Home| Professor of Diabetes and Clinical Research |
Contact details:
| Tel: | +44 20 7882 2392 |
| Fax: | +44 20 7882 2186 |
| Email: | p.p.pozzilli@qmul.ac.uk |
| Address: |
Centre for Diabetes, |
Biography
Paolo Pozzilli is Professor of Diabetes and Clinical Research at the Centre for Diabetes at Barts and The London School of Medicine & Dentistry, London , and Professor of Endocrinology & Metabolic Diseases at the University Campus Bio-Medico in Rome , Italy.
He qualified in Medicine in 1976 at "Sapienza" University in Rome and specialized in Endocrinology and Metabolic Diseases in 1979 at the same University. He has participated in 4 Biomed projects of the European Union and 3 NIH projects. He is Member of Ancillary Study Committee for the TRIGR Study (NIH project) and Deputy Chairman for the ACTION LADA Project (EU).
He is the Delegate for University Campus Bio-Medico, Permanent Conference of Rectors of the Italian Universities (CRUI), Member Scientific Advisory Board, Graduate School in Molecular Medicine, University of Ulm and Member Advisory Board, International Diabetes Federation, Group for Diabetes in the Youth.
He coordinates the International PhD programme in Endocrinology and Metabolic Diseases between Queen Mary University of London, University Campus Bio-Medico in Rome and the University of Ulm, Germany.
He is the European Editor of Diabetes Metabolism Research & Reviews and Associate Editor of Nutrition Metabolism and Cardiovascular Disease.
He is Review Editor for the International Diabetes Monitor and Member of the International Commission of the Italian Society of Endocrinology.
He was the recipient of several awards amongst which the Andrew Cudworth Memorial Prize of the British Diabetic Association (1986), the G.B. Morgagni Prize, Young Investigator Award of the European Association of Metabolism (1989), the SID Prize 1994 (Italian Society of Diabetes), the Karol Marcinkowski Medal of the "Poznan Academy of Medicine"(1997), the Mary Jane Kugel Award, Juvenile Diabetes Research Foundation, USA (2003 and 2006) and the Diabetes Honoris Causa, Paulescu Foundation & Romanian Society of Diabetes (2007).
Research Activity
Our research projects focus on the pathogenesis of type 1 diabetes (T1DM) taking advantage of a large database of DNA and sera from patients with T1DM and of the non-obese diabetic (NOD) mouse which is an ideal animal model to study this disease since it develops an autoimmune form of diabetes comparable to the one occurring in humans. These animals retain a high incidence of diabetes, making them a very relevant tool for defining strategies aimed at preventing the onset, delaying the progression and discovering new therapies for the disease.
Presently we are aiming to generate insulin producing cells from different sources of stem cells obtained from the bone marrow and other tissues of NOD mice . We intend to use these stem cells to prevent the development of T1DM and to reverse hyperglycaemia in these animals when they are diagnosed with the disease.
The project includes several steps from the establishment of the best conditions for the isolation and culture of haematopoietic and mesenchymal stem cells obtained from the NOD mice. The proliferation and differentiation of these cells to generate new insulin producing cells and the injection of these cells into NOD mice to establish whether delay or prevention of T1DM can be achieved, represent the core of our projects. The type of cells we use in our study have been selected because they are easily available and may be potentially used safely for transplantation in humans following successful outcome in mice.
Clinical applied programs include studies on genetic and immunological markers of T1DM, and prediction and prevention of this disease. The ongoing collaboration with academic Institutions in Europe allows us to network with them paying special attention to intervention trials for protection of residual beta cell function in T1DM. More recently studies are ongoing on vitamin D status in T1DM, thus offering novel approaches for treatment of this condition.
Key Publications
• Hawa MI, Thivolet C, Mauricio D, Alemanno I, Cipponeri E, Collier D, Hunter S, Buzzetti R, de Leiva A, Pozzilli P, Leslie RD; Action LADA Group. Metabolic syndrome and autoimmune diabetes: action LADA 3. Diabetes Care. 2009 Jan;32(1):160-4.
