Diabetes/Metabolism ReviewsVolume 14, Issue 4 p. 315-324 Review Article Actual perspectives in biohybrid artificial pancreas for the therapy of Type 1, insulin-dependent diabetes mellitus Riccardo Calafiore, Corresponding Author Riccardo Calafiore Department of Internal Medicine and Endocrine and Metabolic Sciences, University of Perugia, ItalyDIMISEM University of Perugia, Via E. dal Pozzo, 06126 Perugia, ItalySearch for more papers by this author Riccardo Calafiore, Corresponding Author Riccardo Calafiore Department of Internal Medicine and Endocrine and Metabolic Sciences, University of Perugia, ItalyDIMISEM University of Perugia, Via E. dal Pozzo, 06126 Perugia, ItalySearch for more papers by this author First published: 15 February 1999 https://doi.org/10.1002/(SICI)1099-0895(199812)14:4<315::AID-DMR235>3.0.CO;2-2Citations: 9AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume14, Issue4December 1998Pages 315-324 RelatedInformation
Recent experimental work has challenged and shattered the old concept of a sequestration of pancreatic islet antigens from developing T-cells within the thymic environment. There is now compelling evidence that the central immunological tolerance of the whole insulin family may be induced during the process of T-cell ontogeny in the thymus. Transcripts of insulin-like growth factor II (IGF-II), IGF-I and insulin genes have been characterized in human, rat and mouse thymuses. At the peptide level, IGF-II was shown to be the dominant polypeptide of the insulin family in the thymus from different species. Data are presented which support a dual role of thymic IGF-II both in T-cell development as well as in T-cell negative selection. Using animal models of autoimmune diabetes, current research is investigating the hypothesis that a defect of thymic T-cell education to the insulin family is implicated in the pathophysiology of human Type 1 diabetes. An efficient and secure prevention of Type 1 diabetes could be designed on the basis of the strong natural tolerogenic properties of the thymus.
The relationship between Fas-mediated apoptosis and Type 1 diabetes is currently under investigation. Fas/Fas ligand interaction could be involved both in the insulitis process and in beta-cell death. Nevertheless, different mechanisms appear to be involved in human Type 1 diabetes and in NOD mice. In the present work, we review recent evidence of the role of the Fas/Fas ligand system in human and NOD mouse diabetes, describing possible hypotheses for its involvement in the pathogenesis of the disease, with possible implications for therapy and islet transplantation.
Fibrocalculous pancreatic diabetes (FCPD) is a unique form of diabetes secondary to chronic pancreatitis seen in developing countries of the world associated with either overt protein-calorie malnutrition or, more likely, with deficiency of certain micronutrients. FCPD affects young individuals and runs an aggressive course to reach the endpoints of diabetes, pancreatic calculi and exocrine pancreatic dysfunction (steatorrhoea) in the majority of cases. There are characteristic features of FCPD radiologically, ultrasonographically, on endoscopic retrograde cholangiopancreatography and on histopathology which distinguish it from chronic pancreatitis of other aetiologies seen in temperate zones, e.g. alcoholic chronic pancreatitis. Although a secondary form of diabetes, specific diabetes-related complications like retinopathy and nephropathy do occur in FCPD. There appears to be a high risk of developing pancreatic carcinoma. Although the aetiology of FCPD is still unclear, the role of micronutrient (antioxidant) deficiency is emerging as a possible aetiological or predisposing factor. The contribution of genetic factors and environmental toxins, e.g. cyanogenic glycosides or other nutritional/toxic factors, merit further study. Studies on FCPD, a good model of a secondary form of diabetes, could lead to improved understanding of other primary forms of diabetes as well. If the underlying aetiological factors are identified, it may also be possible to prevent this type of diabetes. (C) 1998 John Wiley & Sons, Ltd.
