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B Billaudel

Publications and source records attributed to B Billaudel.

32 records · Page 2Linked to original sources
PubMed1983

Comparison of the cationic and secretory response of pancreatic islets to gliclazide and/or potassium.

The concept that hypoglycemic sulfonylureas stimulate Ca2+ inflow and insulin release in the pancreatic B-cell by causing the gating of voltage-sensitive Ca2+ channels was tested by comparing the cationic and secretory response of perifused pancreatic islets to gliclazide and/or an increase in extracellular K+ concentration. In the presence of glucose (2.8 mM), both procedures resulted in an immediate and sustained stimulation of 45Ca and insulin release from prelabelled islets. The capacity of gliclazide to stimulate 45Ca and insulin release persisted, to a limited extent, in islets exposed to 20 mM K+, but was abolished in islets exposed to 50 mM K+. At the latter concentration, however, K+ was still able to augment 45Ca outflow and insulin secretion from islets first exposed to gliclazide. These findings support the view that the depolarization of the B-cell membrane plays a critical role in the stimulus-secretion coupling of sulfonylurea-induced insulin release.

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PubMed1982

Immediate in-vivo effect of corticosterone on glucose-induced insulin secretion in the rat.

The effect of infused corticosterone (300 micrograms/h per kg body wt) on the concentrations of insulin in the plasma of the rat was examined (1) when glucose concentration was basal, (2) at standardized glucose levels attained by modulated glucose infusion and (3) in response to a standard or a modulated glucose pulse. There was no effect of corticosterone on the levels of plasma insulin when the glucose concentrations were either basal or raised in response to the standard pulse of glucose. However, when glucose was infused a significantly reduced plasma level of insulin was detected after 60 min when the glucocorticoid was present and this level remained significantly reduced after the modulated pulse of glucose. Thus the infusion of corticosterone leads to an acute depression of the concentrations of insulin in the plasma and of their response to a glucose pulse only when the hormone acts in the presence of a concentration of glucose in the plasma that is insulin-stimulatory.

Animals↗
PubMed1982

Effect of corticosterone upon insulin biosynthesis and storage by isolated rat Langerhans islets.

A rapid inhibitory effect of corticosterone upon glucose- or leucine-induced insulin release being established, steroid action upon insulin biosynthesis of rat Langerhans islets was studied as a function of time. Islet proinsulin and insulin content was reduced after two hours of incubation in presence of corticosterone (0.2 mg/l) with a 16.7 mmoles/l glucose stimulation. L (-) [4-5(3)H] leucine incorporation into proinsulin and insulin was lowered at all time (points examined: 1, 2 and 3 hours). Incorporation ratio between proinsulin and insulin remained stable, so an interaction at the proinsulin biosynthetic level may be possible. Corticosterone had no effect upon biosynthesis of other islet proteins. Our data suggest that the corticosterone inhibition of insulin biosynthesis is specific.

Animals↗
PubMed1981

Modulation of the direct effect of corticosterone upon glucose-induced insulin secretion of rat isolated islets of Langerhans.

As a direct inhibiting effect of corticosterone (0.2 mg/l) has been shown upon 16.7 mmoles/l glucose-induced insulin secretion rate of rat islets of Langerhans, modulations of this inhibition were studied. The inhibitory effect was observed over a wide range of stimulatory glucose concentrations (8.3--33.4 mmoles/l), but not with non-stimulating glucose values (0-4.2 mmoles/l). During the steady-state insulin secretory rate induced by glucose 16.7 mmoles/l, the inhibiting effect needed about fifteen minutes to become statistically significant; it persisted as long as the glucose stimulation was maintained, independently of corticosterone presence. The inhibition during a subsequent incubation without corticosterone after a preincubation period with the steroid and glucose concentrations between 4.2 and 11.1 mmoles/l, appeared only if the glucose concentration during the preincubation period was a stimulating one. A minimal steroid presence time (10 min) appeared to be necessary for the induction of the subsequent inhibitory effect of corticosterone in presence of 16.7 mmoles/l glucose. Our data suggest that the inhibition of insulin secretion is constant over a wide range of glucose concentrations on condition that the hormone presence lasts more than ten minutes and glucose concentration is a stimulating one; then it persists as long as a stimulatory glucose concentration is provided.

Animals↗
PubMed1979

Direct effect of corticosterone upon insulin secretion studied by three different techniques.

The immediate effect of corticosterone upon insulin secretion rates estimated by three different techniques (perfusior of isolated rat pancreas and perifusion or incubation of isolated islets of Langerhans) was studied for one hour. Three corticosterone concentrations were used: 0.02, 0.2 or 20 mg/l. With 4.2 mmol/l glucose, corticosterone did not affect insulin secretion, whereas, with a stimulating glucose concentration (16.7 mmol/l), insulin secretion was inhibited by the three corticosterone concentrations tested during incubation experiments, and by only the two physiological ones (0.02 and 0.2 mg/l) during islets perifusion and pancreas perfusion experiments. Moreover the inhibitory effect appeared more rapid with perifused islets than perfused pancreas, where only the second insulin secretory phase was disturbed.

