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8. Eighth annual meeting of the European Association for the Study of Diabetes: Madrid, Spain September, 6–8, 1972

Author

Alberti, K. G. M. M., Darley, J., Emerson, Pauline M., Hockaday, T. D. R., Amherdt, M., Like, A. A., Blondel, B., Marliss, B., Wollheim, C., Orci, L., Andersen, O. Ortved, Andersson, Arne, Antonini, F. M., Fumagalli, C., Petruzzi, E., Bertini, G., Mori, S., Tinti, P., Ashcroft, S. J. H., Weerasinghe, L. C. C., Randle, P. J., Assan, R., Slusher, N., Guy-Grand, B., Girard, F., Soufflet, E., Attali, J. R., Ballerio, G., Boillot, J., Atkins, T., Matty, A. J., Bailey, C. J., Aynsley-Green, A., Bloom, S. R., Bacchus, R. A., Meade, L. G., London, D. R., Balant, L., Zahnd, G., Petitpierre, B., Fabre, J., Balasse, E. O., Neef, M. A., Barta, L., Brooser, G., Molnar, Maria, Bataille, D. P., Freychet, P., Kitabgi, P., Rosselin, G. E., Berne, Christian, Beyer, J., Cordes, U., Sell, G., Rosak, C., Schöffling, K., Birkner, B., Henner, J., Wagner, P., Erhardt, F., Dieterle, P., Bloom, S. R., Vaughan, N. J. A., Edwards, A. V., Boquist, L., Brand, I., Söling, H. D., Brandenburg, D., Gliemann, J., Ooms, H. A., Puls, W., Wollmer, A., Camerini-Davalos, R. A., Bloodworth, Jr., J. M. B., Limburg, B., Oppermann, W., Campbell, A. K., Siddle, K., Cañadell, J. M., Barraquer, J., Muiños, A., Heredia, C. D., Castillo-Olivares, J., Guijo, J., Pallardo, L. F., Cerasi, E., Efendić, S., Luft, R., Cerasi, E., Wahren, J., Luft, R., Felig, P., Christensen, Niels Juel, Christiansen, A. H., Vølund, A., Connon, J. J., Trimble, E., Copinschi, G., Leclercq, R., Bruno, O. D., Cordes, U., Sell, G., Beyer, J., Haupt, E., Schöffling, K., Creutzfeldt, C., Track, N. S., Cuendet, G. S., Wollheim, C. B., Cameron, D. P., Balant, L., Stauffacher, W., Marliss, E. B., Czyzyk, A., Lao, B., Bartosiewicz, W., Szczepanik, Z., De Nobel, E., Laar, A. Van't, Koene, R. A. P., Benraad, Th. J., Dietze, G., Hepp, K. D., Wickmayr, M., Mehnert, H., Dixon, K., Exon, P. D., Hughes, H. R., Jones, D. W., Elkeles, R. S., Exon, P. D., Dixon, K., FitzGerald, M. G., Malins, J. M., Falorni, A., Massi-Benedetti, F., Gallo, G., Maffei, S., Fedele, D., Tiengo, A., Muggeo, M., Fabris, P., Crepaldi, G., Federlin, K., Helmke, K., Slijepčević, M., Pfeiffer, E. F., Felber, J. P., Oulès, J., Schindler, Ch., Chabot, V., Fernandez-Cruz, Jr., A., Catalán, E., Otero, M. Luque, Hermida, O. Garcia, Otero, M. Luque, Catalán, E., Flatt, J. P., Blackburn, G., Randers, G., Förster, H., Hoos, I, Lerche, D., Förster, H., Hoos, I., Matthäus, M., Franckson, J. R. M., Ooms, H. A., Frerichs, H., Daweke, H., Gries, F., Grüneklee, D., Hessing, J., Jahnke, K., Keup, U., Miss, H., Otto, H., Puls, W., Schmidt, D., Zumfelde, C., Funcke, H. v., Löffler, G., Wieland, O., Galton, D. J., Guttman, R., Gazzola, G. C., Franchi, R., Ronchi, P., Saibene, V., Guidotti, G. G., Gligore, V., Hîncu, N., Tecuceanu, Rodica, Goberna, R., Garcia-Albertos, F., Tamarit-Rodriguez, J., del