Diabetes/Metabolism ReviewsVolume 14, Issue 2 p. 191-192 Commentary CD95 ligand expression on alpha cells: protection or killing? Giovina Ruberti, Giovina Ruberti Department of Immunobiology, Institute of Cell Biology, National Research Council, Rome, 00137 ItalySearch for more papers by this authorAlberto Signore, Alberto Signore Nu.M.E.D. Group Clinica Medica 2, University ‘La Sapienza’, Rome, 00161 ItalySearch for more papers by this author Giovina Ruberti, Giovina Ruberti Department of Immunobiology, Institute of Cell Biology, National Research Council, Rome, 00137 ItalySearch for more papers by this authorAlberto Signore, Alberto Signore Nu.M.E.D. Group Clinica Medica 2, University ‘La Sapienza’, Rome, 00161 ItalySearch for more papers by this author First published: 21 December 1998 https://doi.org/10.1002/(SICI)1099-0895(199806)14:2<191::AID-DMR5210>3.0.CO;2-0AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. Volume14, Issue2June 1998Pages 191-192 RelatedInformation
Diabetes/Metabolism ReviewsVolume 14, Issue 3 p. 258-259 Commentary Gluten: is it also a determinant of islet autoimmunity? Ezio Bonifacio, Corresponding Author Ezio Bonifacio Istituto Scientifico San Raffaele, University of Milan, 20132 Milan, ItalyIstituto Scientifico San Raffaele, University of Milan, 20132 Milan, ItalySearch for more papers by this authorAnnette-G Ziegler, Annette-G Ziegler Diabetes Research Institute, Krankenhaus München-Schwabing, GermanySearch for more papers by this authorMichael Hummel, Michael Hummel Diabetes Research Institute, Krankenhaus München-Schwabing, GermanySearch for more papers by this authorJulia Dittler, Julia Dittler Diabetes Research Institute, Krankenhaus München-Schwabing, GermanySearch for more papers by this authorVito Lampasona, Vito Lampasona Istituto Scientifico San Raffaele, University of Milan, 20132 Milan, ItalySearch for more papers by this authorMatteo Rocco Pastore, Matteo Rocco Pastore Istituto Scientifico San Raffaele, University of Milan, 20132 Milan, ItalySearch for more papers by this authorEmanuele Bosi, Emanuele Bosi Istituto Scientifico San Raffaele, University of Milan, 20132 Milan, ItalySearch for more papers by this author Ezio Bonifacio, Corresponding Author Ezio Bonifacio Istituto Scientifico San Raffaele, University of Milan, 20132 Milan, ItalyIstituto Scientifico San Raffaele, University of Milan, 20132 Milan, ItalySearch for more papers by this authorAnnette-G Ziegler, Annette-G Ziegler Diabetes Research Institute, Krankenhaus München-Schwabing, GermanySearch for more papers by this authorMichael Hummel, Michael Hummel Diabetes Research Institute, Krankenhaus München-Schwabing, GermanySearch for more papers by this authorJulia Dittler, Julia Dittler Diabetes Research Institute, Krankenhaus München-Schwabing, GermanySearch for more papers by this authorVito Lampasona, Vito Lampasona Istituto Scientifico San Raffaele, University of Milan, 20132 Milan, ItalySearch for more papers by this authorMatteo Rocco Pastore, Matteo Rocco Pastore Istituto Scientifico San Raffaele, University of Milan, 20132 Milan, ItalySearch for more papers by this authorEmanuele Bosi, Emanuele Bosi Istituto Scientifico San Raffaele, University of Milan, 20132 Milan, ItalySearch for more papers by this author First published: 21 December 1998 https://doi.org/10.1002/(SICI)1099-0895(1998090)14:3<258::AID-DMR221>3.0.CO;2-JCitations: 4AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article.Citing Literature Volume14, Issue3September 1998Pages 258-259 RelatedInformation
The Nobel prize-winning discovery of MHC restriction by Zinkernagel and Doherty has led to some of the most exciting advances in immunology over the past two decades. The ongoing progress in our conceptual understanding of the processes governing the immunology to infection, tolerance to self and consequently the immune dysregulation in autoimmunity have all assimilated the laws of restriction as a central tenet. The focus of much of this research has been the T-cell and its interactions. Refinement of the paradigm of MHC restriction at the molecular level has allowed a view of the pathogenesis of insulin-dependent diabetes mellitus (IDDM), a prototypic autoimmune disease, unprecedented in its detail. This article discusses the impact of MHC restriction on the central themes of immunology, and focuses on its utility as a framework in understanding the role of the T-cell in the pathogenesis of IDDM. Copyright (C) 1998 John Wiley & Sons, Ltd.
Recent advances in the understanding of the pathogenesis of insulin-dependent diabetes mellitus (IDDM) have led to the first trials of disease prevention in susceptible individuals. Two main trials (nicotinamide and insulin) are now running but first results will not be available before the turn of the century. Pilot trials using different approaches, most of them based on the induction of immunotolerance, are also under way and should offer new insight for establishing larger multicentre studies including attempts aimed at primary prevention by removal of diabetogenic components in cow's milk. The field is moving fast and it is expected that intervention for IDDM prevention will be offered to an increasing number of individuals found at risk of developing the disease.
