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Start Over Author "F. Massara" Journal diabetologia
9 results on '"F. Massara"'

1. Seventh Annual Meeting of the European Association for the Study of Diabetes

Author

Bo Hellman, G. C. Palmieri, N. Mihalache, P. Siltanen, G. Bagnariol, W. K. Waldhäusl, M. Javicoli, U. Klör, F.A. Van Assche, M. Rathery, O. Melogli, D. Fedele, E. F. Pfeiffer, G. K. Rastogi, M. Bretán, R. R. de Mowbray, Poul Ebbe Nielsen, A. E. Lambert, Aa. Prange Hansen, Guido Tamburrano, J. C. Sodovez, B. Riveline, J. Canivet, Bartelt Km, S. Efendic, Franco Camanni, J. P. Bali, J. R. Claude, C. Rouiller, B. Schulz, M. Hinz, E. Eschwege, M. M. Mariani, M. Vigas, L. Kammerer, G. Enzi, M. Prud'homme, F. Massi-Benedetti, P. P. Foà, A. Ghidoni, I. M. Burr, L. Niklas, L. Nye, Sotirios Raptis, U. Brinck, B. Meyer, Hamish W. Sutherland, H. Laube, W. R. Drucker, B. Lesobre, H. J. Quabbe, M. A. Page, Åke Lernmark, Raimundo Goberna, M. Muggio, A. van't Laar, R. F. Murphy, Jens F. Rehfeld, Rolf Luft, C. E. Østerby, H. Karmann, K. E. Schröder, Ch. Thum, K. A. Munday, N. Mosora, Y. Kanazawa, D. P. Cameron, C. V. Tompkins, R. E. Levett, P. H. Sönksen, Domenico Andreani, R. D. M. Scott, P. J. Reeds, R. Fellin, A. Loubatières, M. J. Smith, J. Samsel, H. Iwatsuka, A. J. Valleron, S. Persson, K. Pyörälä, Victor Conard, J. M. Warnet, P. Polosa, R. Sparthe, A. Gordon, Y. Abdel Rahman, E. Fusco, Felix P. N. Schennetten, M. C. Srivastava, K. Johansen, D. Wübbens, F. Dauchy, Keith D. Buchanan, J. Marco, W. Teller, W. Poser, J. D. N. Nabarro, M. Rousselet, A. Hasselblatt, G. Rothenbuchner, H. Ørskov, G. M. Molinatti, J. Schönborn, A. Vitelli, A. M. McCarroll, Inge Bert Täljedal, M. Amherdt, R. Knussman, F. A. Gries, L. Orci, Beyer J, F. Jallet, J. Schlichtkrull, Z. Skrabalo, J. Vincze, W. Korp, Schöffling K, Ev. Kriedstein, E. B. Möller, J. Landon, S. Frezzato, H. Wingstrand, F. Massara, G. E. Rosselin, G. J. A. I. Snodgrass, H. L. Fehm, D. Michaelis, S. Le Guilcher, K. Seyer-Hansen, C. Kruger, D. M. Kipnis, J. Mirouze, María L. Villanueva, O. Oelz, P. J. Lefèbvre, V. Duma, Per Westermark, E. Giangrandi, M. R. Turner, H. Bibergeil, G. R. Brisson, J. Birk, T. Mincu, I. M. Baroja, M. R. P. Hall, G. Wick, Patricia Metzger, Werner Oppermann, E. Jutzi, Guido Pozza, P. Jacquet, A. Kopf, J Ostman, N. Conte, R. Fuchs, Theodore Ehrenreich, I. Mincu, Barbara Rudas, A. S. Luyckx, A. E. Renold, A. Schirmann, U. Klemens, R. E. Haist, V. Nuteanu, L. Papoz, R. Spaethe, G. Tohobroutsky, W. Hildmann, V. Gligore, B. Morell, G. Tchobroutsky, Willy Malaisse, J. Sterne, G. Löffler, N. S. Track, E. B. Marliss, EskoA. Nikkilä, C. R. C. Heard, Tr. Baciu, F. Fallucca, E. Krug, J. Trap-Jensen, Isabel Valverde, Rafael A. Camerini-Davalos, S. Klahr, L. Stimmler, C. Rosak, M. Motocou, K. W. Taylor, H. Otto, O. Wieland, K. Lundbak, Th. Koschinsky, R. Assan, E. Cerasi, M. Toeller, S. Triggs, W. Stauffacher, Haupt E, R. J. Dash, C. Scandellari, E. R. Froesch, F. J. Woodroffe, L. Balant, M. Verry, M. Lunetta, A. Tiengo, D. G. Parry, L. Weiss, M. Kikuchi, Uwe Panten, G. C. Viberti, B. Blondel, J. D. Teale, J. C. Dunbar, N. S. Bricker, C. E. Ruth, M. K. Sinha, W. Braun, M.R. Taskinen, D. H. Williamson, U. Loos, O. Steingaszner, Giovanni Federspil, L. Herberg, S. Georgescu, R. Fussgänger, J. Hewitt, A. L. Bergström, S. Levin Nielsen, H. Schatz, E. Lehtovirta, Jurgen Steinke, I. Lozano, F. Sodovez-Goffaux, D. R. Langslow, E. Speich, I. Neumann, G. Menzinger, A. Tinant, S. Munkgaard Rasmussen, Janove Sehlin, C. Dumitrescu, N. Katsilambros, A. Tognetti, Ligia Simionesco, C. Oliver, C. E. Mogensen, A. E. Pappalettera, P. Vague, K. Sträub, L. Motta, J. Vague, A. Orsetti, Mme A. Serre, B. M. Freeman, A. Trisotto, R. Korec, M. Diaz-Fierros, F. Stadil, S. Campeanu, J. Sabin, H. P. T. Ammon, P. Mialhe, F. Legros, C. Rogister, R. Schröder, V. Maier, Risto Pelkonen, F. Scaroina, M. Parvulescu, and K. E. Schenk

