Research Topics
Genomes and GenesSpecies | Edward LeiterSummaryAffiliation: The Jackson Laboratory Country: USA Publications
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Publications
Animal models have little to teach us about type 1 diabetes: 2. In opposition to this proposalE H Leiter
The Jackson Laboratory, 600 Main St, Bar Harbor, Maine, USA
Diabetologia 47:1657-60. 2004- Differential endocrine responses to rosiglitazone therapy in new mouse models of type 2 diabetesEdward H Leiter
The Jackson Laboratory, Bar Harbor, Maine 04609, USA
Endocrinology 147:919-26. 2006..In summary, longitudinal profiling of multiple plasma analytes identified PAI-1 as a useful biomarker to monitor for differential pharmacogenetic responses to Rosi in these new mouse models of T2D... - Differential levels of diabetogenic stress in two new mouse models of obesity and type 2 diabetesEdward H Leiter
Jackson Laboratory, Bar Harbor, Maine 04609, USA
Diabetes 53:S4-11. 2004..These RCSs are differentially sensitive to adverse side effects of thiazolidinediones and thus should be particularly useful for pharmacogenetic analyses... - Novel leptin receptor mutation in NOD/LtJ mice suppresses type 1 diabetes progression: I. Pathophysiological analysisChul Ho Lee
The Jackson Laboratory, 600 Main St, Bar Harbor, ME 04609, USA
Diabetes 54:2525-32. 2005.... - Mouse models and the genetics of diabetes: is there evidence for genetic overlap between type 1 and type 2 diabetes?Edward H Leiter
The Jackson Laboratory, 600 Main St, Bar Harbor, Maine 04609, USA
Diabetes 54:S151-8. 2005..The conclusion is that although overlap exists in the pathophysiological insults leading to beta-cell destruction in the currently studied rodent models, the genetic bases seem quite distinct... - Novel leptin receptor mutation in NOD/LtJ mice suppresses type 1 diabetes progression: II. Immunologic analysisChul Ho Lee
The Jackson Laboratory, 600 Main St, Bar Harbor, ME 04609, USA
Diabetes 55:171-8. 2006.... - Adipokine and insulin profiles distinguish diabetogenic and non-diabetogenic obesities in miceEdward H Leiter
The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA
Obesity (Silver Spring) 15:1961-8. 2007..To use longitudinal profiling of plasma adipokines to distinguish diabetogenic vs. non-diabetogenic obesity syndrome in two new mouse models of polygenic obesity... - Nonobese diabetic mice and the genetics of diabetes susceptibilityEdward H Leiter
The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA
Curr Diab Rep 5:141-8. 2005..An understanding of how variable collections of genes interact with each other and with environmental cues offers important insights as to the complexities of T1D inheritance in humans... - Unexpected functional consequences of xenogeneic transgene expression in beta-cells of NOD miceE H Leiter
The Jackson Laboratory, Bar Harbor, ME 04609, USA
Diabetes Obes Metab 9:14-22. 2007..These findings emphasize the need for careful characterization of genetically manipulated NOD mouse stocks to insure that model characteristics have not been compromised... - Mice with targeted gene disruptions or gene insertions for diabetes research: problems, pitfalls, and potential solutionsE H Leiter
The Jackson Laboratory, Bar Harbor, Maine 04609 1500, USA
Diabetologia 45:296-308. 2002..This review focuses on certain complications inherent in the methodologies, and outlines steps that can be taken to distinguish effects of the genetic manipulation from unexpected contributions from the genetic background... - NOD x 129.H2(g7) backcross delineates 129S1/SvImJ-derived genomic regions modulating type 1 diabetes development in miceEdward H Leiter
The Jackson Laboratory, Bar Harbor, ME, USA
Diabetes 58:1700-3. 2009..Our objective was to identify 129S1/SvJ non-MHC regions contributing type 1 diabetes resistance or susceptibility in backcross to NOD/LtJ... - Deconstructing and reconstructing obesity-induced diabetes (diabesity) in micePeter C Reifsnyder
Jackson Laboratory, Bar Harbor, Maine 04609 1500, USA
Diabetes 51:825-32. 2002.... - The diabetes-prone NZO/HlLt strain. I. Immunophenotypic comparison to the related NZB/BlNJ and NZW/LacJ strainsBradford D Haskell
The Jackson Laboratory, Bar Harbor, Maine 04609, USA
Lab Invest 82:833-42. 2002..Further, these results, combined with the pancreatic histopathology contained in the companion manuscript, suggest that B lymphocytes may be important contributors to diabetes pathogenesis in the NZO mouse... - Pharmacogenetic analysis of rosiglitazone-induced hepatosteatosis in new mouse models of type 2 diabetesHuei-Ju Pan