Diabetes/Metabolism ReviewsVolume 14, Issue 3 p. 252-254 Commentary How does antibody combination really predict IDDM in the general population? Fortune telling—not fortune spending Orit Pinhas-Hamiel, Corresponding Author Orit Pinhas-Hamiel National Center For Childhood Diabetes, Institute of Endocrinology, Schneider’s Children’s Medical Center, Kaplan 14, Petah-Tikva, Tel-Aviv University, IsraelNational Center For Childhood Diabetes, Institute of Endocrinology, Schneider’s Children’s Medical Center, Kaplan 14, Petah-Tikva, Tel-Aviv University, IsraelSearch for more papers by this authorElliot Sprecher, Elliot Sprecher National Center For Childhood Diabetes, Institute of Endocrinology, Schneider’s Children’s Medical Center, Kaplan 14, Petah-Tikva, Tel-Aviv University, IsraelSearch for more papers by this authorPnina Vardi, Pnina Vardi National Center For Childhood Diabetes, Institute of Endocrinology, Schneider’s Children’s Medical Center, Kaplan 14, Petah-Tikva, Tel-Aviv University, IsraelSearch for more papers by this author Orit Pinhas-Hamiel, Corresponding Author Orit Pinhas-Hamiel National Center For Childhood Diabetes, Institute of Endocrinology, Schneider’s Children’s Medical Center, Kaplan 14, Petah-Tikva, Tel-Aviv University, IsraelNational Center For Childhood Diabetes, Institute of Endocrinology, Schneider’s Children’s Medical Center, Kaplan 14, Petah-Tikva, Tel-Aviv University, IsraelSearch for more papers by this authorElliot Sprecher, Elliot Sprecher National Center For Childhood Diabetes, Institute of Endocrinology, Schneider’s Children’s Medical Center, Kaplan 14, Petah-Tikva, Tel-Aviv University, IsraelSearch for more papers by this authorPnina Vardi, Pnina Vardi National Center For Childhood Diabetes, Institute of Endocrinology, Schneider’s Children’s Medical Center, Kaplan 14, Petah-Tikva, Tel-Aviv University, IsraelSearch for more papers by this author First published: 21 December 1998 https://doi.org/10.1002/(SICI)1099-0895(1998090)14:3<252::AID-DMR217>3.0.CO;2-KCitations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume14, Issue3September 1998Pages 252-254 RelatedInformation
Diabetes/Metabolism ReviewsVolume 14, Issue 1 p. 108-109 Commentary Intervention at neonatal age: can we intervene? Shiva Reddy, Corresponding Author Shiva Reddy Department of Paediatrics, School of Medicine, University of Auckland, Private Bag 92019, Auckland, New ZealandDepartment of Paediatrics, School of Medicine, University of Auckland, Private Bag 92019, Auckland, New ZealandSearch for more papers by this author Shiva Reddy, Corresponding Author Shiva Reddy Department of Paediatrics, School of Medicine, University of Auckland, Private Bag 92019, Auckland, New ZealandDepartment of Paediatrics, School of Medicine, University of Auckland, Private Bag 92019, Auckland, New ZealandSearch for more papers by this author First published: 21 December 1998 https://doi.org/10.1002/(SICI)1099-0895(199803)14:1<108::AID-DMR4204>3.0.CO;2-KCitations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume14, Issue1March 1998Pages 108-109 RelatedInformation
Diabetes/Metabolism ReviewsVolume 14, Issue 3 p. 260-261 Commentary IDDM preventive trials: what’s new? Paolo Pozzilli, Corresponding Author Paolo Pozzilli Università Campus Biomedico, CISD, Largo, Marchiafava I, 00161 Rome, ItalyUniversità Campus Biomedico, CISD, Largo, Marchiafava I, 00161 Rome, ItalySearch for more papers by this author Paolo Pozzilli, Corresponding Author Paolo Pozzilli Università Campus Biomedico, CISD, Largo, Marchiafava I, 00161 Rome, ItalyUniversità Campus Biomedico, CISD, Largo, Marchiafava I, 00161 Rome, ItalySearch for more papers by this author First published: 21 December 1998 https://doi.org/10.1002/(SICI)1099-0895(1998090)14:3<260::AID-DMR223>3.0.CO;2-%23Citations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume14, Issue3September 1998Pages 260-261 RelatedInformation
