| dc.description.abstract | The past decade has witnessed for high prevalence of various metabolic, lifestyle, and diet-related maladies such as diabetes. Currently, one of the new treatment methods and approaches for controlling chronic degenerative diseases such as diabetes is dissecting the disease's molecular mechanisms. The aim of this study was to evaluate the beneficial effects of sodium butyrate and inulin supplementation on the beta-cell function and inflammatory responses through molecule-based mechanisms in patients with Type 2 diabetes. In this clinical trial, 60 patients with Type 2 diabetes were recruited from the north-western part of Iran. The participants were allocated to one of the four treatment orders. Group A took six capsules of 100 mg of NaBut daily, group B took 10 g of HP inulin supplement powder daily, group C consumed both the supplements, and group D took placebo. Before and after the intervention, we assessed the thioredoxin-interacting protein (TXNIP), interleukin-6, and interleukin-10 mRNA expression, as well as noting the plasmatic levels of the miR-204, miR-200c, and miR-21. A homeostasis model assessment of beta-cells (HOMA-?) was used to evaluate the function of the pancreatic beta-cells. The results showed that TXNIP expression was over three times higher in the placebo group as compared to the butyrate + inulin group (p = 0.045). Furthermore, the plasmatic levels of miR-200c expression decreased in the groups A (butyrate) and C (butyrate + inulin) (p < 0.001), as opposed to its constant level in the placebo. Interestingly, IL-6 mRNA expression decreased after butyrate (p < 0.001) and butyrate + inulin supplementation (p < 0.001). Our results revealed new insights into how TXNIP functions have a role in controlling diabetes. The newly identified TXNIP-miR-200c-IL-6-beta-cell function pathway may contribute to diabetes progression. Inhibiting TXNIP and miR-200c activity may be a potential pharmacological target to promote beta-cell function. © 2018 Elsevier Ltd | |