Subjects
medicine.medical_specialty, business.industry, Endocrinology, Diabetes and Metabolism, Association (object-oriented programming), Family medicine, Ophthalmology, Diabetes mellitus, Internal Medicine, medicine, Human physiology, business, medicine.disease
Published
1972
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2. Depressed tolbutamide-induced insulin response in subjects treated with propranolol

Author

Strumia E, Franco Camanni, G. M. Molinatti, and F. Massara

Subjects
Adult, Blood Glucose, Male, Drug, medicine.medical_specialty, Tolbutamide, Endocrinology, Diabetes and Metabolism, media_common.quotation_subject, Administration, Oral, Propranolol, Pharmacology, Internal medicine, Insulin Secretion, Insulin response, Internal Medicine, medicine, Humans, Insulin, Insulin secretion, media_common, business.industry, Human physiology, Middle Aged, Endocrinology, Depression, Chemical, Injections, Intravenous, Female, Plasma insulin, business, medicine.drug
Abstract

The effect of propranolol on 1 g i.v. tolbutamide-induced insulin response was studied in 11 subjects. The drug depressed this response, the effect being more noticeable in the patients receiving 200 mg/ dayper os for three days. The corresponding blood glucose curves, however, were unaffected by propranolol. The finding suggest that the beta-receptors play a part in sulphonylurea-induced insulin secretion in man.

Published
1971
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3. Glucagon induced hyperkalaemia in diabetes

Author

F. Massara, Enrico Cagliero, and G. M. Molinatti

Subjects
medicine.medical_specialty, Hyperkalemia, business.industry, Endocrinology, Diabetes and Metabolism, Human physiology, Glucagon, medicine.disease, Endocrinology, Internal medicine, Diabetes mellitus, Diabetes Mellitus, Internal Medicine, medicine, Humans, medicine.symptom, business
Published
1983
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4. Glucagon-induced increase in plasma potassium levels in type 1 (insulin-dependent) diabetic subjects

Author

Enrico Cagliero, G. M. Molinatti, V. Martina, and F. Massara

Subjects
Adult, Blood Glucose, Male, medicine.medical_specialty, Adolescent, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Potassium, chemistry.chemical_element, Glucagon, Internal medicine, Diabetes mellitus, Mole, Internal Medicine, medicine, Diabetes Mellitus, Humans, Insulin, Decompensation, Saline, medicine.disease, Somatostatin, Endocrinology, chemistry, Female
Abstract

To investigate the hypothesis that in Type 1 (insulin-dependent) diabetes the increase in plasma potassium during decompensation may be due to a rise in glucagon concentrations, we have measured plasma glucose, potassium and glucagon levels in five diabetic patients during two tests with 0.154 mol/l saline or somatostatin (500 micrograms/h) performed on two successive days. The patients were maintained normoglycaemic overnight by means of a continuous insulin infusion. After insulin withdrawal during the saline infusion, glucose and potassium levels rose markedly (delta maximum: glucose, 12.0 +/- 1.5 mmol/l; potassium, 0.73 +/- 0.12 mmol/l), while glucagon showed a slight, but significant increment (delta maximum: 10.6 +/- 1.0 pmol/ml, p less than 0.05). The potassium increment was not mediated by a reduction in blood pH. Somatostatin abolished the rise in glucagon concentration and simultaneously markedly inhibited the rise in potassium and glucose levels. It is concluded that in acute insulin deficiency, glucagon could be one of the factors that contributes to hyperkalaemia.