Rio, E., Roca, R., Gomez-Acebo, José, Creco, A. V., Fedeli, G., Ghirlanda, G., Fenici, R., Lucente, M., Gutman, A., Agam, G., Nahas, N., Cazalis, P., Gylfe, E., Hellman, B., Hadden, D. R., Connolly, J. H., Montgomery, D. A. D., Weaver, J. A., Hellerström, Claes, Howell, Simon, Andersson, Arne, Edwards, John, Sehlin, J., Täljedal, I. -B., Heptner, W., Neubauer, H. B., Herchuelz, A., Pipeleers, D. G., Malaisse, W. J., Herrera, E., Montoya, Eladio, Hommel, H., Fischer, IT., Schmid, B., Fiedler, H., Bibergeil, H., Iversen, J., Iynedjian, P. B., Peters, G., Jacquemin, C., Lambert, B., Sutter, B. Ch. J., Jakob, A., Zapf, J., Froesch, E. R., Jansen, F. K., Freytag, G., Herberg, L., Jarrett, R. J., Baker, I. A., Jarrousse, C., Rancon, F., Rosselin, G. E., Job, D., Tchobroutsky, G., Eschwege, E., Guyot-Argenton, C., Aubry, J. P., Déret, M., Karman, H., Mialhe, P., Kissebah, A., Tulloch, B., Fraser, Russell, Kissebah, A., Tulloch, B., Vydelingum, N., Fraser, Russell, Kissing, J., Raptis, S., Dollinger, H., Faulhaber, J., Rothenbuchner, G., Pfeiffer, E. F., Kleineke, J., Sauer, H., Söling, H. D., Kloeze, J., Kohner, Eva M., Sutcliffe, Barbara A., Tudball, M., Dollery, C. T., Korp, W., Neubert, J., Bruneder, H., Lenhardt, A., Levett, R. E., Koschinsky, T., Gries, F. A., Landgraf-Leurs, M. M. C., Landgraf, R., Hörl, R., Langslow, D. R., Laube, H., Fussgänger, R., Mayer, R., Pfeiffer, E. F., Laube, H., Fussgänger, R., Klör, H., Pfeiffer, E. F., Lázaro, E., Leclercq-Meyer, V., Marchand, J. J., Malaisse, W., Ledet, Thomas, Lefébvre, P. J., Luyckx, A. S., Le Marchand, Y., Assimacopoulos, F., Singh, A., Amherdt, M., Rouiller, Ch., Jeanrenaud, B., Lenti, G., Frezzotti, R., Angotzi, G., Bardelli, A. M., Pagano, G., Basetti-Sani, A., Galli, M., Lernmark, Å., Fex, G., Lindsay, D. G., Loge, O., Lopez-Quijada, C., Chiva, L., Rodriguez-Lopez, M., Loten, E. G., Loubatières, A. L., Loubatières-Mariani, M. M., Ribes, G., Chapal, J., Lubetzki, J., Duprey, J., Sambourg, Cl., Lefebvre, P. J., Maier, V., Hinz, M., Schatz, H., Nierle, C., Pfeiffer, E. F., Malaisse, W. J., Pipeleers, D. G., Malaisse-Lagae, F., Orci, L., Malaisse-Lagae, F., Amherdt, M., Ravazzola, M., Stauffacher, W., Orci, L., Renold, A. E., Manzano, P., Rojas-Hidalgo, E., Marco, J., Diaz-Fierros, D., Calle, C., Roman, D., Villanueva, M. L., Valverde, I., Marliss, E. B., Wollheim, C. B., Blondel, B., Orci, L., Like, A., Amherdt, M., Stauffacher, W., Massi-Benedetti, F., Luycks, A. L., Fracassini, F., Lefebvre, P. J., Falorni, A., Menzel, R., Michaelis, D., Neumann, I., Bibergeil, H., Schulz, B., Wilke, W., Wulfert, P., Krämer, K., Menzinger, G., Fallucca, F., Tamburrano, F., Carratu', R., Andreani, D., Metzger, P., Franken, P., Balasse, E. O., Michael, R., Hildmann, W., Jutzi, E., Michl, J., Fankhauser, S., Schlichtkrull, J., Mirouze, J., Orsetti, A., Vierne, Y., Arnoux, N., Mølsted-Pederson, L., Tygstrup, Inge, Villumsen, Åge