radioactivity released from the cells was identical in the three conditions and the radioactivity was released throughout the experiments. Complete degradation of the released insulin was observed by gel filtration when the previous binding was 0.4 ng insulin/10(6) cells. When the dose of associated insulin increased (25 ng/10(6) cells) 3.5% of non-degraded insulin was liberated and when the dose was 14,300 ng/10(6) cells, the insulin released was 44.3%. In one experiment during the first 30 min, the insulin released was 52.88% and in the last 45 min 39.59%. To study the biologic behavior of the insulin released from cells, a group of mice were injected with this insulin (8.4 mU/mouse) and blood glucose was measured. The released insulin behaved as intact insulin as far as blood glucose responses were concerned. We may conclude that liver cells have the ability to internalize insulin and release biologically active insulin after accumulation.

Animals↗
PubMedDate not supplied

Insulin secretion induced by alloantigens. Mechanisms of action.

Basal insulin secretion stimulated by allogeneic lymphocyte injection was inhibited by SRIF, diazoxide and verapamil but was not affected by theophylline or imidazole. Glucose stimulated insulin secretion induced by alloantigens was inhibited by imidazole. Maximum insulin secretion was achieved with 2.1 mg/ml theophylline in allogeneized mouse pancreata and with 4.2 mg/ml in control pancreata. Propranolol also blocked allogen-induced glucose-stimulated insulin secretion. Phentolamine enhanced insulin secretion from both experimental groups, but phentolamine plus epinephrine only stimulated insulin secretion in control pancreata. Verapamil, diazoxide and SRIF diminished insulin secretion in both experimental groups. These results suggest that: a) basal insulin secretion induced by alloantigens may be mediated by an increase in calcium translocation, and b) glucose-stimulated insulin secretion induced by alloantigen may be mediated by a rise in B-cell cAMP.

Animals↗