The Jackson Laboratory, 600 Main St, Bar Harbor, ME 04609, USA
Diabetes 54:1854-62. 2005..Thus, these RCSs present a panel of new mouse models exhibiting differential levels of obesity and diabetes as well as different drug responses. This panel can be used to screen for treatments for type 2 diabetes and its complications... - Selecting the "right" mouse model for metabolic syndrome and type 2 diabetes researchEdward H Leiter
The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA
Methods Mol Biol 560:1-17. 2009.... - Major histocompatibility complex-linked diabetes susceptibility in NOD/Lt mice: subcongenic analysis localizes a component of Idd16 at the H2-D end of the diabetogenic H2(g7) complexDarcy P Pomerleau
The Jackson Laboratory, 600 Main St, Bar Harbor, ME 04609, USA
Diabetes 54:1603-6. 2005..33 mB, distinguishing D.R2 from D.R3. Evidence supporting the candidacy of the ALR/CTS-shared H2-D(dx) MHC class I variant present in both diabetes-resistant stocks, but not the susceptible stock, is discussed... - Targeted disruption of CD38 accelerates autoimmune diabetes in NOD/Lt mice by enhancing autoimmunity in an ADP-ribosyltransferase 2-dependent fashionJing Chen
The Jackson Laboratory, Bar Harbor, ME 04609, USA
J Immunol 176:4590-9. 2006..Unexpectedly, diabetes development in the combined CD38/ART2 stock was strongly suppressed, possibly through epistatic interactions between genes linked to the targeted CD38 on Chromosome 5 and the ART2 complex on Chromosome 7... - Genetic control of neutrophil superoxide production in diabetes-resistant ALR/Lt miceClayton E Mathews
The Jackson Laboratory, Bar Harbor, ME, USA
Free Radic Biol Med 32:744-51. 2002.... - Genetic analysis of resistance to Type-1 Diabetes in ALR/Lt mice, a NOD-related strain with defenses against autoimmune-mediated diabetogenic stressClayton E Mathews
The Jackson Laboratory, Bar Harbor, ME 04609, USA
Immunogenetics 55:491-6. 2003..Two additional ALR-contributed resistance loci may be ALR-specific and contribute to this strain's ability to dissipate free-radical stress... - Cdcs1, a major colitogenic locus in mice, regulates innate and adaptive immune response to enteric bacterial antigensJason Beckwith
The Jackson Laboratory, Bar Harbor, Maine 04609 1500, USA
Gastroenterology 129:1473-84. 2005..We developed reciprocal Cdcs1 congenic stocks on both interleukin 10-deficient backgrounds to identify the susceptibility gene and its function... - Caspase-1 is not required for type 1 diabetes in the NOD mouseWilliam H Schott
The Jackson Laboratory, Bar Harbor, Maine 04609, USA
Diabetes 53:99-104. 2004..These findings show that caspase-1 processing of IL-1 beta and IL-18 is not absolutely required for mediation of spontaneous or chemically induced diabetes pathogenesis in the NOD mouse... - Tracking autoimmune T cells in diabetesDavid V Serreze
The Jackson Laboratory, 600 Main Street, Bar Harbor, Maine 04609, USA
J Clin Invest 112:826-8. 2003..Methodologies to track the development, migration, and functional activation of one class of such T cells (CD4 T cells) have been limited. However, it now appears that this limitation has been overcome... - New mouse model to study islet transplantation in insulin-dependent diabetes mellitusClayton E Mathews
The Jackson Laboratory, Bar Harbor, ME 04609, USA
Transplantation 73:1333-6. 2002..This report examines the insulin sensitivity of mice that carry Ins2Akita and their responsiveness to engraftment with syngeneic pancreatic islets... - Bone marrow expressing a diabetes resistance MHC class II allele: diabetes deviation by chronic immune stimulationPeter Reifsnyder
The Jackson Laboratory, Bar Harbor, ME 04609, USA
Novartis Found Symp 292:32-46; discussion 46-9, 122-9, 202-3. 2008.... - "Agouti NOD": identification of a CBA-derived Idd locus on Chromosome 7 and its use for chimera production with NOD embryonic stem cellsJing Chen
The Jackson Laboratory, 600 Main Street, Bar Harbor, Maine 04609 1500, USA
Mamm Genome 16:775-83. 2005..CBALs- Tyr(+)/Lt blastocysts produced approximately 50% live-born mice, of which approximately 11% were chimeric. Presumably because of high genomic instability, no germline transmission was observed... - CD38 is required for the peripheral survival of immunotolerogenic CD4+ invariant NK T cells in nonobese diabetic miceYi Guang Chen
The Jackson Laboratory, Bar Harbor, ME 04609, USA
J Immunol 177:2939-47. 2006..Therefore, this study documents a previously unrecognized role for CD38 in maintaining survival of an iNKT cell subset that preferentially contributes to the maintenance of immunological tolerance... - Four additional mouse crosses improve the lipid QTL landscape and identify Lipg as a QTL geneZhiguang Su