Animals↗
PubMed1978

Simultaneous determination of insulin secretion and glucose oxidation rates during incubation of isolated rat islets of Langerhans.

Insulin secretion being related to glucose metabolism of the B cell, it seemed of interest to develop a suitable system to measure these two parameters on the same islet pool, in order to overcome the great individual differences observed when these are measured in separate experiments. For this reason, we used an incubation system allowing the measurement of insulin secretion concomitantly with the determination of the corresponding oxidation rate. The results obtained agree well with those described by several authors using separate experimental procedures. Thus, our experimental design appears to be a reliable method for simultaneous determination of insulin secretion and glucose oxidation rates.

Animals↗
PubMed1975

Existence in fetal and adult rat of several forms of material reacting with anti-insulin antibody (IRI).

The double antibody procedure detects 3 peaks in the elution fractions of adult or fetal rat sera, after passage on Sephadex G50 or G100 columns. Peak A (apparent MW 6000) contains insulin monomer; peak B (apparent MW 10-12000) is tentatively attributed to proinsulin (or proinsulin like substances); peak C (apparent MW 50-100000) is similar to the so called "big big" insulin. During intravenously induced hyperglycemia, the 3 peaks show parallel increases, but, after the disappearance of peaks A and B in streptozotocin treated rats, peak C remains unaltered. Pancreatic extracts and secreta present a very minor and inconstant peak C, the bulk of their immunoreactive material belonging to peaks A and B. A companion paper further discusses the nature of peaks B and C materials.

Animals↗
PubMed1975

[Immuno-reactive insulin-like substances in the rat].

Chromatography on G50 or G100 sephadex column of rat plasma or serum divides up the insulin-like immunoreactive material into three peaks: monomere insulin, proinsulin and a fraction of molecular weight between 50 and 100,000. This fraction is virtually absent (less than 1%) from immunoreactive material extracted from the pancreas. Comparison of the results obtained by methods using double or simple antibodies (charcoal dextran) and study of fixation in vitro of labelled insulin, taken up by various plasma proteins, suggest that the high molecular weight material includes insulin more or less broken down and linked to proteins. Furthermore, when one uses a double antibody method, the alpha globulins and albumin in the rat present also an insulin-like reactivity. This disadvantage does not occur with the charcoal dextran method which is more specific.

Animals↗
PubMedDate not supplied

Is 1,25-dihydroxyvitamin D3 the specific vitamin D3 metabolite active on insulin release and calcium handling by islets from vitamin D3-deprived rats?

Vitamin D3 treatment can improve within 3 days the low insulin secretion of vitamin D3-deficient rats. One of its metabolite active in vivo, 1,25(OH)2D3 cannot stimulate the insulin secretion in vitro within 2 h, except when islets came from 24 h-vitamin D3 prepared rats. These findings led us to determine the respective in vitro activity of three vitamin D3 metabolites [1,25(OH)2D3; 24,25(OH)2D3 and 25(OH)D3] on cellular events in perifused islets derived from vitamin D3-deficient rats which were injected with vitamin D3 24 h earlier. Three experimental conditions were studied: either a rise in metabolite concentration during a steady-state 8.3 mmol/l glucose medium, or without glucose, or a rise in glucose concentration (16.7 mmol/l) during a steady-state vitamin D3 metabolite concentration. The 1,25(OH)2D3 was the only of the 3 metabolites active both on insulin release and 45Ca2+ efflux. None of the three metabolites modified K+ fluxes (86Rb as a tracer). The in vitro specific stimulatory action of 1,25(OH)2D3 on B cell was rapidly seen within a few minutes, and occurred only in the presence of glucose stimulation. These results suggest that 1,25(OH)2D3 might potentiate the insulin response to glucose by an action on Ca2+ handling, either by enhancing Ca2+ entry in the B cell and/or Ca2+ mobilization from intracellular organelles.

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PubMedDate not supplied

Direct in vitro effect of 1,25-dihydroxyvitamin D3 on islets insulin secretion in vitamin deficient rats: influence of vitamin D3 pretreatment.

Vitamin D3 deficiency decreased glucose-induced insulin release from isolated rat islets. In vivo, vitamin D3 treatment restored the B-cell response within 3 days; this delay suggests an effect of vitamin D3 metabolites. The effect of 1,25-dihydroxyvitamin D3 was studied in vitro on isolated islets from vitamin D3 deficient rats. When it was added to the incubation medium, it increased in a dose-dependent manner islet insulin secretion. However this effect only occurred when the vitamin D3-deficient rats received at least a single injection of vitamin D3 24 hours earlier; these results sustain the hypothesis of a direct but delayed in vitro stimulation of B cell function by 1,25-dihydroxyvitamin D3.

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