L., Pedersen, Jørgen, Montague, W., Howell, S. L., Moody, A. J., Agerbak, G. S., Sundby, F., Muggeo, M., Crepaldi, G., Fedele, D., Baritussio, A., Naeser, Peter, Navalesi, R., Pilo, A., Lenzi, S., Cecchetti, P., Corsini, G., Donato, L., Nerup, J., Andersen, O. Ortved, Bendixen, G., Egeberg, J., Poulsen, J. E., Nielsen, J. Høiriis, Hansen, F. Mølgaard, Gliemann, J., Niki, A., Niki, H., Koide, T., Lin, B. J., Nikkels, R. E., Terpstra, J., Gay, A., Oakman, R. H., Lazarus, Norman R., Orci, L., Amherdt, M., Stauffacher, W., Like, A. A., Rouiller, C., Renold, A. E., Malaisse-Lagae, F., Ravazzola, M., Ostman, J., Backman, L., Cerasi, E., Luft, R., Hallberg, D., Ostrowski, K., Panten, U., Christians, J., Parving, H. -H., Rasmussen, S. Munkgaard, Marichal, M., Platilovà, H., Dufek, M., Konopàsek, E., Pozuelo, V., Tamarit, J., Suner, A., Castell, C., Pruett, E. D. R., Maehlum, S., Raptis, S., Grebe, B., Chrissiku, M., Rothenbuchner, G., Müller, R., Hinze, H. J., Pfeiffer, E. F., Reinauer, H., Müller-Ruchholtz, E. R., Rietzler, X., Passa, P., Canivet, J., Schatz, H., Otto, J., Hinz, M., Maier, V., Nierle, C., Behrens, G., Bücher, T., Pfeiffer, E. F., Schlumpf, U., Morell, B., Zingg, A., Schönborn, J., Westphal, P., Panten, U., Bloom, G. D., Idahl, L. -A., Lernmark, A., Söderberg, M., Rios, M. Serrano, Hawkins, F. G., Escobar, F., Mato, J. M., Larrodera, L., de Oya, M., Rodriguez-Miñon, J. L., Shafrir, E., Gutman, A., Sitbon, G., Mialhe, P., Skrabalo, Z., Panajatović, N., Papić, Z., Posinovec, J., Stavljenić, A., Lipovac, V., Aganović, I., Soler, N. G., Bennett, M. A., Söling, H. D., Peters, H., Janson, G., Sönksen, P. H., Srivastava, M. C., Tompkins, C. V., Nabarro, J. D. N., Sørensen, N. Schwartz, Ladefoged, K., Wildenhoff, K. E., Sorge, F., Diehl, H. -J., Hoffmann, H., Schwartzkopff, W., Standl, E., Kolb, H., Standl, A., Mehnert, H., Sutherland, H. W., Stowers, J. M., Whetham, J. C. G., Sutter, B. C. J., Billaudel, B., Sutter, B. Ch. J., Sutter-Dub, M. T., Leclercq, R., Jacquot, R., Täljedal, I. B., Tamarit, J., Tamarit-Rodriguez, J., Goberna, R., Gobema, R., Tamás, Jr., Gy., Baranyi, Éva, Baranyi, A., Radvanyi, A., Tatoń, J., Hinek, A., Wiśniewska, A., Tattersall, R. B., Pyke, D. A., Terpstra, J., Slot, J. Bruins, Sande, P. L. M. v. d., Radder, J. K., Waldeok, K. J. J., Muijden, R. C. P. A. v., Tiengo, A., Assan, R., Frerichs, H., Creutzfeldt, W., Turner, D. S., Baker, R. W., Gent, W. G. L., Shabaan, A., Marks, V., Young, D. A. B., Vague, Ph., Heim, H., Laval, C. Martin, Vegezzi, M., Campo, C.Di, Rahamandridona, G., Garron, D., Heyraud, B., Vague, J., Valverde, I., Villanueva, M. L., Lozano, I., Diaz-Fierros, M., Marco, J., Van Assche, F. A., Gepts, W., Van Obberghen, E., Somers, G., Devis, G., Vaughan, G. D., Malaisse-Lagae, F., Orci, L., Malaisse, W. J., Veleminsky, J., Spirova, E., Waldhäusl, W., Frisch, H., Haydl, H., Weiss, L., Löffler, G., Wieland, O., Willms, B., Deuticke, U., Wollheim, C. B., Marliss, E. B., Blondel, B., Orci, L., Like, A., Renold, A. E., Zrůstová, M., and Roštlapil, J.