Diabetes/Metabolism ReviewsVolume 14, Issue 1 p. 105-106 Commentary Dietary intervention for diabetes prevention in the neonate Fraser W. Scott, Corresponding Author Fraser W. Scott Nutrition Research Division, Health Canada, Ottawa, Canada, KIA 0L2. Diabetes Research Institute, University of Düsseldorf, Düsseldorf, 40225 GermanyNutrition Research Division, Health Canada, Ottawa, Canada, KIA 0L2. Diabetes Research Institute, University of Düsseldorf, Düsseldorf, 40225 GermanySearch for more papers by this authorHubert Kolb, Hubert Kolb Nutrition Research Division, Health Canada, Ottawa, Canada, KIA 0L2. Diabetes Research Institute, University of Düsseldorf, Düsseldorf, 40225 GermanySearch for more papers by this author Fraser W. Scott, Corresponding Author Fraser W. Scott Nutrition Research Division, Health Canada, Ottawa, Canada, KIA 0L2. Diabetes Research Institute, University of Düsseldorf, Düsseldorf, 40225 GermanyNutrition Research Division, Health Canada, Ottawa, Canada, KIA 0L2. Diabetes Research Institute, University of Düsseldorf, Düsseldorf, 40225 GermanySearch for more papers by this authorHubert Kolb, Hubert Kolb Nutrition Research Division, Health Canada, Ottawa, Canada, KIA 0L2. Diabetes Research Institute, University of Düsseldorf, Düsseldorf, 40225 GermanySearch for more papers by this author First published: 21 December 1998 https://doi.org/10.1002/(SICI)1099-0895(199803)14:1<105::AID-DMR204>3.0.CO;2-QCitations: 2AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume14, Issue1March 1998Pages 105-106 RelatedInformation
Diabetes/Metabolism ReviewsVolume 14, Issue 1 p. 106-107 Commentary Neonatal prevention of IDDM? William E. Winter, Corresponding Author William E. Winter Departments of Pathology and Pediatrics, University of Florida, Gainsville, Florida 32610, USADepartments of Pathology and Pediatrics, University of Florida, Gainsville, Florida 32610, USASearch for more papers by this authorDesmond Schatz, Desmond Schatz Departments of Pathology and Pediatrics, University of Florida, Gainsville, Florida 32610, USASearch for more papers by this author William E. Winter, Corresponding Author William E. Winter Departments of Pathology and Pediatrics, University of Florida, Gainsville, Florida 32610, USADepartments of Pathology and Pediatrics, University of Florida, Gainsville, Florida 32610, USASearch for more papers by this authorDesmond Schatz, Desmond Schatz Departments of Pathology and Pediatrics, University of Florida, Gainsville, Florida 32610, USASearch for more papers by this author First published: 21 December 1998 https://doi.org/10.1002/(SICI)1099-0895(199803)14:1<106::AID-DMR1204>3.0.CO;2-PCitations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume14, Issue1March 1998Pages 106-107 RelatedInformation
Diabetes/Metabolism ReviewsVolume 14, Issue 2 p. 192-193 Commentary A pragmatic answer to the use of animal models for Type 1 diabetes Karsten Buschard, Karsten Buschard Bartholin Instituttet, Kommunehospitalet, DR-1399 Copenhagen K, DenmarkSearch for more papers by this author Karsten Buschard, Karsten Buschard Bartholin Instituttet, Kommunehospitalet, DR-1399 Copenhagen K, DenmarkSearch for more papers by this author First published: 21 December 1998 https://doi.org/10.1002/(SICI)1099-0895(199806)14:2<192::AID-DMR7210>3.0.CO;2-YAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume14, Issue2June 1998Pages 192-193 RelatedInformation
A combination of genetic and environmental factors is most likely the cause of Type 1 diabetes. Results from twin data, familial clustering of the disease and difference in incidence according to ethnicity infer the presence of specific disease genes. The genetic component of Type 1 diabetes cannot be classified according to a classical model of inheritance but is due to an interaction between different genes and environmental factors. The major genes are within the HLA region that are responsible for 40% of the genetic susceptibility, although other genes are important (non-HLA genes). To date, more than 10 specific loci have been localized on different chromosomes. The gene involved has been characterized only for two of such loci, IDDM1 and IDDM2, while in the other cases the presence of some susceptibility genes can be envisaged and their identification represents the goal of genetic research in coming years. Fine mapping of the loci will certainly increase our understanding of the genetics of Type 1 diabetes; the limitation in detecting some of the remaining genes by linkage studies can be overcome by association studies. That is possible via the collection of a large number of affected families (over 1000) in homogeneous populations.
