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Biomedical subjects

B Billaudel

Publications and source records attributed to B Billaudel.

At least 19 recordsLinked to original sources
PubMed1988

Vitamin D and pancreatic islet function. I. Time course for changes in insulin secretion and content during vitamin D deprivation and repletion.

After weaning, rats were given free access to a control or vitamin D-deprived diet for 2 to 5 weeks. In the vitamin D deficient rats, plasma concentrations of 25-(OH)D3, 1,25-(OH)2D3,24,25-(OH)2D3 calcium, glucose and insulin were all decreased. After an overnight fast, the plasma insulin concentration was also decreased even when the plasma glucose concentration was not significantly affected. The food intake and body growth was also impaired in vitamin D-deficient rats. Administration of vitamin D3 in oil for 3 to 6 days to vitamin D-deficient rats increased the plasma concentration of vitamin D metabolites, calcium and insulin, but not that of glucose, and stimulated food intake and body growth to a larger extent than in rats treated by oil alone. Vitamin D deprivation decreased and vitamin D treatment increased the insulin content of the whole pancreas or isolated islets and the secretory response of the islets to D-glucose. The changes in insulin release remained significant when the hormonal output was expressed relative to the insulin content of the islets. These findings confirm that vitamin D deficiency causes alterations of pancreatic B-cell function. Moreover, the time course for changes in biological variables during vitamin D deprivation and treatment suggests that such an alteration cannot be solely accounted for by concomitant abnormalities in either plasma calcium or glucose concentrations.

Animals↗
PubMed1988

Vitamin D and pancreatic islet function. II. Dynamics of insulin release and cationic fluxes.

Pancreatic islets were prepared from control and vitamin D-deprived rats 2 or 5 weeks after weaning and, in the latter case, after 3 or 6 days treatment with exogenous vitamin D3 (60 nmol per day). The islets were prelabelled with both 86Rb and 45Ca and placed in a perfusion chamber. Vitamin D deprivation or administration failed to affect 86Rb outflow whether prior or after stimulation of the islets by a rise in either extracellular D-glucose or Ca2+ concentration. However, vitamin D deprivation decreased and vitamin D administration enhanced the basal 45Ca fractional outflow rate, as well as the magnitude of changes in both 45Ca and insulin release evoked by the rise in either D-glucose or extracellular Ca2+. It is proposed that the alteration in 45Ca fluxes and insulin release attributable to changes in the supply of vitamin D are, to a large extent, independent of the changes in nutrient catabolism conceivably associated with vitamin D deprivation and administration.

Animals↗
PubMed1987

Effects of constant magnetic fields on the B-cells and insulin target cells in the rat.

Young male rats were exposed to constant uniform magnetic fields of 400 and 800 millitesia (mT). No changes were observed in the body and in the pancreas weight, in the pancreatic insulin content and in the in vitro insulin release of Langerhans islets, in glucose and insulin plasma levels. The magnetic fields abolished the insulin effect on glucose uptake of diaphragms, but not on 1-14C-glucose oxidation. In adipocytes 400 mT increased insulin-stimulated 1-14C-glucose oxidation, when expressed as percentage of mean basal oxidation, and 800 mT diminished it.

Adipose Tissue↗
PubMed1985

Cholinergic stimulation of ion fluxes in pancreatic islets.

Cholinergic agents are known to stimulate the hydrolysis of polyphosphoinositides in pancreatic islets. The effect of carbamylcholine upon ion fluxes in the islet cells was investigated. Carbamylcholine provoked a rapid but poorly sustained increase in 45Ca and 86Rb outflow from perifused islets. Such a cationic response was observed at different glucose concentrations (zero to 16.7 mM), at three concentrations of carbamylcholine (10 microM, 100 microM and 1.0 mM), and in the absence or presence of extracellular Ca2+. It coincided with a biphasic stimulation of insulin release, both the cationic and secretory responses being abolished in the presence of atropine (10 microM). At variance with nutrient secretagogues, carbamylcholine failed to affect the net production of cyclic AMP and caused a transient decrease in 32P outflow from islets prelabelled with [32P]phosphate. It is proposed that cholinergic agents mobilize Ca2+ from intracellular sites, possibly through generation of inositol, 1,4,5-triphosphate from phosphatidylinositol 4,5-bisphosphate. The intracellular redistribution of Ca2+ does not appear sufficient, however, to account fully for the secretory response, which may also involve activation of protein kinase C by diacylglycerol.

Animals↗
PubMed1985

Facilitation of insulin release by N-p-tosylglycine.

N-p-tosylglycine, which inhibits transglutaminase activity in islet homogenates, was found to cause a rapid and sustained facilitation of insulin release evoked by D-glucose, L-leucine or the association of Ba2+ and theophylline in intact islets. Such a facilitating action could not be attributed to any obvious effect upon either nutrient oxidation or 45Ca net uptake and outflow. It failed to be reproduced by glycine, N alpha-p-tosyl-L-arginine methyl ester or N alpha-p-tosyl-L-lysine methyl ester. N-p-tosylglycine (5.0 mM) slightly enhanced insulin release evoked by a high concentration of glucose (16.7 mM) and failed to affect significantly the secretory response to the association of L-leucine and L-glutamine or that of D-glucose and gliclazide. N-p-tosylglycine failed to affect the incorporation of [2,5-3H]histamine in trichloroacetic acid-precipitable material in intact islets. These results suggest that N-p-tosylglycine interferes with a late event in the secretory sequence, possibly at the level of the cell boundary, rather than inhibiting the crosslinking of intracellular proteins.