Published
1973
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11. European Association for the study of Diabetes First Annual Meeting, Montecatini Terme, 20. IV.-22.IV. 1965

Author

Manchester, K. L., Clausen, T., Azerad, E., Lubetzki, J., Feiedlek, D., Kreis, H., Duprey, J., Ammon, J., Ditschuneit, H., Oster, W., Telib, M., Gutte, B., Brinkhoff, O., Zahn, H., Butterfield, W. J. H., Abrams, M. E., Boyns, D. R., Buckle, A. L. J., Cox, B. D., Hanley, T., Hartley, S., Sells, R., Sterky, G., Veall, N., Whichelow, M. J., Wigglesworth, A., Zampa, G. A., McIntyre, N., Turner, D. S., Holdsworth, C. D., Hansson, Göran, Angervall, Lennart, Ceresa, F., Segre, G., Vitelli, A., Martino, P., Martini, P. F., Ghemi, F., Welborn, T., Samaan, N., Fraser, R., Brown, J., Felber, J. P., Mody, A. J., Franckson, J. R. M., Conard, V., Malaisse, W., BaLasse, E., Rasio, E., Bastenie, P. A., Schwarz, K., Bottermann, P., Gordon, Edgar S., Kinsell, L. W., Schlierf, G., Han, Y., Samols, Ellis, Jones, Valerie, Pellegrini, G., Maggi, G., Rodari, T., Specchia, G., Abquilla, E. R., Ooms, H. A., Heding, Lise, Korec, R., Mialhe, P., Sutter, B., Meyer, V., Halmos, T., Loozka, B., Salamonv, F., Beyer, J., Schöffling, K., Melani, F., Walter, A., Althoff, P., Melant, F., Pfeiffer, B. F., Sonksen, P. H., Ellis, J., Lowy, C., Rütherford, A., Nabarro, J. D. N., Humbel, R. E., Müller, W. A., Bürgi, B., Ginsberg, J. L., Labhart, A., Froesch, E. R., Jörgensen, K. R., Derot, M., Assan, R., Rathery, M., Tchobroutsky, G., Rosselin, G., Löffler, G., Weinges, K. F., Daweke, H., Oberdisse, K., Reinwein, D., Bethge, H., Schilling, W., Pirart, J., Lauvaux, J. P., Pallardo, L. -F., Bermejo, A. Garcia, Giner, G., Tarreo, J. L. Muñoz, Cerrato, J. Cabezas, Polosa, P., Motta, L., Turrisi, E., Frerichs, H., Creutzfeldt, W., Houtsmuller, A. J., Lestradet, H., Labram, Cl., Grégoire, J., Gout, M., Loubatières, A., Mariani, M. M., Chapal, J., Taylor, J., Houareau, M. H., Rondot, A. M., Czyzyk, A., Lawecki, J., Söling, H. D., Kneer, P., Mooshagen, D., Scutella, E., Struck, E., Geyer, S., Wieland, O., Škrabalo, Z., Stavrinić, A., Črepinko, I., Jaksic, Z., Pieri, A., Scarpelli, P. T., Hansen, Østerby, Gregersen, R. G., Lundbaek, K., Olsen, S., Keen, H., Chlouverakis, C., Reske-Nielsen, E., and Rafaelsen, O. J.

Published
1965
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14. Evidence for two different types of P2 receptors stimulating insulin secretion from pancreatic B cell

Author

Petit, P, Hillaire-Buys, D, Manteghetti, M, Debrus, S, Chapal, J, and Loubatières-Mariani, M M

Subjects
Male, Potassium Channels, Receptors, Purinergic P2, Sodium Chloride Symporter Inhibitors, Diazoxide, Thionucleotides, Rats, Adenosine Diphosphate, Islets of Langerhans, Adenosine Triphosphate, Glucose, Papers, Insulin Secretion, Animals, Insulin, Rats, Wistar, Diuretics, Rubidium Radioisotopes
Abstract

Adenine nucleotides have been shown to stimulate insulin secretion by acting on P2 receptors of the P2Y type. Since there have been some discrepancies in the insulin response of different analogues of ATP and ADP, we investigated whether two different types of P2 receptors exist on pancreatic B cells. The effects of alpha,beta-methylene ATP, which is more specific for the P2X subtype, were studied in vitro in pancreatic islets and isolated perfused pancreas from rats, in comparison with the potent P2Y receptor agonist ADPbetaS. In isolated islets, incubated with a slightly stimulating glucose concentration (8.3 mM), alpha,beta-me ATP (200 microM) and ADPbetaS (50 microM) similarly stimulated insulin secretion; by contrast, under a non stimulating glucose concentration (3 mM), alpha,beta-me ATP was still effective whereas ADPbetaS was not. In the same way, in islets perifused with 3 mM glucose, alpha,beta-me ATP but not ADPbetaS induced a partial but significant reduction in the peak 86Rb efflux induced by the ATP-dependent potassium channel opener diazoxide. In the isolated pancreas, perfused with a non stimulating glucose concentration (4.2 mM), ADPbetaS and alpha,beta-me ATP (5-50 microM), administered for 10 min, induced an immediate, transient and concentration-dependent increase in the insulin secretion; their relative potency was not significantly different. In contrast, with a slightly stimulating glucose concentration (8.3 mM), ADPbetaS was previously shown to be 100 fold more potent than alpha,beta-me ATP. Furthermore, at 4.2 mM glucose a second administration of alpha,beta-me ATP was ineffective. In the same way, ADPbetaS was also able to desensitize its own insulin response. At 3 mM glucose, alpha,beta-me ATP as well as ADPbetaS (50 microM) induced a transient stimulation of insulin secretion and down regulated the action of each other. These results give evidence that pancreatic B cells, in addition to P2Y receptors, which potentiate glucose-induced insulin secretion, are provided with P2X receptors, which transiently stimulate insulin release at low non-stimulating glucose concentration and slightly affect the potassium conductance of the membrane.

