Fagopyrum tataricum ethanol extract ameliorates symptoms of hyperglycemia by regulating gut microbiota in type 2 diabetes mellitus mice.

Type 2 diabetes mellitus (T2DM) is typically accompanied by sudden weight loss, dyslipidemia-related indicators, decreased insulin sensitivity, and altered gut microbial communities. Fagopyrum tataricum possesses many biological activities, such as antioxidant, hypolipidemic, and hypotensive activities. However, only a few studies have attempted to elucidate the regulatory effects of F. tataricum ethanol extract (FTE) on intestinal microbial communities and its potential relationships with T2DM. In this study, we established a T2DM mouse model and investigated the regulatory effects of FTE on hyperglycemia symptoms and intestinal microbial communities. FTE intervention significantly improved the levels of fasting blood glucose, the area under the curve of oral glucose tolerance test (OGTT), and glycosylated serum protein, as well as pancreas islet function correlation index. In addition, FTE effectively improved hepatic and cecum injuries and insulin secretion due to T2DM. It was also revealed that the potential hypoglycemic mechanism of FTE was involved in the regulation of protein kinase B (AKT-1) and glucose transporter 2 (GLUT-2). Furthermore, compared with the Model group, the FTE-H intervention exhibited a significantly decreased ratio of Firmicutes to Bacteroidetes at the phylum level, reduced relative abundance of pernicious bacteria at the genus level, such as Desulfovibrio, Oscillibacter, Blautia, Parabacteroides, and Erysipelatoclostridium, and ameliorated inflammatory response and insulin resistance. Moreover, the correlation between gut microbiota and hypoglycemic indicators was predicted. The results showed that Lachnoclostridium, Lactobacillus, Oscillibacter, Bilophila, and Roseburia have the potential to be used as bacterial markers for T2DM. In conclusion, our research showed that FTE alleviates hyperglycemia symptoms by regulating the expression of AKT-1 and GLUT-2, as well as intestinal microbial communities in T2DM mice.

Protein-rich yeast extract (®fermgard) has potential antioxidant and anti-aging activities.

There existed a deficiency in the research on the nutritional activities of microbial (yeast) active substances in antioxidant and anti-aging activities, although the research objects were concentrated in animals and plants in recent years. In this study, the anti-oxidant and anti-aging activities of protein-rich yeast extract (®fermgard) (YE) were investigated through Caenorhabditis elegans (C. elegans). The results indicated that YE could improve the lifespan and anti-stress ability by up-regulating the activities of antioxidant enzymes in C. elegans. Meanwhile, the mRNA transcriptional level of daf-16, skn-1 and sod-3 was significantly up-regulated. In addition, the composition and level of the gut microbiota and metabolite were modulated. YE exerts antioxidant and anti-aging activities by regulating the expression of anti-oxidation-related mRNA, gut microbiota and metabolites in C. elegans, providing a basis for exploring the deep mechanism of YE improving health. At the same time, it provides new ideas for the development of functional foods.

Anti-fatigue property of the oyster polypeptide fraction and its effect on gut microbiota in mice.

We aimed to evaluate the anti-fatigue effects of the oyster polypeptide (OP) fraction and its regulatory effect on the gut microbiota in mice. Our exhaustive swimming experiment showed that the swimming time of the low-, middle- and high-dose groups of the OP fraction was increased by 1.82, 2.18 and 2.44 times compared with the control group, respectively. Besides, the liver glycogen levels of the three groups were increased by 19.3%, 42.02% and 65.07%, while the lactate levels were decreased by 18.85%, 21.18% and 28.74%, respectively. Moreover, administration of the OP fraction upregulated the expressions of PEPCK and AMPK, but downregulated the TNF-α expression. Correlation analysis between the gut microbiota and fatigue-related biochemical indicators showed that Faecalibacterium, Desulfovibri and Intestinibacter were negatively correlated with the swimming time, blood lactate, blood urea nitrogen, liver glycogen and muscle glycogen, while Yaniella and Romboutsia were positively correlated. Therefore, the OP fraction had anti-fatigue effects, and could regulate the abundance of gut microbiota and maintain its balance.

[Efficacy and safety of № I Empirical Prescription for Chronic Prostatitis in the treatment of type ⠢ refractory chronic prostatitis].

OBJECTIVE: To evaluate the efficiency and safety of № I Empirical Prescription for Chronic Prostatitis (№ I EPCP) in the treatment of type Ⅲ refractory chronic prostatitis. METHODS: We randomly assigned 53 cases of type Ⅲ refractory chronic prostatitis with damp-heat and blood stasis to an experimental and a control group to receive № I EPCP at 1 dose per day and saw palmetto extract at 160 mg bid), respectively, all for 8 weeks. Before and after 4 and 8 weeks of treatment, we obtained The National Institute of Health Chronic Prostatitis Symptom Index (NIH-CPSI) scores, Traditional Chinese Medicine Syndrome Scores (TCMSS), maximum urinary flow rate (Qmax), average urinary flow rate (Qavg), Hamilton Depression Rating Scale (HAMD) scores and Hamilton Anxiety Rating Scale (HAMA) scores, and compared them between the two groups of patients. RESULTS: Totally 48 of the patients completed the medication and follow-up, 25 in the experimental and 23 in the control group. Compared with the baseline, the NIH-CPSI scores after 8 weeks of treatment were significantly decreased in the experimental (27.82 ± 7.25 vs 15.46 ± 4.77, P <0.05) and the control group (25.98 ± 6.47 vs 21.06 ± 5.74, P <0.05), and so were the TCMSSs (24.64 ± 9.82 vs 16.42 ± 6.33 and 9.15 ± 3.74, P <0.05, and 23.67 ± 8.73 vs 18.55 ± 5.92 and 13.48 ± 4.45, P <0.05); the Qmax at 8 weeks were dramatically increased in the experimental group (ï¼»18.45 ± 7.81ï¼½ vs ï¼»23.44 ± 8.73ï¼½ ml/s, P <0.05) and the control (ï¼»17.58 ± 6.92ï¼½ vs ï¼»21.26 ± 8.32ï¼½ ml/s, P <0.05), and so was the Qavg (ï¼»11.27 ± 5.33ï¼½ vs ï¼»16.51 ± 7.36ï¼½ ml/s, P <0.05 and ï¼»10.66 ± 5.82ï¼½ vs ï¼»13.44 ± 6.16ï¼½ ml/s, P <0.05); the HAMD scores were remarkably reduced in the experimental group (22.74 ± 6.37 vs 17.62 ± 5.71 and 12.54 ± 5.22, P <0.05) and the control (23.55 ± 7.14 vs 22.34 ± 6.88 and 21.62 ± 5.63, P <0.05), and so were the HAMA scores (21.37 ± 7.15 vs 18.42 ± 6.35 and 14.63 ± 7.11, P <0.05 and 20.54 ± 6.77 vs 19.87 ± 6.24 and 19.42 ± 7.04, P <0.05). No obvious adverse reactions were observed in either of the two groups during the medication. CONCLUSIONS: № I EPCP deserves promotion and clinical application for its definite effectiveness and safety in the treatment of type Ⅲ refractory chronic prostatitis with damp-heat and blood stasis.

Milk osteopontin, a nutritional approach to prevent alcohol-induced liver injury.

Alcohol consumption is a leading cause of liver disease worldwide; thus, there is an urgent need to develop novel therapeutic interventions. Key events for the onset and progression of alcoholic liver disease result in part from the gut-to-liver interaction. Osteopontin is a cytokine present at high concentration in human milk, umbilical cord, and infants' plasma with beneficial potential. We hypothesized that dietary administration of milk osteopontin could prevent alcohol-induced liver injury perhaps by maintaining gut integrity and averting hepatic inflammation and steatosis. Wild-type mice were fed either the control or the ethanol Lieber-DeCarli diets alone or in combination with milk osteopontin for 3 wk, and parameters of gut and liver damage were measured. Milk osteopontin protected the stomach and the gut by increasing gland height, crypt cell plus enterocyte proliferation, and mucin content in addition to lowering macrophages, plasmacytes, lymphocytes, and neutrophils in the mucosa and submucosa in alcohol-fed mice. Milk osteopontin targeted the gut-liver axis, preserving the expression of tight-junction proteins in alcohol-fed mice thus maintaining intestinal integrity and permeability. There was protection from liver injury since transaminases, the activity scores, triglyceride levels, neutrophil infiltration, 3-nitrotyrosine residues, lipid peroxidation end products, translocation of gram-negative bacteria, lipopolysaccharide levels, and tumor necrosis factor-α were lower in cotreated than in ethanol-fed mice. Furthermore, milk osteopontin diminished ethanol-mediated liver injury in OPN knockout mice. Milk osteopontin could be a simple effective nutritional therapeutic strategy to prevent alcohol hepatotoxicity due, among others, to gut protective, anti-inflammatory, and anti-steatotic actions.