Epigenetic and Diabetes Mellitus Type 1 | ||
| Suez Canal Veterinary Medical Journal. SCVMJ | ||
| Article 14, Volume 21, Issue 2, December 2016, Pages 163-169 PDF (521.27 K) | ||
| Document Type: Review Article | ||
| DOI: 10.21608/scvmj.2016.62696 | ||
| Author | ||
| Aliaa Hassan* | ||
| Biochemistry Division | ||
| Abstract | ||
| Type 1 diabetes mellitus (T1D) is one of the commonest chronic autoimmune diseases. It’s characterized by formation of islet specific T cells and autoantibodies leading to chronic inflammation in the islelets, i.e. inflammatory destruction of the β cells resulting in an insulin deficiency. T1D resulting from the interplay of genetic, epigenetic, and environmental factors. Worldwide, the T1D epidemic represents an increasing global public health burden,Egypt ranked 8th highest in the world. The incidence of T1D among the children has been rising. There has been an overall increase in the incidence of T1D of 3% to 5% per year. Suggested the interaction between genetic predisposition and environmental factors. The low disease concordance rate in adult-onset T1D (<20%) suggests that environmental and epigenetic changes may play a predominant role. Circulating miRNA is now a biomarker for example miRNA 375. miRNA 375 control cellular growth, proliferation and cellular function, and it released when β cell destruction and so it can be used as a novel T1D marker .itearly detected in plasma, while T1D is usually diagnosed when >80 % of pancreatic β cells are destroyed. miRNA 375 easily detectable can detected blood, can found in serum, plasma and urine. Also miRNA 375is stable even against boiling low or high pH, multiple freeze throw cycle. Diane Mathis, Benoist and co-worker at Harvard medical school and GlaxoSmithKline reported that an epigenetic drug called BET151 can effectively prevent T1D in mouse model for these diseases. This is by neutralizing the cytokines, blocking the interaction of T cells and antigen presenting cell and regeneration of β cells. A novel epigenetic drugs for treatment of T1D by transdifferantiation of human dermal fibroblasts into insulin cell producing cells by inducing the expression of insulin through increasing acetylation and decrease methylation by two epigenetic modified compounds romidepsin a histone deacetylase inhibitor and Azacytidine that cant methylated. | ||
| Keywords | ||
| Epigenetic; diabetes mellitus type 1 | ||
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