Published
1998

15. Effects of homocysteine on acetylcholine- and adenosine-induced vasodilatation of pancreatic vascular bed in rats

Author

Quéré, I, Hillaire-Buys, D, Brunschwig, C, Chapal, J, Janbon, C, Blayac, J P, Petit, P, and Loubatières-Mariani, M M

Subjects
Male, Adenosine, Vasodilator Agents, Muscle, Smooth, In Vitro Techniques, Acetylcholine, Rats, Perfusion, Vasodilation, Ileum, Papers, Animals, Humans, Endothelium, Vascular, Rats, Wistar, Homocysteine, Pancreas, Cell Division, Cells, Cultured, Muscle Contraction
Abstract

1. Epidemiological and experimental data have shown that homocysteine may provoke vascular lesions and that moderate homocysteinaemia may constitute an independent risk factor for vascular disease. It is now documented that homocysteine damages human endothelial cells in culture, possibly by producing hydrogen peroxide in an oxygen-dependent reaction. 2. In this study, we have examined the direct effect of this sulphur amino acid on pancreatic vascular resistance. Experiments were performed on the vascular bed of the rat isolated pancreas perfused at constant pressure; thus, any change in pancreatic vascular resistance resulted in a change in the flow rate. D,L-Homocysteine perfused for one hour at three different concentrations (200 microM, 2 mM, 20 mM) did not induce any significant change in the flow rate per se. Homocysteine infusion for 30 min at a concentration of 200 microM or 2 mM abolished the endothelium-dependent vasodilatation induced by acetylcholine (0.05 microM), but did not modify adenosine (1.5 microM)-induced vasodilatation. 3. The effect of D,L-homocysteine (200 microM or 2 mM) cannot be ascribed to a direct antimuscarinic effect since 30 min pretreatment of rat ileum with these concentrations did not significantly change the contractile effect of increasing concentrations of acetylcholine (0.015-15 microM). 4. Preincubation of human umbilical vein endothelial cells with D,L-homocysteine (0.2-5.0 mM) had no significant effect on overall cell number or viability during 18 h of incubation; the endothelial cells exposed to concentrations up to 5 mM exhibited a spindle-shaped, whirled pattern. This pattern was reversed 48 h after the removal of homocysteine. A cytotoxic effect was seen after 18 h incubation in 10 mM D,L-homocysteine. 5. In conclusion, an acute infusion of homocysteine altered acetylcholine endothelium-induced vasodilation, whereas the adenosine vasodilatator effect was insensitive to the deleterious action of homocysteine in vitro.

Published
1997

31. Untitled.

Author

Laurent, F., Hillaire-Buys, D., Chapal, J., Dietz, S., Portet, K., Cros, G., Petit, P., and Michel, A.

Abstract

In the present work, we have studied adenosine-induced vasodilation in streptozotocin-induced diabetic rats and compared it to that observed in normal age-matched or weight-matched animals. Experiments were performed on a vascular bed, the isolated perfused pancreas, and a large vessel, the thoracic aorta, provided from the same animal. Vasodilator activity was assessed, for isolated pancreas, as the increase in flow induced by the infusion of 2 µM adenosine for 30 min, or for noradrenaline-contracted aortae, as the relaxant response to adenosine (1 µM–1 mM). In both preparations the results obtained with selective adenosine receptors ligands (CPA, CGS 21680 and NECA) agreed with the presence of adenosine receptor of A2a subtype. In normal animals, adenosine vasodilator activity on both preparations diminished with advancing age in the rat, while diabetes was associated with a decreased or increased responsiveness to adenosine in pancreatic vascular bed or aorta, respectively. Further, the involvement of nitric oxide (NO), in relaxant responses, was evaluated by the use of the NO synthase inhibitor N ω-nitro- l-arginine methyl ester ( l-NAME). In all groups of animals, the flow rate of isolated pancreas dropped in the presence of 200 µM l-NAME, but was restored by adenosine to the level observed without l-NAME. l-NAME (10 µM) significantly reduced the dilator response to adenosine in aortic rings from diabetic animals, but not in those from normal rats. These results showed that adenosine vasorelaxant activity is significantly but differentially altered by diabetes according to the origin of the vascular preparation, and suggest that NO is involved in the vasorelaxant activity of adenosine in large vessels of diabetic animals. The potential pathophysiological role of adenosine in the vascular complications of diabetes remains to be determined. [ABSTRACT FROM AUTHOR]

Published
1999
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34. Insulino-s�cr�tion �tudi�e sur Ie pancr�as isol� et perfus� du rat

