A novel fasting regimen revealed protein reservation and complement C3 down-regulation after 14-day's continual dietary deprivation.

Objectives: The aim is to evaluate the effect of a novel 14-day fasting regimen on the balance between skeletal muscle and adipose tissue composition which might associate with inflammatory factors. Our analysis includes basic physical examinations, clinical laboratory analysis, bioelectrical impedance and biochemical analytic assessments of healthy volunteers. Methods: Eight healthy subjects were randomly selected from a pool of volunteers to undergo a continual dietary deprivation (CDD) regimen. Individuals were assigned to take Flexible Abrosia (FA, prebiotic combination) plus appropriate mineral supplement of potassium and magnesium at 3 mealtime every day to prevent potential injury from starved intestinal flora and avoid spasms of smooth muscle due to hunger. Physical and medical examinations were conducted and blood samples were collected at following timepoints: before CDD as self-control (0D), day 7 and day 14 during fasting, and 7-21days and/or 2~3mo after refeeding. Results: The combination of FA and mineral supplements significantly decreased self-reported physical response of starvation, with tolerable hunger-mediated sensations experienced during CDD. Bioelectrical and biochemical results indicated significant reduction in both muscle lean and fat mass on day 7. Meanwhile, markers related to fat composition consistently decreased during and after CDD. In addition, most biochemical marker levels, including serum proteins, reached their inflection points at the 7th day of CDD as compared to the control measurements. Levels of these factors started to show a relative plateau, or reversed direction upon the 14th day of CDD. The exceptions of above factors were myostatin and complement protein C3, which remained at lower concentrations in the blood throughout CDD, and were unable to fully recover toward baseline levels even after 3 months' refeeding. Conclusion: Our results indicated that human subjects undergoing prolonged dietary restriction were well protected by FA and mineral ions from gut injury or physical discomfort of starvation. Most factors showed a relative plateau response at the end of 14D-CDD. The muscle tissues were well preserved during prolonged fasting, and an improved protein/lipid ratio was observed. Upon refeeding, constant lower levels of myostatin and complement C3 were maintained after CDD implies a long-term beneficial effect in dealing with anti-aging and inflammation.

Soy isoflavone genistein inhibits hsa_circ_0031250/miR-873-5p/FOXM1 axis to suppress non-small-cell lung cancer progression.

The foods of plants provide the rich nutrition and have protective function in human diseases, including cancers. Genistein is a major isoflavone constituent in soybeans, which has an anti-cancer role in non-small-cell lung cancer (NSCLC). Nevertheless, the mechanism underlying the anti-cancer function of genistein in NSCLC remains largely unknown. NSCLC cells (H292 and A549) were exposed to genistein. Circular RNA hsa_circ_0031250 (circ_0031250), microRNA (miR)-873-5p and forkhead box M1 (FOXM1) abundances were examined via quantitative reverse transcription polymerase chain reaction and Western blotting. The function of genistein, circ_0031250, miR-873-5p, and FOXM1 on NSCLC progression was investigated via Cell Counting Kit-8, colony formation, transwell well, wound healing, flow cytometry, Western blotting and xenograft model. The target relationship was analyzed by dual-luciferase reporter analysis and RNA immunoprecipitation. Results showed that genistein inhibited NSCLC cell viability in dose-time-dependent patterns. circ_0031250 abundance was elevated in NSCLC samples and cell lines, and it was reduced via genistein exposure. circ_0031250 knockdown aggravated genistein-caused suppression of cell proliferation, migration and invasion and elevation of apoptosis. miR-873-5p expression was decreased in NSCLC samples and cells. miR-873-5p was targeted via circ_0031250, and miR-873-5p knockdown attenuated the influence of circ_0031250 silence on NSCLC progression in the presence of genistein. FOXM1 was regulated via circ_0031250/miR-873-5p axis. miR-873-5p constrained cell proliferation, migration and invasion and increased apoptosis via regulating FOXM1 in genistein-treated cells. circ_0031250 knockdown enhanced the inhibitive function of genistein on NSCLC cell growth in xenograft model. Collectively, genistein repressed NSCLC progression by modulating circ_0031250/miR-873-5p/FOXM1 axis.