Date Published: March 18, 2018
Publisher: Tabriz University of Medical Sciences
Author(s): Abed Ghavami, Neda Roshanravan, Shahriar Alipour, Meisam Barati, Behzad Mansoori, Faezeh Ghalichi, Elyas Nattagh- Eshtivan, Alireza Ostadrahimi.
Purpose: The worldwide prevalence of metabolic disorders such as diabetes is increasing rapidly. Currently, the complications of diabetes are the major health concern. The aim of this study was to investigate the effect of high performance (HP) inulin supplementation on glucose homeostasis via KLF5 mRNA expression in adults with type 2 diabetes.
Diabetes mellitus (DM) as a complex metabolic disorder influenced by various environmental and genetic factors has become a common health problem in the entire world.1 According to recent reports it is estimated that by the year 2030, at least 366 million people will suffer from diabetes.2 Recent scientific advances point to manipulation of gut microbiota as contributing factors for preventing or controlling diabetes.2,3
The study flowchart is shown in Figure 1. A total of 46 diabetic patients completed the study and were interred in the final analyses. No adverse side-effects were reported by diabetic patients following the HP inulin or placebo supplementation. General characteristics (demographic variables and baseline values of anthropometric indices) of the participants are presented in Table 1. None of the demographic and anthropometric variables were different between the study groups, at baseline (P>0.05). As specified in Table 2, no differences were seen in the percent changes of few of the variables such as HbA1c, Weight, BMI, anthropometric indices (WC, HC and WHR) and blood lipids (TC, TG, HDL-C, LDL-C) after Inulin supplementation compared to the placebo group (P>0.05). However, Inulin supplementation significantly decreased FPG in comparison to the placebo group (P<0.001). Also, a statistically insignificant increase was observed in fasting insulin level after inulin supplementation. Intra-group statistical analysis indicated that Inulin supplementation significantly reduced FPG, WC and HC (P<0.05). Inulin supplementation significantly decreased WC from 97.47± 8.41 to 96.28±8.03 (p=0.009). Our findings provide strong evidence for modulation of glycemic indices via miR-375 as an important regulator for KLF5 mRNA expression in type 2 diabetic patients after HP inulin supplementation. The findings of the present study indicated that HP inulin supplementation decreased FPG and KLF5 mRNA expression significantly. Interestingly, miR-375 expression increased remarkably in the intervention group compared with the placebo group. Additionally, our study revealed that the levels of FPG, WC and HC decreased in inulin group compared to the placebo one. According to the effectiveness of inulin supplementation on glucose homeostasis through effective mechanisms like genes expression, this survey can be considered as a novel therapeutic approach in controlling diabetes. Our results revealed new insights into how KLF5 functions play a role in controlling diabetes. The newly identified KLF5- miR-375 pathway may contribute to diabetes progression. Inhibiting KLF5 may be a potential pharmacological intervention in controlling diabetes. With descriptions above, inulin supplementation maybe considered an adjunctive therapy for diabetic patients. The authors would like to thank all the study participants, as well as nurses and doctors in the diabetes clinics in East Azerbaijan, Iran for their collaboration. The present study did not achieve any grants. The Ethics committee of Tabriz University of Medical Science (Ethic code: IR.TBZMED.REC.1395.671) approved the research protocol of the study and a written informed consent document was obtained from all patients. The study was registered in the Iranian Registry of Clinical Trials website (IRCT ID: IRCT201610212017N31). The authors would like to gratitude the individuals who participated in this study. HP: high performance; KLF5: kruppel like factor 5; FPG: fasting plasma glucose; PBMCs: Peripheral blood mononuclear cells. Source: http://doi.org/10.15171/apb.2018.005