Author

Chapal J, Mariani Mm, and Loubatières Al

Subjects
Glibenclamide, Tolbutamide, Chemistry, Endocrinology, Diabetes and Metabolism, Internal Medicine, medicine, Human physiology, Insulin secretion, Molecular biology, medicine.drug
Abstract

Nos experiences effectuees sur le pancreas isole et perfuse du rat montrent que: 1. En l'absence de glucose, le pancreas secrete seulement une tres petite quantite d'insuline: c'est la secretion basale. — 2. Quand on utilise des concentrations croissantes de glucose, le debit d'insuline augmente en fonction de la concentration de glucose (suivant une courbe sigmoide). — 3. Le tolbutamide seul, en l'absence de glucose, augmente legerement la secretion basale. — 4. Le tolbutamide potentialise les effets insulino-secreteurs de concentrations croissantes de glucose. En presence de tolbutamide, la quantite supplementaire d'insuline secretee s'eleve en meme temps que la concentration de glucose, jusqu'a 2 g/1; a 3 g/1 elle diminue. — 5. A forte concentration (100 mg/1), l'effet potentialisateur du tolbutamide sur l'insulino-secretion due au glucose (1.5 g/1) se prolonge bien au dela de l'arret de l'infusion du sulfamide. A faible concentration (5 mg/1) il cesse des que l'infusion est supprimee. — 6. Le glibenclamide (a faible concentration: 1 μg/1), non seulement potentialise l'action du glucose, mais aussi prolonge son action stimulante sur la cellule beta, longtemps apres la suppression du sulfamide hypoglycemiant. — 7. Dans nos conditions experimentales, l'administration repetee de tolbutamide, en presence de glucose, ne modifie pas la reponse insulino-secretoire du pancreas a ce sulfamide.

Published
1970
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35. Studies of the cholinergic receptors involved in the secretion of insulin using isolated perfused rat pancreas

Author

Alric R, Loubatières Al, Chapal J, and M. M. Loubatières-Mariani

Subjects
Atropine, medicine.medical_specialty, Sensory Receptor Cells, Physostigmine, Endocrinology, Diabetes and Metabolism, Stimulation, In Vitro Techniques, Biology, Islets of Langerhans, chemistry.chemical_compound, Parasympathetic Nervous System, Internal medicine, Insulin Secretion, Muscarinic acetylcholine receptor, Internal Medicine, medicine, Muscarinic acetylcholine receptor M4, Animals, Insulin, Muscarine, Muscarinic acetylcholine receptor M3, Muscarinic acetylcholine receptor M2, Acetylcholine, Rats, Perfusion, Glucose, Endocrinology, Parasympathomimetics, chemistry, Cholinergic, medicine.drug
Abstract

Studies of the role and nature of the cholinergic receptors acting on the secretion of isolated perfused rat pancreas have shown the following: The infusion of acetylcholine at a dose of 2.5 μM in the presence of a concentration of glucose of 1.5 g/1, provoked a first phase of immediate and important stimulation of the secretion of insulin; this initial peak of insulin secretion was followed by a second phase during which a new less intense stimulation occurred; the latter was followed by an inhibition appearing at a time that depended on the pancreas used. At a dose of 0.5 μM of acetylcholine, the first phase of stimulation always appeared; during the second phase some pancreases were inhibited, others remained stimulated. — The peak of insulin secretion obtained by stimulation with acetylcholine during the first phase was dose related. — Eserine intensified the effects of acetylcholine. — The presence of glucose was essential for the insulinsecretory action of acetylcholine. The muscarinic nature of the cholinergic receptors implicated in the secretion of insulin was demonstrated by the use of: — Atropine which completely blocked the effects of acetylcholine, — Muscarine which produced the same effects as acetylcholine on our pancreas preparation, effects which were equally inhibited by atropine. The cholinergic receptors of the endocrine beta cell of the islet of Langerhans of the pancreas are therefore of the muscarinic type.

Published
1973
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36. Action nocive de l'adr�naline pour la structure histologique des �lots de Langerhans du pancr�as. Action protectrice de la dihydroergotamine

Author

M. M. Mariani, Rondot Am, J. Taylor, M. H. Houareau, A. Loubatières, and Chapal J

Subjects
Gynecology, medicine.medical_specialty, business.industry, Endocrinology, Diabetes and Metabolism, Internal Medicine, medicine, Human physiology, business
Abstract

