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Micronutrients in Prevention and Improvement of the Standard Therapy in Diabetes
Published in Kedar N. Prasad, Micronutrients in Health and Disease, 2019
Downregulation of miR-200b increased the levels of its target proteins VEGF (vascular endothelial growth factor), zinc finger-box-binding homebox, TGF-β1 (transforming growth factor-β1), and p300 in the heart of diabetic mice. Overexpression of this microRNA prevented the rise in the levels of these proteins in mouse heart endothelial cells (MHECs), In streptozotocin-induced diabetic mice, reduced expression of miR-133 caused increased levels of its target proteins TGF-β1, connective tissue growth factor (CTGF), fibronectin (FN1), and COL4A1 (alpha 1 subunit of collagen type IV) causing cardiac fibrosis. These effects were decreased in mice overexpression of miR-133a.83 MiR-503 expression was upregulated in ECc cells growing in the presence of high glucose that generates excessive amounts of free radicals and reduced its target proteins cdc25A (Cell Division Cycle 25 Homolog A) and CCNE1 (Cyclin E1).84 Additionally, deleting the expression of miR-503 improved function of ECs growing under high glucose concentrations. In the β-cells from mouse, overexpression of miR-483 increased insulin secretion by downregulating its target protein SOCS3, while increased expression of this microRNA in α-cells reduced the secretion of glucagon. Additionally, overexpression of miR-483 protected β-cells against pro-inflammatory cytokine-induced apoptosis, and enhanced beta-cells mass in the islets of pre-diabetic (db/db) mice.85 Overexpression of miR-200 downregulated the levels of its target proteins Dnajc3 (also known as p58IPK) and Xiap, an inhibitor of caspase, and induced apoptosis in the beta cells in diabetic mice. On the other hand, ablation of miR-200 reduced the apoptosis of beta-cells and prevented development of diabetes.86 The expression of miR-9 was enhanced and its target protein Sirt1 (NSD-dependent protein deacetylase reduced during glucose-dependent insulin secretion in mouse beta-cells secreting insulin. Therefore, miR-9 could be a therapeutic target for diabetes.87 In type 2 diabetes, increased expression of miR-185 was associated decreased its target protein homeodomain-interacting protein kinase-3 (HIPK3) and decreased glucose-stimulated secretion of insulin (GSIS) in islet cells compared with normal controls. Decreased expression of miR-185 increased its target protein SOCS3 and reduced insulin secretion in mice as well as in humans with diabetes.88
Lactiplantibacillus plantarum 299v supplementation modulates β-cell ER stress and antioxidative defense pathways and prevents type 1 diabetes in gluten-free BioBreeding rats
Published in Gut Microbes, 2022
Pinar Sargin, Mark F. Roethle, Shuang Jia, Tarun Pant, Ashley E. Ciecko, Samantha N. Atkinson, Nita H. Salzman, Ru-Jeng Teng, Yi-Guang Chen, Susanne M. Cabrera, Martin J. Hessner
The DRlyp/lyp HCD+Lp299v islet transcriptome exhibited higher abundance of transcripts related to translation initiation, positive regulation of insulin secretion, chaperone binding and protein processing (Figure 3b). This included eukaryotic initiation factors, including Eif4g1 which regulates glucose homeostasis and β-cell function,52 and Eif3f a translational enhancer that improves protein synthesis efficiency.53Eef2 and Eef1d, which encode translation elongation factors, were also most abundant in DRlyp/lyp HCD+Lp299v islets. DRlyp/lyp HCD+Lp299v islets exhibited reduced abundance of translational repressors (Paip2, Eif4g2, Fmr, Cirbp), while showing high abundance of transcripts encoding products required for protein processing within the ER. These included Ssr2 and Sec61a1, necessary for translocating nascent peptides into the ER, and chaperones/co-chaperones (Cdc37, Creld2, Dnajb11, Hsp90b1, Pfdn1, Serpinh1, Sil1) including Dnajc3 which maintains insulin-folding homeostasis.54 Transcripts encoding isomerases (Ppib, Fkbp11, Pdia6) and oxidases necessary for protein maturation within the ER exhibited higher abundance in DRlyp/lyp HCD+Lp299v islets, this included quiescin sulfhydryl oxidase 1 (Qsox1), which also acts to inhibit autophagy.