The Jackson Laboratory, Bar Harbor, ME 04609, USA
J Lipid Res 50:2083-94. 2009..The data from these crosses further increase the ability to perform haplotype analyses that can lead to the identification of causal lipid genes... - Lipid metabolome-wide effects of the PPARgamma agonist rosiglitazoneSteven M Watkins
Lipomics Technologies, Inc, 2545 Boatman Ave, West Sacramento, CA 95691, USA
J Lipid Res 43:1809-17. 2002..Because many of the effects of rosiglitazone on tissue metabolism were reflected in the plasma lipid metabolome, metabolomics has excellent potential for developing clinical assessments of metabolic response to drug therapy... - Resistance of C57BL/6 mice to amoebiasis is mediated by nonhemopoietic cells but requires hemopoietic IL-10 productionShinjiro Hamano
Division of Infectious Diseases and International Health, University of Virginia, Charlottesville, VA 22908, USA
J Immunol 177:1208-13. 2006..We conclude that nonhemopoietic cells mediate the natural resistance to intestinal amoebiasis of B6 mice, yet this resistance depends on hemopoietic IL-10 activity... - A polymorphism in New Zealand inbred mouse strains that inactivates phosphatidylcholine transfer proteinHuei Ju Pan
Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan
FEBS Lett 580:5953-8. 2006..Consistent with the structure-based predictions, functional studies demonstrated that Arg120His PC-TP was inactive, suggesting that this mutation contributes to the deficiencies in phosphatidylcholine metabolism observed in NZO mice... - Absence of a reductase, NCB5OR, causes insulin-deficient diabetesJianxin Xie
Hematology Division, Brigham and Women s Hospital, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 101:10750-5. 2004..Four-week-old Ncb5or-/- mice have enhanced sensitivity to the diabetogenic agent streptozotocin. NCB5OR appears to play a critical role in protecting pancreatic beta cells against oxidant stress... - Hyperglycemia, maturity-onset obesity, and insulin resistance in NONcNZO10/LtJ males, a new mouse model of type 2 diabetesYou Ree Cho
Department of Internal Medicine, Section of Endocrinology and Metabolism, Yale University School of Medicine, New Haven, Connecticut, USA
Am J Physiol Endocrinol Metab 293:E327-36. 2007.... - Adverse hepatic and cardiac responses to rosiglitazone in a new mouse model of type 2 diabetes: relation to dysregulated phosphatidylcholine metabolismHuei-Ju Pan
Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan
Vascul Pharmacol 45:65-71. 2006..This model system demonstrates how the power of mouse genetics can be used to identify the metabolic signatures of individuals who may be prone to drug side effects... - The diabetes-prone NZO/Hl strain. Proliferation capacity of beta cells in hyperinsulinemia and hyperglycemiaCarsten Lange
Evangelisches Krankenhaus, Dusseldorf, Germany
Arch Physiol Biochem 112:49-58. 2006..As shown by morphometric measurements, beta cell expansion in diabetic mice was limited, in spite of high IKi-67 values. This suggested increased death rates of beta cells... - Contributions of dysregulated energy metabolism to type 2 diabetes development in NZO/H1Lt mice with polygenic obesityRobert A Koza
Pennington Biomedical Research Center, Baton Rouge, LA, USA
Metabolism 53:799-808. 2004..This is the first report demonstrating the effects of dietary beta(3)-agonist in preventing the onset of diabesity in a polygenic rodent model of type 2 diabetes... - P2X7 receptor-dependent and -independent T cell death is induced by nicotinamide adenine dinucleotideHiroki Kawamura
Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, CA 90033, USA
J Immunol 174:1971-9. 2005..Adding either NAD or ADPR also triggers a different set of mechanisms, not requiring ART-2 or P2X7 receptors that more slowly induce cell death... - ALS/Lt: a new type 2 diabetes mouse model associated with low free radical scavenging potentialClayton E Mathews
Department of Pediatrics, The University of Pittsburgh, Pittsburgh, Pennsylvania 15213, USA
Diabetes 53:S125-9. 2004..This mouse model with reduced ability to diffuse free radical stress is of obvious interest because free radical-mediated damage is implicated in the pathogenesis and complications of both type 1 and type 2 diabetes... - Mechanisms underlying resistance of pancreatic islets from ALR/Lt mice to cytokine-induced destructionClayton E Mathews
Diabetes Institute, Children s Hospital of Pittsburgh, University of Pittsburgh School of Medicine, 3460 5th Avenue, Pittsburgh, PA 15221, USA