Des perfusions de doses non hypertensives d'adrenaline (0,5 μg/kg/min) ont ete effectuees pendant 2 a 6 heures chez le chien par la voie de l'artere gastroepiploique droite, branche de l'artere pancreatico-duodenale. Dans certaines experiences le pancreas a ete maintenu intact; dans d'autres la portion splenique ainsi que le ≪processus uncinatus≫ ont ete extirpes. Des biopsies pancreatiques ont ete pratiquees a divers stades de la perfusion. Les cellules des ilots et particulierement les cellules beta ont ete trouvees gravement lesees; cependant le tissu exocrine etait relativement conserve. La glycemie s'est elevee pendant la perfusion puis est redescendue vers la normale. Les jours suivants 35 pour 100 des animaux porteurs seulement de la portion duodenale du pancreas ont presente un diabete persistant; 65 pour 100 ont gueri. La dihydroergotamine s'oppose a l'action nocive de l'adrenaline pour les cellules des ilots. La noradrenaline a paru moins nocive que l'adrenaline. Ces faits sont discutes en ce qui concerne la pathologie du diabete et en particulier pour l'interpretation du diabete concomitant de pheochromocytomes.

Published
1965
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38. 2-Thioether 5‘-O-(1-Thiotriphosphate)adenosine Derivatives as New Insulin Secretagogues Acting through P2Y-Receptors

Author

Fischer, B., Chulkin, A., Boyer, J. L., Harden, K. T., Gendron, F.-P., Beaudoin, A. R., Chapal, J., Hillaire-Buys, D., and Petit, P.

Abstract

P2-Receptors (P2-Rs) represent significant targets for novel drug development. P2-Rs were identified also on pancreatic B cells and are involved in insulin secretion. Therefore, novel P2Y-R ligands, 2-thioether 5‘-O-phosphorothioate adenosine derivatives (2-RS-ATP-α-S), were synthesized as potential insulin secretagogues. An efficient synthesis of these nucleotides and a facile method for separation of the chiral products are described. The enzymatic stability of the compounds toward pig pancreas type I ATPDase was evaluated. The rate of hydrolysis of 2-hexylthio-5‘-O-(1-thiotriphosphate)adenosine (2-hexylthio-ATP-α-S) isomers by ATPDase was 28% of that of ATP. Some 2-thioether 5‘-(monophosphorothioate)adenosine derivatives (2-RS-AMP-S) exerted an inhibitory effect on ATPDase. The apparent affinity of the compounds to P2Y1-R was determined by measurement of P2Y-R-promoted phospholipase C activity in turkey erythrocyte membranes. 2-RS-ATP-α-S derivatives were agonists, stimulating the production of inositol phosphates with K0.5 values in the nanomolar range. 2-RS-AMP-S derivatives were full agonists, although 2 orders of magnitude less potent. All the compounds were more potent than ATP. The effect on insulin secretion and pancreatic flow rate was evaluated on isolated and perfused rat pancreas. A high increase, up to 500%, in glucose-induced insulin secretion was due to addition of 2-hexylthio-ATP-α-S in the nanomolar concentration range, which represents 100-fold enhancement of activity relative to ATP. 2-Hexylthio-AMP-S was 2.5 orders of magnitude less effective.

Published
1999

39. Involvement of K+channel permeability changes in the L‐NAME and indomethacin resistant part of adenosine‐5′‐O‐(2‐thiodiphosphate)‐induced relaxation of pancreatic vascular bed

Author

Hillaire‐Buys, D, Chapal, J, Linck, N, Blayac, J P, Petit, P, and Loubatières‐Mariani, M M

