Search Results - (Author, Cooperation:R. Buzzetti)
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1A. Ichimura ; A. Hirasawa ; O. Poulain-Godefroy ; A. Bonnefond ; T. Hara ; L. Yengo ; I. Kimura ; A. Leloire ; N. Liu ; K. Iida ; H. Choquet ; P. Besnard ; C. Lecoeur ; S. Vivequin ; K. Ayukawa ; M. Takeuchi ; K. Ozawa ; M. Tauber ; C. Maffeis ; A. Morandi ; R. Buzzetti ; P. Elliott ; A. Pouta ; M. R. Jarvelin ; A. Korner ; W. Kiess ; M. Pigeyre ; R. Caiazzo ; W. Van Hul ; L. Van Gaal ; F. Horber ; B. Balkau ; C. Levy-Marchal ; K. Rouskas ; A. Kouvatsi ; J. Hebebrand ; A. Hinney ; A. Scherag ; F. Pattou ; D. Meyre ; T. A. Koshimizu ; I. Wolowczuk ; G. Tsujimoto ; P. Froguel
Nature Publishing Group (NPG)
Published 2012Staff ViewPublication Date: 2012-02-22Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Adipocytes/metabolism/pathology ; Adipogenesis ; Adipose Tissue/metabolism/pathology ; Animals ; Calcium Signaling ; Cell Differentiation ; DNA Mutational Analysis ; Diet, High-Fat ; Energy Metabolism ; Europe/ethnology ; European Continental Ancestry Group/genetics ; Exons/genetics ; Fatty Liver/complications/genetics ; Gene Expression Regulation ; Glucagon-Like Peptide 1/secretion ; Glucose/metabolism ; Glucose Intolerance/complications ; Humans ; Insulin/metabolism ; Insulin Resistance ; Lipogenesis ; Liver/metabolism ; Macrophages/metabolism ; Mice ; Mutation/genetics ; Obesity/complications/genetics/*metabolism/pathology ; Receptors, G-Protein-Coupled/deficiency/genetics/*metabolism ; Signal Transduction/geneticsPublished by: -
2Copeman, J.B. ; Cucca, F. ; Hearne, C.M. ; Cornall, R.J. ; Reed, P.W. ; Rønningen, K.S. ; Undlien, D.E. ; Nisticò, L. ; Buzzetti, R. ; Tosi, R. ; Pociot, F. ; Nerup, J. ; Cornélis, F. ; Barnett, A.H. ; Bain, S.C. ; Todd, J.A.
[s.l.] : Nature Publishing Group
Published 1995Staff ViewISSN: 1546-1718Source: Nature Archives 1869 - 2009Topics: BiologyMedicineNotes: [Auszug] The role of human chromosome 2 in type 1 diabetes was evaluated by analysing linkage and linkage disequilibrium at 21 microsatellite marker loci, using 348 affected sibpair families and 107 simplex families. The microsatellite D2S152 was linked to, and associated with, disease in families from ...Type of Medium: Electronic ResourceURL: -
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ISSN: 1432-0428Source: Springer Online Journal Archives 1860-2000Topics: MedicineType of Medium: Electronic ResourceURL: -
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ISSN: 1432-0428Source: Springer Online Journal Archives 1860-2000Topics: MedicineType of Medium: Electronic ResourceURL: -
5Staff View
ISSN: 1432-0428Source: Springer Online Journal Archives 1860-2000Topics: MedicineType of Medium: Electronic ResourceURL: -
6Pozzilli, P. ; Visalli, N. ; Signore, A. ; Baroni, M. G. ; Buzzetti, R. ; Cavallo, M. G. ; Boccuni, M. L. ; Fava, D. ; Gragnoli, C. ; Andreani, D. ; Lucentini, L. ; Matteoli, M. C. ; Crinò, A. ; Cicconetti, C. A. ; Teodonio, C. ; Paci, F. ; Amoretti, R. ; Pisano, L. ; Pennafina, M. G. ; Santopadre, G. ; Marozzi, G. ; Multari, G. ; Suppa, M. A. ; Campea, L. ; Mattia, G. C. De
Springer
Published 1995Staff ViewISSN: 1432-0428Keywords: Key words Nicotinamide ; insulin-dependent diabetes mellitus ; C-peptide ; insulin therapy.Source: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary Nicotinamide has been recently introduced, in addition to intensive insulin therapy for patients with recent-onset insulin-dependent diabetes mellitus (IDDM) to protect beta cells from end-stage destruction. However, available data are conflicting. A double blind trial in 56 newly-diagnosed IDDM patients receiving nicotinamide for 12 months at a dose of 25 mg/kg body weight or placebo was designed in order to determine whether this treatment could improve the integrated parameters of metabolic control (insulin dose, glycated haemoglobin and C-peptide secretion) in the year after diagnosis. In addition to nicotinamide or placebo, patients received three to four insulin injections daily to optimize blood glucose levels. Patients treated with nicotinamide or placebo received similar doses of insulin during follow-up and 1 year after diagnosis with comparable glycated haemoglobin levels (6.7 ± 1.8 % nicotinamide vs 7.1 ± 0.6 % placebo). Basal and glucagon stimulated C-peptide secretion detectable at diagnosis were similarly preserved in the course of 12 months follow-up both in nicotinamide and placebo treated patients. No adverse effects were observed in patients receiving nicotinamide. When age at diagnosis was taken into account, nicotinamide treated older patients ( 〉 15 years of age) showed significantly higher stimulated C-peptide secretion than placebo treated patients (p 〈 0.02). These results suggest that nicotinamide can preserve and improve stimulated beta-cell function only in patients diagnosed after puberty. We conclude that in these patients nicotinamide can be added to insulin at the time of disease diagnosis to maintain and possibly improve residual beta-cell function. However, further studies on patients diagnosed after puberty are needed to confirm whether nicotinamide can be considered an additional tool to insulin in early-onset IDDM. [Diabetologia (1995) 38: 848–852]Type of Medium: Electronic ResourceURL: -
7Pozzilli, P. ; Pitocco, D. ; Visalli, N. ; Cavallo, M. G. ; Buzzetti, R. ; Crinò, A. ; Spera, S. ; Suraci, C. ; Multari, G. ; Cervoni, M. ; Manca Bitti, M. L. ; Matteoli, M. C. ; Marietti, G. ; Ferrazzoli, F. ; Cassone Faldetta, M. R. ; Giordano, C. ; Sbriglia, M. ; Sarugeri, E. ; Ghirlanda, G.
Springer
Published 2000Staff ViewISSN: 1432-0428Keywords: Keywords Type I diabetes ; oral insulin ; insulin antibodies ; prevention.Source: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract Aims/hypothesis. Induction of tolerance to insulin is achievable in animal models of Type I (insulin-dependent) Diabetes mellitus by oral treatment with this hormone, which can lead to prevention of the disease. In the Diabetes Prevention Trial of Type I diabetes (DPT-1), oral insulin is given with the aim of preventing disease insurgence. We investigated whether if given at diagnosis of Type I diabetes in humans, oral insulin can still act as a tolerogen and therefore preserve residual beta-cell function, which is known to be substantial at diagnosis. Methods. A double-blind trial was carried out in patients (mean age ± SD: 14 ± 8 years) with recent-onset Type I diabetes to whom oral insulin (5 mg daily) or placebo was given for 12 months in addition to intensive subcutaneous insulin therapy. A total of 82 patients with clinical Type I diabetes ( 〈 4 weeks duration) were studied. Basal C peptide and glycated haemoglobin were measured and the insulin requirement monitored every 3 months up to 1 year. Insulin antibodies were also measured in 27 patients treated with oral insulin and in 18 patients receiving placebo at the beginning of the trial and after 3, 6 and 12 months of treatment. Results. The trial was completed by 80 patients. Overall and without distinction between age at diagnosis, at 3, 6, 9 and 12 months baseline mean C-peptide secretion in patients treated with oral insulin did not differ from that of those patients treated with placebo. In patients younger than 15 years a tendency for lower C-peptide values at 9 and 12 months was observed in the oral insulin group. Insulin requirement at 1 year was similar between the two groups as well as the percentage of glycated haemoglobin. Finally, IgG insulin antibodies were similar in the two groups at each time point. Conclusion/interpretation. The results of this study indicate that the addition of 5 mg of oral insulin does not modify the course of the disease in the first year after diagnosis and probably does not statistically affect the humoral immune response against insulin. [Diabetologia (2000) 43: 1000–1004]Type of Medium: Electronic ResourceURL: -
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ISSN: 1432-5233Keywords: Key words Insulin-dependent diabetes mellitus (type 1) ; CTLA-4 gene ; Non-HLA genes ; IDDM pathogenesisSource: Springer Online Journal Archives 1860-2000Topics: MedicineType of Medium: Electronic ResourceURL: -
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ISSN: 1432-5233Keywords: Insulin-dependent diabetes mellitus (type 1) ; CTLA-4 gene ; Non-HLA genes ; IDDM pathogenesisSource: Springer Online Journal Archives 1860-2000Topics: MedicineType of Medium: Electronic ResourceURL: