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Biomedical subjects

B Blondel

Publications and source records attributed to B Blondel.

At least 163 records · Page 9Linked to original sources
PubMed1979

Perturbation of hormone storage and release induced by cyproheptadine in rat pancreatic islets in vitro.

The effects of cyproheptadine (CPH) added in vitro were studied in rat pancreatic islets maintained in culture medium. CPH added over 6 days resulted in either an increase (5 X 10(-7) M CPH) or a marked, but reversible decrease (5 X 10(-5 M) in insulin content of islets when related to that of controls. At both concentrations, however, total recoverable insulin from islets, cells detached from islets, and medium was decreased relative to control cultures. The increased insulin content observed after 6 days with 5 X 10(-7) M CPH may be explained by the partial inhibition of insulin release, preventing the normally occurring early drop in insulin content of control islets. The decreased total recoverable insulin in the culture system with 5 X 10(-5) M CPH (17% of the initial insulin content of the islets placed into the CPH-containing culture medium) was not acounted for by the combined effects of insulin degradation in the culture medium and inhibition of insulin biosynthesis. Together and by exclusion these data suggest increased insulin degradation within beta-cells as a result of exposure to 5 X 10(-5) M CPH. Since increased intracellular insulin degradation was not found at 5 X 10(-7) M CPH, the data suggest that only severe inhibition of insulin release (5 X 10(-5) M CPH) increases intracellular insulin degradation. CPH added in vitro irreversibly decreased islet glucagon content; the data suggest that these effects are due to alterations in the physical properties of the peripheral cell layers of isolated islets. Studies with 5 X 10(-5) M CPH on the biosynthesis of insulin immunoreactive material failed to link the appearance of flocculent material in dilated cisternae of the rough endoplasmic reticulum (observed by electron microscopy) with accumulation of an immunoreactive biosynthetic precursor for insulin.

Animals↗
PubMed1978

[Outcome of pregnancy and prenatal care among immigrant women (author's transl)].

A retrospective survey on a representative sample of births in France in 1972 relating to more than 11000 women showed the amount of perinatal pathology among immigrants as compared with French women: a higher rate of foetal or neonatal distress, a three to four times higher stillbirth rate among Portuguese and North African women, a prematurity rate more than twice as higher among North African women. When differences in parity and socio-cultural level between immigrant and French women were allowed for, there remained a higher rate of perinatal pathology among immigrants. Prenatal care was also more often inadequate among immigrants, even when taking into account their low socio-cultural standard. Attitude towards prenatal care was highly influenced by the level of adaptation in France. But, even with equal prenatal care, perinatal pathology was higher among immigrant women: being an immigrant is a risk factor in itself.

Acculturation↗
PubMed1977

Somatostatin inhibition of pancreatic glucagon release from monolayer cultures and interactions with calcium.

The effects of somatostatin (SRIF) on glucagon release have been studied in the monolayer culture of newborn rat pancreas. It was found that SRIF inhibited glucagon release rapidly and in a dose dependent manner at concentrations of 1-1000 ng/ml. SRIF inhibited glucagon release under basal conditions and after stimulation by arginine, 3-isobutyl-1-methylxanthine (IBMX), high Ca++ concentrations, ionophore A23187 and Ca++, and Ba++. SRIF inhibited ionophore-induced glucagon release over 60 min when a low concentration of A23187 was used (0.1 microgram/ml) but not when a high concentraion (10 microgram/ml) was used. The stimulant effect of 10 microgram/ml A23187 was, however, inhibited by SRIF during short periods of incubation. The per cent inhibition of arginine-stimulated glucagon release due to SRIF remained unchanged when the Ca++ concentration in the medium was varied from 1-10 mM. It is concluded that SRIF promptly inhibits glucagon release under basal conditions or when stimulated by a variety of agents. Thus, the action of SRIF appears to be basic to the granule release process and not specifically antagonisitc to any particular stimulants. Further, as SRIF inhibits release due to raised cytosol Ca++ (e.g., ionophore-Ca++ or high Ca++ experiments) the action is probably at a late point in the release mechanism.

Animals↗
PubMed1976

Calcium induced glucagon release in monolayer culture of the endocrine pancreas. Studies with ionophore A23187.