J Immunol 175:1248-56. 2005.... - Anti-insulin receptor autoantibodies are not required for type 2 diabetes pathogenesis in NZL/Lt mice, a New Zealand obese (NZO)-derived mouse strainMarcia F McInerney
Department of Medicinal and Biological Chemistry, University of Toledo College of Pharmacy, Toledo, OH 43606, USA
Exp Diabesity Res 5:177-85. 2004..Also, unlike NZO/HlLt mice that are difficult to breed, the NZL/Lt strain breeds well and thus offers clear advantages to obesity/diabetes researchers... - Adoptive transfer of islet antigen-autoreactive T cell clones to transgenic NOD.Ea(d)mice induces diabetes indicating a lack of I-E mediated protection against activated effector T cellsSamantha A Roberts
Department of Biology, Wittenberg University, Ward St. at N. Wittenberg Ave, Springfield, OH 45501-0720, USA
J Autoimmun 21:139-47. 2003.... - The diabetes-prone NZO/Hl strain. II. Pancreatic immunopathologyErika Junger
Diabetes Research Institute, Auf'm Hennekamp, , Germany
Lab Invest 82:843-53. 2002.... - CD38 controls ADP-ribosyltransferase-2-catalyzed ADP-ribosylation of T cell surface proteinsChristian Krebs
Institute of Immunology, University Hospital, Hamburg, Germany
J Immunol 174:3298-305. 2005.... - Proteasome inhibition alters glucose-stimulated (pro)insulin secretion and turnover in pancreatic {beta}-cellsKajorn Kitiphongspattana
Division of Nutritional Sciences, Department of Animal Sciences, Institute for Genomic Biology, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA
J Biol Chem 280:15727-34. 2005..Collectively, these data indicate beta-cells may balance glucose-stimulated (pro)insulin synthesis and secretion with the activity of the proteasome to regulate protein concentrations in the ER... - Refined histopathologic scoring system improves power to detect colitis QTL in miceAndre Bleich
Institute for Laboratory Animal Science and Central Animal Facility, Hannover Medical School, 30625 Hannover, Germany
Mamm Genome 15:865-71. 2004.... - Flow cytometric and immunoblot assays for cell surface ADP-ribosylation using a monoclonal antibody specific for ethenoadenosineChristian Krebs
Institute of Immunology, University Hospital, Martinistrasse 52, D-20246, Hamburg, Germany
Anal Biochem 314:108-15. 2003..The immunoblot 1G4 staining assay can also be used to identify etheno-ADP-ribosylated target proteins. These new assays hold promise for many interesting applications in biochemistry and cell biology...
Research Grants
- GENETICS AND PATHOLOGY OF NON-OBESE DIABETIC (NOD) MICEEdward Leiter; Fiscal Year: 1993..Results from these proposed studies will guide geneticists in their search for non-MHC linked diabetogenic susceptibility genes in humans and enhance understanding of their interactions with diabetogenic MHC genes...
- GENETICS AND PATHOLOGY OF NONOBESE DIABETIC (NOD) MICEEdward Leiter; Fiscal Year: 2002..The combination of approaches proposed should permit not only molecular identification of major non-MHC associated IDDM susceptibility genes, but also establishment of their pathogenic contributions at a cellular level. ..
- NEW MOUSE MODELS OF DIABESITYEdward Leiter; Fiscal Year: 2002..Collectively, these studies will permit genetic and metabolic characterization of key events in the transition from simple obesity to diabesity in thee novel mouse models. ..
- New Insights into Animals Models of DiabetesEdward Leiter; Fiscal Year: 2003..The meeting is planned for 200 participants. Because of limited seating capacity in The Jackson Laboratory's auditorium, the meeting venue will be the Bar Harbor Regency Hotel, where participants will be housed and fed. ..
- PATHOGENESIS OF AUTOIMMUNE DIABETES IN MICEEdward Leiter; Fiscal Year: 2004..Understanding the contributions of diabetes modifying genes in the extended mouse MIHC may identify human HLA orthologs whose presence has recently been established. ..
- PATHOGENESIS OF AUTOIMMUNE DIABETES IN MICEEdward Leiter; Fiscal Year: 1993....
- GENETICS AND PATHOLOGY OF NON-OBESE DIABETESEdward Leiter; Fiscal Year: 1990..The proposed studies employing manipulation of the immune system should allow an understanding of how defects in immunoregulation in a diabetes-susceptible genotype can trigger pathogenetic sequelae leading to overt diabetes...
- GENETICS AND PATHOLOGY OF NON-OBESE DIABETIC (NOD) MICEEdward Leiter; Fiscal Year: 2005..These latter investigations are of particular importance in view of an ongoing NIDDK trial to prevent T1D in humans deemed at high risk by oral insulin treatment. ..