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10.1038/s41598-018-23026-w

http://scihub22266oqcxt.onion/10.1038/s41598-018-23026-w
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C5854601!5854601!29545618
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suck abstract from ncbi


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pmid29545618      Sci+Rep 2018 ; 8 (ä): ä
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  • Carbamazepine, a beta-cell protecting drug, reduces type 1 diabetes incidence in NOD mice #MMPMID29545618
  • Lee JTC; Shanina I; Chu YN; Horwitz MS; Johnson JD
  • Sci Rep 2018[]; 8 (ä): ä PMID29545618show ga
  • Pancreatic beta-cells are selectively destroyed by the host immune system in type 1 diabetes. Thus, drugs that preserve beta-cell mass and/or function have the potential to prevent or slow the progression of this disease. We recently reported that the use-dependent sodium channel blocker, carbamazepine, protects beta-cells from inflammatory cytokines in vitro. Here, we tested the effects of carbamazepine treatment in female non-obese diabetic (NOD) mice by supplementing LabDiet 5053 with 0.5% w/w carbamazepine to achieve serum carbamazepine levels of 14.98?±?3.19?µM. Remarkably, diabetes incidence over 25 weeks, as determined by fasting blood glucose, was ~50% lower in carbamazepine treated animals. Partial protection from diabetes in carbamazepine-fed NOD mice was also associated with improved glucose tolerance at 6 weeks of age, prior to the onset of diabetes in our colony. Less insulitis was detected in carbamazepine treated NOD mice at 6 weeks of age, but we did not observe differences in CD4+ and CD8+ T cell composition in the pancreatic lymph node, as well as circulating markers of inflammation. Taken together, our results demonstrate that carbamazepine reduces the development of type 1 diabetes in NOD mice by maintaining functional beta-cell mass.
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