Abstract

We have previously demonstrated that adenosine‐5′‐O‐(2‐thiodiphosphate) (ADPβS), a potent P2Y‐purinoceptor agonist, relaxed pancreatic vasculature not only through prostacyclin (PGI2) and nitric oxide (NO) release from the endothelium but also through other mechanism(s). In this study, we investigated the effects of an inhibitor of the Na+/K+pump, of ATP‐sensitive K+(KATP) channels and of small (SKCa) or large (BKCa) conductance Ca2+‐activated K+channels. Experiments were performed at basal tone and during the inhibition of NO synthase and cyclo‐oxygenase.In control conditions, ADPβS (15 μM) induced an initial transient vasoconstriction followed by a progressive and sustained vasodilatation. In the presence of Nω‐nitro‐L‐arginine methyl ester (L‐NAME, 200 μM) the transient vasoconstriction was reversed into a one minute vasodilator effect, which was then followed by a progressive and sustained vasodilatation similar to that observed with ADPβS alone. The addition of indomethacin (10 μM) did not significantly modify the profile of ADPβS‐induced vasodilatation.Ouabain (100 μM) decreased basal pancreatic flow rate and did not modify ADPβS‐induced relaxation. This inhibitor of the Na+/K+pump increased the pancreatic vasoconstriction induced by L‐NAME or by the co‐administration of L‐NAME and indomethacin. Ouabain did not modify either the L‐NAME or the L‐NAME/indomethacin resistant part of the ADPβS vasodilatation.The KATPinhibitor tolbutamide (185 μM) did not significantly modify basal pancreatic flow rate and ADPβS‐induced relaxation. This inhibitor which did not change L‐NAME‐induced vasoconstriction, significantly diminished the L‐NAME resistant part of ADPβS‐induced vasodilatation. Tolbutamide intensified the vasoconstriction induced by the co‐administration of L‐NAME and indomethacin. In contrast, the L‐NAME/indomethacin resistant part of ADPβS vasodilatation was not changed by the closure of KATP.The SKCainhibitor apamin (0.1 μM) did not significantly change pancreatic vascular resistance whatever the experimental conditions (in the absence or in presence of L‐NAME or L‐NAME/indomethacin). In the presence of L‐NAME, the closure of SKCachannels changed the one minute vasodilator effect of ADPβS into a potent vasoconstriction and thereafter modified only the beginning of the second part of the L‐NAME‐resistant part of the ADPβS‐induced vasodilatation. In contrast, the L‐NAME/indomethacin resistant part of ADPβS‐induced relaxation remained unchanged in the presence of apamin.Charybdotoxin (0.2 μM), an inhibitor of BKCa, increased pancreatic vascular resistance in the presence of L‐NAME/indomethacin. In the presence of L‐NAME, the closure of BKCachannels reversed the one minute vasodilator effect of ADβPS into a potent vasoconstriction and drastically diminished the sustained vasodilatation. In contrast the L‐NAME/indomethacin resistant part of ADPβS‐induced relaxation was not modified by the presence of charybdotoxin. Under L‐NAME/indomethacin/charybdotoxin/apamin infusions, ADPβS evoked a drastic and transient vasoconstriction reaching a maximum at the second minute, which was followed by a sustained increase in the flow rate throughout the ADPβS infusion. The maximal vasodilator effect of ADPβS observed was not modified by the addition of apamin.The results suggest that the L‐NAME‐resistant relaxation induced by ADPβS in the pancreatic vascular bed involves activation of BKCa, KATPand to a lesser extent of SKCachannels, but the L‐NAME/indomethacin resistant part of ADPβS‐induced relaxation is insensitive to the closure of KATP, SKCaand BKCachannels.

Published
1998
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40. Different effects of hypothermia on insulin and glucagon secretion from the isolated perfused rat pancreas

Author

Chapal J, Raymond Puech, F. Lignon, G. Valette, and Marie-Madeleine Loubatières-Mariani

Subjects
medicine.medical_specialty, Arginine, Tolbutamide, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Glucagon, Hypothermia, Induced, Internal medicine, Insulin Secretion, Internal Medicine, medicine, Animals, Insulin, Pancreas, Chemistry, Glucagon secretion, Hypothermia, Acetylcholine, Rats, Insulin oscillation, Perfusion, Glucose, Endocrinology, medicine.symptom, medicine.drug
Abstract

Two series of experiments with the isolated perfused rat pancreas were performed in parallel. The conditions differed only with respect to temperature, which was 37.5 degrees C in one series and 28 degrees C in the other. The lowering of the temperature decreased insulin secretion induced by glucose as well as the insulin response to tolbutamide and acetylcholine. Unlike insulin, glucagon secretion was not significantly modified by hypothermia. Our results suggest that the mechanisms involved in glucagon and insulin secretion are different.

Published
1980
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41. Purine nucleotides and insulin secretion

Author

G. Valette, Chapal J, and Marie-Madeleine Loubatières-Mariani

Subjects
chemistry.chemical_classification, Purine, chemistry.chemical_compound, chemistry, Biochemistry, Nucleotide, Insulin secretion
Published
1978
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42. Analysis of the stimulating action of tolbutamide on the secretion of insulin using mannoheptulose and diazoxide

Author

Chapal J, M. M. Loubatières-Mariani, and Loubatières Al

Subjects
medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Tolbutamide, In Vitro Techniques, chemistry.chemical_compound, Internal medicine, Insulin Secretion, Internal Medicine, medicine, Diazoxide, Animals, Insulin, Secretion, Drug Interactions, Insulin secretion, Pancreas, Chemistry, Human physiology, Heptoses, Stimulation, Chemical, Rats, Perfusion, Endocrinology, Glucose, Sulfonylurea Compounds, Mannoheptulose, medicine.drug
Abstract

The stimulating action of tolbutamide on insulin secretion presents two components; the first is independent of the presence of glucose in the medium which perfuses the beta cells; the second is, on the contrary, dependent upon glucose. D-mannoheptulose and diazoxide permit the dissociation of these two components; the antagonistic effect of the first exerts itself uniquely on that part of the stimulating action of tolbutamide which is gluco-dependent; on the contrary, the antagonistic effect of the second exerts itself on both phases of the stimulating action of the sulfonamide.

Published
1973

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