White common bean extract remodels the gut microbiota and ameliorates type 2 diabetes and its complications: A randomized double-blinded placebo-controlled trial.

Objective: Excessive carbohydrate intake is a high risk factor for increased morbidity of type 2 diabetes (T2D). A novel regimen for the dietary care of diabetes that consists of a highly active α-amylase inhibitor derived from white common bean extract (WCBE) and sufficient carbohydrates intake was applied to attenuate T2D and its complications. Furthermore, the role of gut microbiota in this remission was also investigated. Methods: We conducted a 4-month randomized double-blinded placebo-controlled trial. During the intense intervention period, ninety subjects were randomly assigned to the control group (Group C) and WCBE group (Group W). Subjects in Group C were supplemented with 1.5 g of maltodextrin as a placebo. Subjects in Group W took 1.5 g of WCBE half an hour before a meal. Fifty-five participants continued the maintenance intervention receiving the previous dietary intervention whereas less frequent follow-up. The variation in biochemical, vasculopathy and neuropathy indicators and the structure of the fecal microbiota during the intervention was analyzed. Result: Glucose metabolism and diabetic complications showed superior remission in Group W with a 0.721 ± 0.742% decline of glycosylated hemoglobin after 4 months. The proportion of patients with diabetic peripheral neuropathy (Toronto Clinical Scoring System, TCSS ≥ 6) was significantly lower in Group W than in Group C. Both the left and right sural sensory nerve conduction velocity (SNCV-left sural and SNCV-right sural) slightly decreased in Group C and slightly increased in Group W. Additionally, the abundances of Bifidobacterium, Faecalibacterium and Anaerostipes were higher in Group W, and the abundances of Weissella, Klebsiella, Cronobacter and Enterobacteriaceae_unclassified were lower than those in Group C at month 2. At the end of month 4, Bifidobacterium remained more abundant in Group W. Conclusion: To our knowledge, this is the first report of improvement to diabetes complications by using a dietary supplement in such a short-term period. The enrichment of SCFA-producing bacteria might be responsible for the attenuation of T2D and its complications. Clinical trial registration number: http://www.chictr.org.cn/edit.aspx?pid=23309&htm=4, identifier ChiCTR-IOR-17013656.

Long non-coding RNA FOXD2-AS1 promotes proliferation, migration and invasion of ovarian cancer cells via regulating the expression of miR-4492.

The aim of the present study was to determine the role of long non-coding RNA (lncRNA) forkhead box D2 antisense 1 (FOXD2-AS1) in the development of ovarian cancer, investigate the underlying mechanisms and provide a potential diagnostic biomarker for ovarian cancer. A total of 39 ovarian cancer patients were included, and the ovarian cancer tissues and paracancer tissues were obtained. The ovarian cancer cell lines SKOV3 and OVCAR3 and the human ovarian normal epithelial cell line IOSE80 were cultured. The expression of lncRNA FOXD2-AS1 and miR-4492 was detected by reverse transcription-quantitative PCR. Small interfering RNA targeting FOXD2-AS1 (si-FOXD2-AS1), microRNA (miR)-4492 mimics, miR-4492 inhibitor and their corresponding controls were transfected into cells. The proliferation was detected with a Cell-Couting-Kit-8 assay, and migration and invasion were determined using Transwell assays. The mutual binding site of lncRNA FOXD2-AS1 and miR-4492 was predicted with the miRDB database and verified by a luciferase reporter assay. Finally, a rescue assay was performed. The results suggested that lncRNA FOXD2-AS1 was upregulated in ovarian cancer tissues and cell lines. si-FOXD2-AS1 was able to inhibit the proliferation, migration and invasion of ovarian cancer cells. lncRNA FOXD2-AS1 was confirmed to directly target miR-4492. The expression of lncRNA FOXD2-AS1 and miR-4492 exhibited a negative correlation. In a rescue experiment, miR-4492 inhibitor abrogated the effect of siFOXD2-AS1 in SKOV3 and OVCAR3 cell lines. In conclusion, lncRNA FOXD2-AS1 promotes the proliferation and invasion of ovarian cancer cells via regulating the expression of miR-4492. It may be a novel potential diagnostic biomarker and therapeutic target for ovarian cancer.