Published
1983

5. Influence of glucagon on plasma levels of potassium in man

Author

F. Massara, Franco Camanni, Enrico Cagliero, S. Martelli, and G. M. Molinatti

Subjects
Adult, Blood Glucose, Male, endocrine system, medicine.medical_specialty, Hyperkalemia, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Potassium, chemistry.chemical_element, Glucagon, chemistry.chemical_compound, Diabetes mellitus, Internal medicine, Internal Medicine, medicine, Humans, Insulin, Saline, Aldosterone, Chemistry, medicine.disease, Endocrinology, Somatostatin, Female, medicine.symptom, hormones, hormone substitutes, and hormone antagonists
Abstract

To investigate the role played by glucagon in the regulation of plasma potassium, we have examined the behaviour of this ion during four 2 h infusions of saline, glucagon (200 ng/min), cyclic somatostatin (priming dose of 50 microgram followed by 5.8 microgram/min) and somatostatin plus glucagon in 6 normal volunteers. Glucagon alone produced no change in potassium, despite an increase in insulin. Somatostatin, in addition to depressing insulin, produced a slight but significant (P0.01) increase in potassium (delta max: 0.2-0.8 mmol/1: mean +/- SEM, 0.4 +/- 0.1). Infusion of somatostatin together with glucagon suppressed the glucagon-induced increase in insulin and greatly augmented the increase in blood glucose. Potassium rose significantly more (P0.02) than after somatostatin alone (delta max: 0.5-1.3 mmol/l; mean 0.9 +/- 0.1), indicating that hyperkalaemia results from hyperglucagonaemia in the absence of insulin. Evidence is presented that this last phenomenon is not mediated by hyperglycaemia or by a reduction in aldosterone secretion. It is suggested that low blood insulin and increased glucagon could be one of the mechanisms that underlie or magnify the hyperkalaemia observed in cases of serious stress or decompensated diabetes.

Published
1980

7. Glucagon-induced increase in plasma potassium levels in type 1 (insulin-dependent) diabetic subjects.

Author

Cagliero E, Martina V, Massara F, and Molinatti GM

Subjects
Adolescent, Adult, Blood Glucose analysis, Diabetes Mellitus drug therapy, Female, Glucagon blood, Humans, Insulin therapeutic use, Male, Somatostatin pharmacology, Diabetes Mellitus blood, Glucagon physiology, Potassium blood
Abstract

To investigate the hypothesis that in Type 1 (insulin-dependent) diabetes the increase in plasma potassium during decompensation may be due to a rise in glucagon concentrations, we have measured plasma glucose, potassium and glucagon levels in five diabetic patients during two tests with 0.154 mol/l saline or somatostatin (500 micrograms/h) performed on two successive days. The patients were maintained normoglycaemic overnight by means of a continuous insulin infusion. After insulin withdrawal during the saline infusion, glucose and potassium levels rose markedly (delta maximum: glucose, 12.0 +/- 1.5 mmol/l; potassium, 0.73 +/- 0.12 mmol/l), while glucagon showed a slight, but significant increment (delta maximum: 10.6 +/- 1.0 pmol/ml, p less than 0.05). The potassium increment was not mediated by a reduction in blood pH. Somatostatin abolished the rise in glucagon concentration and simultaneously markedly inhibited the rise in potassium and glucose levels. It is concluded that in acute insulin deficiency, glucagon could be one of the factors that contributes to hyperkalaemia.

Published
1983
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8. Influence of glucagon on plasma levels of potassium in man.

Author

Massara F, Martelli S, Cagliero E, Camanni F, and Molinatti GM

Subjects
Adult, Aldosterone biosynthesis, Blood Glucose analysis, Female, Humans, Hyperkalemia etiology, Insulin blood, Male, Somatostatin pharmacology, Glucagon pharmacology, Potassium blood
Abstract

To investigate the role played by glucagon in the regulation of plasma potassium, we have examined the behaviour of this ion during four 2 h infusions of saline, glucagon (200 ng/min), cyclic somatostatin (priming dose of 50 microgram followed by 5.8 microgram/min) and somatostatin plus glucagon in 6 normal volunteers. Glucagon alone produced no change in potassium, despite an increase in insulin. Somatostatin, in addition to depressing insulin, produced a slight but significant (P < 0.01) increase in potassium (delta max: 0.2-0.8 mmol/1: mean +/- SEM, 0.4 +/- 0.1). Infusion of somatostatin together with glucagon suppressed the glucagon-induced increase in insulin and greatly augmented the increase in blood glucose. Potassium rose significantly more (P < 0.02) than after somatostatin alone (delta max: 0.5-1.3 mmol/l; mean 0.9 +/- 0.1), indicating that hyperkalaemia results from hyperglucagonaemia in the absence of insulin. Evidence is presented that this last phenomenon is not mediated by hyperglycaemia or by a reduction in aldosterone secretion. It is suggested that low blood insulin and increased glucagon could be one of the mechanisms that underlie or magnify the hyperkalaemia observed in cases of serious stress or decompensated diabetes.

Published
1980
Full Text
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9. Depressed tolbutamide-induced insulin response in subjects treated with propranolol.

Author

Massara F, Strumia E, Camanni F, and Molinatti GM

Subjects
Administration, Oral, Adult, Blood Glucose, Depression, Chemical, Female, Humans, Injections, Intravenous, Insulin blood, Insulin Secretion, Male, Middle Aged, Propranolol administration & dosage, Tolbutamide antagonists & inhibitors, Insulin metabolism, Propranolol pharmacology, Tolbutamide administration & dosage
Published
1971
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