Acyltransferases↗
PubMed1984

Adrenal interference of insulin secretion after 14-days oestradiol treatment in female rats.

Ovarian-adrenal interactions on insulin secretion during oestradiol treatment were studied in sham-operated, ovariectomized and adrenalectomized-ovariectomized female rats, the latter thus treated to suppress interference from endogenous hormones. Islets of Langerhans isolated from oestradiol or oestradiol + corticosterone treated and control rats were incubated with various glucose concentrations. Oestradiol treatment enhanced basal and glucose stimulated insulin secretion from sham-operated (+12%) or ovariectomized rats (+24%). This effect disappeared in adrenalectomized-ovariectomized rats but reappeared when adrenalectomized-ovariectomized rats were treated with oestradiol + corticosterone (+37%). A 14-day oestradiol treatment had a trophic effect on total protein content independent of adrenal presence (+14%; +15%; +31%; +23% versus respective control groups). Our data demonstrate that corticosterone is necessary for the stimulating effect of oestradiol on insulin secretion.

Adrenal Glands↗
PubMed1984

Methylamines and islet function: cationic aspects.

Methylamine (2 to 10 mM) caused a dose-related inhibition of insulin release evoked in rat pancreatic islets by nutrient or non nutrient secretagogues. Trimethylamine exerted comparable effects upon insulin release. Methylamine (2 mM) inhibited insulin secretion but failed to affect 45Ca uptake and efflux in response to a rise in extracellular K+ concentration, suggesting that methylamine acts, to a certain extent at least, at a distal site in the secretory sequence. Methylamine, however, also exerted untoward ionic effects. First, methylamine (2 to 10 mM) apparently caused a dose-related increase in cellular pH. Second, methylamine (2mM) augmented 86Rb outflow from islets perifused either in the absence or presence of glucose or gliclazide, and inhibited Ca2+ inflow (as judged from the net uptake or efflux of 45Ca) in islets stimulated by D-glucose, L-leucine or 2-ketoisocaproate. This multiplicity of ionic and other effects may account for the fact that, in the presence of distinct secretagogues, the secretory process appeared more or less sensitive towards methylamine, depending on the relative importance of changes in cellular pH, K+ permeability and intracellular Ca2+ distribution as determinants of the secretory response.

Acyltransferases↗
PubMed1984

Inhibition by corticosterone of calcium inflow and insulin release in rat pancreatic islets.

Corticosterone (0.6 mumol/l) inhibited both 45Ca outflow and insulin release evoked by glucose, the combination of leucine and glutamine, 2-ketoisocaproate, gliclazide or the association of gliclazide and a tumour-promoting phorbol ester in rat pancreatic islets perifused at normal extracellular Ca2+ concentration (1.0 mmol/l). In all cases, the inhibitory action of corticosterone reached statistical significance within 10-22 min of exposure to this steroid and failed to be rapidly reversible. Corticosterone failed to affect basal 45Ca outflow and insulin release. The steroid also failed to affect the inhibitory action of glucose upon 45Ca outflow, as judged from either the glucose-induced early fall in effluent radioactivity from islets maintained at normal extracellular Ca2+ concentration or the steady-state values for 45Ca outflow from glucose-stimulated but Ca2+-deprived islets. Corticosterone caused a modest increase in 86Rb outflow from islets perifused in the presence of glucose (16.7 mmol/l). It is concluded that corticosterone impairs Ca2+ inflow into the islet cells and, by doing so, causes a progressive inhibition of insulin release. The pancreatic B cell might thus serve as a further model for the study of the rapid biological response to steroids, as presumably mediated by alteration in the biophysical properties of the plasma membrane.

Animals↗
PubMed1984

Influence of extracellular pH upon the ionic and secretory response to gliclazide in pancreatic islets.

The influence of extracellular pH upon the ionic and secretory response to gliclazide was examined in perifused rat islets. Gliclazide usually decreased 86Rb outflow from the islets except in the presence of glucose (7.0 mM) and Ca2+ (1.0 mM) and at low (7.0) or normal (7.4) pH, in which cases it caused a rapid increase in 86Rb output. Gliclazide failed to affect 45Ca outflow in the absence of extracellular Ca2+, whatever the extracellular pH. However, in the presence of Ca2+ and glucose (7.0 mM), gliclazide enhanced 45Ca outflow and insulin release. Under the latter experimental conditions, the gliclazide-induced increment in both 45Ca and insulin output was progressively increased as the pH was raised from 7.0 to 7.4 and 7.8, despite the fact that glucose-induced insulin release was progressively decreased over the same pH range. The gliclazide-induced facilitation of Ca2+ inflow into the islet cells and the subsequent stimulation of insulin release, whatever their precise molecular determinants, thus displayed the same dependency towards extracellular pH as that characterizing the ionophoretic action of the drug. The influence of extracellular pH upon the cationic and secretory response to gliclazide is compatible, therefore, with the view that the insulinotropic action of hypoglycemic sulfonylureas is somehow related to their ionophoretic capacity.

Animals↗
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.

Animals↗
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↗