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Article Abstract

Background Diabetes mellitus is a chronic metabolic disorder that undesirably affects both central and peripheral nervous systems through the apoptosis of neurons. Insulin and insulin-like growth factors (IGFs) inhibit apoptosis of oligodendrocytes. The objective of this study was to determine whether oral insulin in the form of nanoparticles may have similar effects to injectable insulin in increasing the gene expression of IGF1 and IGF2. Methods Insulin-loaded trimethyl chitosan nanoparticles were prepared using the polyelectrolyte complex method and characterized for size, polydispersity index, zeta potential, drug loading, and entrapment efficiency. An in vivo study was performed in different groups of male Wistar rats with diabetes mellitus type 1 treated with insulin-loaded trimethyl chitosan nanoparticles and subcutaneous injection of trade insulin (neutral protamine Hagedorn). The hippocampus of rats were studied for the expression of IGF1 and IGF2 genes by using real-time PCR, and the fold changes in gene expression were evaluated using the 2-ΔΔCt method. Results The expression of IGF1 and IGF2 genes in the groups treated with nano-insulin and injected insulin were significantly higher than that in the diabetic control group (p<0.001) and meaningfully lower than that in the healthy control group. However, there was no significant difference to the treated groups. Conclusion Our findings suggest that future research might provide a new formulation of drugs for treating type 1 diabetes, in the form of oral insulin.

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http://dx.doi.org/10.1515/jbcpp-2019-0147DOI Listing

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Background Diabetes mellitus is a chronic metabolic disorder that undesirably affects both central and peripheral nervous systems through the apoptosis of neurons. Insulin and insulin-like growth factors (IGFs) inhibit apoptosis of oligodendrocytes. The objective of this study was to determine whether oral insulin in the form of nanoparticles may have similar effects to injectable insulin in increasing the gene expression of IGF1 and IGF2.

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