Abstract
Type 1 diabetes (T1D) results from autoimmune destruction of insulin-producing beta-cells in the pancreas, caused by the interplay of genetic and environmental factors. Despite the introduction of advanced technologies for diabetes management, most patients fail to achieve target glycemic control, and T1D still has a high burden of long-term end-organ complications. Over several decades, multiple clinical trials have attempted to find prevention for T1D in at-risk individuals or to stabilize, ultimately reverse, the disease in those with T1D. To date, T1D remains yet incurable condition; however, recently improved understanding of the natural history of the disease may lead to new strategies to preserve or improve beta-cell function in those at increased risk and T1D patients. This publication aims to provide an overview of past experiences and recent findings in the prevention of T1D.
Highlights
Type 1 diabetes (T1D) is one of the most common chronic diseases affecting children, adolescents, and young adults at crucial times of growth and development [1]
After having demonstrated that mucosal administration of insulin is safe, the GPPAD-POInT (Global Platform for the Prevention of Autoimmune Diabetes Primary Oral Insulin Trial) study was initiated to test whether daily administration of oral insulin, from age 4.0 months to 7.0 months until age 36.0 months to children who are genetically at risk will reduce the beta-cell autoantibodies and T1D development
The effect was related to younger age, disease duration
Summary
Type 1 diabetes (T1D) is one of the most common chronic diseases affecting children, adolescents, and young adults at crucial times of growth and development [1]. Numerous putative environmental factors triggering autoimmunity, such as diet, vitamin D intake, infections, and gut microbiota, may play a role in favoring T1D development [3]. Both the immune regulation and the immune response contribute to T1D pathogenesis, in which cellular immunity plays a vital role [4]. Enhanced understanding of the natural history of the disease helped identify earlier pre-symptomatic phases of T1D, from the asymptomatic stage to clinical diagnosis. These include stage 0, in which individuals carrying T1D susceptibility alleles have not yet developed islet autoantibodies. TThhee nnaattuurraall hhiissttoorryy ooff TTyyppee 11 ddiiaabbeetteess ((TT11DD)) iiss bbaasseedd oonn tthhee rreeffeerreenncceedd mmooddeell [[1122]] wwiitthh rreecceennttllyypprrooppoosseeddeeaarrllyyssttaaggeessooffTT11DD[[1133]]aannddpprreevveenntitoionnooppppoorrtutunnitiiteiess
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