The possible role of Ca2+ in glucagon release has been investigated by the use of ionophore A23187. This ionophore permits Ca2+ entry down a suitable concentration gradient by complexing and releasing Ca2+, thereby acting as a carrier in plasma membranes. Cultured cells obtained by enzymatic digestion of pancreases from newborn rats were studied on the third day of culture. As expected the effects of the ionophore were dependent upon the presence of Ca2+ in the medium. However, either stimulation or inhibition of glucagon release resulted when different concentrations of ionophore and Ca2+ were used. With 1.0 mM Ca2+ in the medium, glucagon release was stimulated in the presence of 0.01 and 0.1 mug/ml ionophore, but inhibited in the presence of 3.0 and 10.0 mug/ml. With 0.1 mug/ml ionophore, glucagon release was stimulated by 0.3 and 1.0 mC Ca2+ but not by 2.5 mM Ca2+. With 10 mug/ml ionophore glucagon release was stimulated by 0.03, 0.1 and 0.3 mM Ca2+, whereas at 1.0 mM, glucagon release was depressed. These findings suggest that by increasing Ca2+, glucagon is released from the A-cells, whereas too large an increase in Ca2+ is inhibitory. The effect to stimulate release was not completely specific for Ca2+ in that while the ionophore did not stimulate release in the presence of either Mg2+ or Sr2+ in the absence of Ca2+, it did stimulate release when Ba2+ was tested. Furthermore Ba2+ at 0.3 mM was stimulatory even in the absence of ionophore. Glucagon release in the absence of ionophore was also enhanced by addition of 30 mM Ca2+ or by omission of Ca2+ from the medium. It is concluded that Ca2+, which plays an essential role in the stimulus-secretion coupling in several different cell types, may be involved in the stimulation of glucagon release from the A-cells of the pancreas.

Animals↗
PubMed1976

Stimulatory and inhibitory effects of cyclic AMP on pancreatic glucagon release from monolayer cultures and the controlling role of calcium.

When glucagon release from monolayer cultures of newborn rat pancreas was measured over four hours in media containing 2.5 mM Ca++, a significant cyclic AMP-related inhibition of release was observed. This was noted whether intracellular cyclic AMP levels were raised by the addition of exogenous cyclic AMP or dibutyryl cyclic AMP, by phosphodiesterase inhibition with theophylline, or by the stimulation of adenylate cyclase with cholera toxin. The inhibition was concentration dependent for cyclic AMP and could not be reproduced by the addition of AMP, ADP or ATP. Adenosine also inhibited glucagon release while ATP was stimulatory. From time course studies it appeared that the inhibitory effects of cyclic AMP and cholera toxin were progressive after two hours of incubation. With cholera toxin an early stimulation of glucagon release was observed. The effects of cyclic AMP and cholera toxin on arginine-stimulated glucagon release were to stimulate further the glucagon release during the first hour of the incubation. Thus, the effects of raising intracellular cyclic AMP levels were biphasic in that both an early stimulation and a late inhibition of glucagon release were observed. In examining the nature of these responses a remarkable controlling role for Ca++ was uncovered: at Ca concentrations of 0.3 mM and lower no effect of cyclic AMP on glucagon release was found. With 1 mM Ca++ in the medium cyclic AMP stimulated glucagon release early (30 min) and thereafter had no further effect. In the presence of 2.5 mM Ca++ cyclic AMP did not stimulate early but did cause the delayed inhibition of release. It is concluded that the effect of cyclic AMP on glucagon release can be either stimulatory or inhibitory depending upon the Ca++ concentration of the medium and the duration of exposure to raised cyclic AMP levels.

Adenine Nucleotides↗
PubMed1975

Calcium-induced insulin release in monolayer culture of the endocrine pancreas. Studies with ionophore A23187.

The role of Ca2+ on insulin release has been studied by the use of ionophore A23187. The ionophore complexes divalent cations and permits Ca2+ entry into cells by acting as a carrier in the plasma membranes. Cultured cells obtained by enzymatic digestion of pancreases from newborn rats were studied on the 3rd day of culture. With Ca2+ in the incubation medium the ionophore induced sustained insulin release even in the absence of glucose. Optimal effects of the ionophore were observed at 3 and 10 mug per ml in the presence of 0.3 to 1.0 mM Ca-2+. Under these conditions the insulin release was greater than that caused by 16.7 mM glucose. A graded response was observed to changes in Ca-2+ concentration from 0.1 to 1.0 mM Ca-2+. Higher Ca-2+ concentrations caused a large amount of insulin to be released promptly, but the release was not sustained. Mg-2+ and Sr-2+ were not found to substitute for Ca-2+. Ba-2+ at 0.3 mM stimulated insulin release even in the absence of ionophore. Cyclic adenosine 3':5'-monophosphate was able to increase ionophore-induced insulin release. The alpha-adrenergic effect of epinephrine to inhibit insulin release was not observed in the presence of Ca-2+ and the ionophore, and a stimulatory effect of epinephrine was seen. This unusual stimulatory effect of epinephrine was blocked by propranolol indicating a beta-adrenergic mechanism for epinephrine. It is concluded that Ca-2+, which plays an essential role in the stimulus-secretion coupling, can alone initiate and cause sustained insulin release.

Animals↗