Prevention strategies for type 1 diabetes

Kishiyama, Christopher M.; Chase, H. Peter; Barker, Jennifer M.

doi:10.1007/s11154-006-9015-z

Cited by 11 publications

(6 citation statements)

References 60 publications

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“…In this regard, a lesson can be learned from studies in type 1 diabetes which has a similar model of development of RA where autoantibodies precede the clnical onset of disease, and can be used in a highly accurate fashion to predict future onset of disease (101–103). T1DM investigators have formed large-scale study networks to study both the natural history of T1DM as well as identify subjects for prevention trials.…”

Section: How To Make Ra Prevention a Realitymentioning

confidence: 99%

Can rheumatoid arthritis be prevented?

Deane

2013

Best Practice & Research Clinical Rheumatology

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The discovery of elevations of rheumatoid arthritis (RA)-related biomarkers prior to the onset of clinically apparent RA raises hopes that individuals who are at risk for future RA can be identified in a preclinical phase of disease that is defined as abnormalities of RA-related immune activity prior to the clinically apparent onset of joint disease. Additionally, there is a growing understanding of the immunologic processes that are occurring in preclinical RA, as well as a growing understanding of risk factors that may be mechanistically related to RA development. Furthermore, there are data supporting that treatment of early RA can lead to drug free remission. Taken as a whole, these findings suggest that it may be possible to use biomarkers and other factors to accurately identify the likelihood and timing of onset of future RA, and intervene with immunomodulatory therapies and/or risk factor modification to prevent the future onset of RA in at-risk individuals. Importantly, several clinical prevention trials for RA have already been tried, and one is underway. However, while our understanding of the growing understanding of the mechanisms and natural history of RA development may be leading us to the implementation of prevention strategies for RA, there are still several challenges to be met. These include developing sufficiently accurate methods of predicting those at high risk for future RA so that clinical trials can be developed based on accurate rates of development of arthritis and subjects can be adequately informed of their risk for disease, identifying the appropriate interventions and biologic targets for optimal prevention, and addressing the psychosocial and economic aspects that are crucial to developing broadly applicable prevention measures for RA. These issues notwithstanding, prevention of RA may be within reach in the near future.

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Section: How To Make Ra Prevention a Realitymentioning

confidence: 99%

Can rheumatoid arthritis be prevented?

Deane

2013

Best Practice & Research Clinical Rheumatology

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“…Failure of the immune system to further maintain control of these T cells is probably affected by external stimuli, which are not yet fully characterized (6). Several environmental agents have been suggested to promote the outbreak of the disease, including viral infection (7), dietary factors (8–14), and impaired intestinal mucosal immunity (15). In addition, accelerated growth rate in childhood was associated with increased risk of T1D (16).…”

Section: Introductionmentioning

confidence: 99%

N-Acetyl-l-Cysteine Supplement in Early Life or Adulthood Reduces Progression of Diabetes in Nonobese Diabetic Mice

Frenkel

Rozenfeld

Rozenberg

et al. 2019

Current Developments in Nutrition

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Background Oxidative stress contributes to the pathologic process leading to the development, progression, and complications of type 1 diabetes (T1D). Objective The aim of this study was to investigate the effect of the antioxidant N-acetyl-l-cysteine (NAC), supplemented during early life or adulthood on the development of T1D. Methods NAC was administered to nonobese diabetic (NOD) female mice during pregnancy and lactation, and the development of diabetes was followed in offspring. In an additional set of experiments, offspring of untreated mice were given NAC during adulthood, and the development of T1D was followed. Morbidity rate, insulitis and serum cytokines were measured in the 2 sets of experiments. In addition, markers of oxidative stress, glutathione, lipid peroxidation, total antioxidant capacity and activity of antioxidant enzymes, were followed. Results Morbidity rate was reduced in both treatment protocols. A decrease in interferon γ, tumor necrosis factor α, interleukin 1α, and other type 1 diabetes-associated proinflammatory cytokines was found in mice supplemented with NAC in adulthood or during early life compared with control NOD mice. The severity of insulitis was higher in control NOD mice than in treated groups. NAC administration significantly reduced oxidative stress, as determined by reduced lipid peroxidation and increased total antioxidant capacity in serum and pancreas of mice treated in early life or in adulthood and increased pancreatic glutathione when administrated in adulthood. The activity of antioxidant enzymes was not affected in mice given NAC in adulthood, whereas an increase in the activity of superoxide dismutase and catalase was demonstrated in the pancreas of their offspring. Conclusion NAC decreased morbidity of NOD mice by attenuating the immune response, presumably by eliminating oxidative stress, and might be beneficial in reducing morbidity rates of T1D in high-risk individuals.

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“…Prevention trials, including the Trial to Reduce Type 1 Diabetes in the Genetically at Risk (TRIGR) (3), the Nutritional Intervention to Prevent Diabetes (NIP-Diabetes) trial (4), and the Primary Oral and Intranasal Trial (Pre-POINT) are currently underway in genetically at-risk children. Many of these trials include first-degree relatives of people with diabetes as well as individuals with highrisk HLA genotypes, including DR3/4-DQ8.…”

mentioning

confidence: 99%

Two Single Nucleotide Polymorphisms Identify the Highest-Risk Diabetes HLA Genotype

Barker¹,

Triolo²,

Aly³

et al. 2008

Diabetes

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are at the highest risk of developing type 1 diabetes. We sought to find an inexpensive, rapid test to identify DR3/4-DQ8 subjects using two single nucleotide polymorphisms (SNPs).RESEARCH DESIGN AND METHODS-SNPs rs2040410 and rs7454108 were associated with DR3-DQB1*0201 and DR4-DQB1*0302. We correlated these SNPs with HLA genotypes and with publicly available data on 5,019 subjects from the Type 1 Diabetes Genetic Consortium (T1DGC). Additionally, we analyzed these SNPs in samples from 143 HLA-typed children who participated in the Diabetes Autoimmunity Study of the Young (DAISY) using Taqman probes (rs7454108) and restriction digest analysis (rs2040410).RESULTS-With a simple combinatorial rule, the SNPs of interest identified the presence or absence of the DR3/4-DQ8 genotype. A wide variety of genotypes were tested for both SNPs. In T1DGC samples, the two SNPs were 98.5% (1,173 of 1,191) sensitive and 99.7% (3,815 of 3,828) specific for DR3/4-DQ8. In the DAISY population, the test was 100% (69 of 69) sensitive and 100% (74 of 74) specific. Overall, the sensitivity and specificity for the test were 98.57 and 99.67%, respectively. CONCLUSIONS-

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Prevention strategies for type 1 diabetes

Cited by 11 publications

References 60 publications

Can rheumatoid arthritis be prevented?

Can rheumatoid arthritis be prevented?

N-Acetyl-l-Cysteine Supplement in Early Life or Adulthood Reduces Progression of Diabetes in Nonobese Diabetic Mice

Two Single Nucleotide Polymorphisms Identify the Highest-Risk Diabetes HLA Genotype

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