• Khoo CP, Valorani MG, Brittan M, Alison MR, Warnes G, Johansson U, Hawa M, Pozzilli P. Characterization of endothelial progenitor cells in the NOD mouse as a source for cell therapies. Diabetes Metab Res Rev. 2009 Jan;25(1):89-93.
• Brophy S, Yderstraede K, Mauricio D, Hunter S, Hawa M, Pozzilli P, Schernthaner G, Schloot N, Buzzetti R, Davies H, Leslie D, Williams R; Action LADA Group. Time to insulin initiation cannot be used in defining latent autoimmune diabetes in adults. Diabetes Care. 2008 Mar;31(3):439-41.
• Petrone A, Spoletini M, Zampetti S, Capizzi M, Zavarella S, Osborn J, Pozzilli P, Buzzetti R; Immunotherapy Diabetes (IMDIAB) Group. The PTPN22 1858T gene variant in type 1 diabetes is associated with reduced residual beta-cell function and worse metabolic control. Diabetes Care. 2008 Jun;31(6):1214-8.
• Petrone A, Suraci C, Capizzi M, Giaccari A, Bosi E, Tiberti C, Cossu E, Pozzilli P, Falorni A, Buzzetti R; NIRAD Study Group. The protein tyrosine phosphatase nonreceptor 22 (PTPN22) is associated with high GAD antibody titer in latent autoimmune diabetes in adults: Non Insulin Requiring Autoimmune Diabetes NIRAD) Study 3. Diabetes Care. 2008 Mar;31(3):534
• Greenbaum CJ, Mandrup-Poulsen T, McGee PF, Battelino T, Haastert B, Ludvigsson J, Pozzilli P, Lachin JM, Kolb H; Type 1 Diabetes Trial Net Research Group; European C-Peptide Trial Study Group. Mixed-meal tolerance test versus glucagon stimulation test for the assessment of beta-cell function in therapeutic trials in type 1 diabetes. Diabetes Care. 2008 Oct;31(10):1966-71.
• Noble JA, Martin A, Valdes AM, Lane JA, Galgani A, Petrone A, Lorini R, Pozzilli P, Buzzetti R, Erlich HA. Type 1 diabetes risk for human leukocyte antigen (HLA)-DR3 haplotypes depends on genotypic context: association of DPB1 and HLA class I loci among DR3- and DR4-matched Italian patients and controls. Hum Immunol. 2008 Apr-May;69(4-5):291-300.
• Pozzilli P, Buzzetti R. A new expression of diabetes: double diabetes.Trends Endocrinol Metab. 2007 Mar;18(2):52-7.
• Ou D, Wang X, Metzger DL, James RF, Pozzilli P, Plesner A, Korneluk RG, Verchere CB, Tingle AJ. Synergistic inhibition of tumor necrosis factor-related apoptosis-inducing igand-induced apoptosis in human pancreatic beta cells by Bcl-2 and X-linked inhibitor of apoptosis. Hum Immunol. 2005 Mar;66(3):274-84.
• Guo D, Li M, Zhang Y, Yang P, Eckenrode S, Hopkins D, Zheng W, Purohit S, Podolsky RH, Muir A, Wang J, Dong Z, Brusko T, Atkinson M, Pozzilli P, Zeidler A, Raffel LJ, Jacob CO, Park Y, Serrano-Rios M, Larrad MT, Zhang Z, Garchon HJ, Bach JF, Rotter JI, She JX, Wang CY. A functional variant of SUMO4, a new I kappa B alpha modifier, is associated with type 1 diabetes. Nat Genet. 2004 Aug;36(8):837-41.
• Palmer JP, Fleming GA, Greenbaum CJ, Herold KC, Jansa LD, Kolb H, Lachin JM, Polonsky KS, Pozzilli P, Skyler JS, Steffes MW. C-peptide is the appropriate outcome measure for type 1 diabetes clinical trials to preserve beta-cell function. Diabetes 2004 Jan;53(1):250-64.
