In Vitro Effects of Tartary Buckwheat-Derived Nanovesicles on Gut Microbiota.

Evidence suggests that plant-derived nanovesicles may play a significant role in human health. Tartary buckwheat has several physiological activities; however, its underlying health-promoting mechanism remains unclear. In this study, first, Tartary buckwheat-derived nanovesicles (TBDNs) were collected, their structures were analyzed, and microRNA sequencing was performed. Next, target prediction and functional verification were conducted. Finally, the effects of TBDNs on gut microbiota and short-chain fatty acid levels were evaluated. The average size of TBDNs was 141.8 nm diameter. Through the sequencing analyses, 129 microRNAs, including 11 novel microRNAs were identified. Target gene prediction showed that some microRNAs could target functional genes in Escherichia coli and Lactobacillus rhamnosus-related physiological processes. TBDNs significantly promoted the growth of E. coli and L. rhamnosus, enhanced the diversity of fecal microorganisms and increased the short-chain fatty acid levels. These findings provided a new nutritional perspective for Tartary buckwheat and were conducive to promote the development and utilization of Tartary buckwheat.

The Development of Rickets in Children and Nursing Contributions to Treatment.

Rickets is one of the most prevalent non-communicable diseases in children in the developing world. It is often found in cultures in which children follow strict vegetarian diets and are not exposed to vitamin D-enhanced foods. While a rare occurrence, X-linked hypophosphatemic rickets may be the most frequent type of the disease seen outside the Third World today. However, there is not much credible information on the extent of the development of rickets. Therefore, pediatric nurses must be able to recognize children at risk and provide best practice care for the prevention and treatment of rickets. When caring for children in hospitals, communities or classrooms, nurses play a vital role in identifying children at risk for hypovitaminosis D and advising families to, if possible, follow safe diets and take supplements in order to avoid health complications associated with low levels of vitamin D. This study examines the prevalence and variables contributing to rickets, including hypovitaminosis vitamin D, the consequent orthopedic problems and the role of nurses in preventing and managing the pathogenesis of rickets and ultimately avoiding extreme deficits that result in bone deformities and the need for corrective surgery.

YY1 deficiency in ß-cells leads to mitochondrial dysfunction and diabetes in mice.

BACKGROUND: The transcription factor YY1 is an important regulator for metabolic homeostasis. Activating mutations in YY1 lead to tumorigenesis of pancreatic ß-cells, however, the physiological functions of YY1 in ß-cells are still unknown. Here, we investigated the effects of YY1 ablation on insulin secretion and glucose metabolism. METHODS: We established two models of ß-cell-specific YY1 knockout mice. The glucose metabolic phenotypes, ß-cell mass and ß-cell functions were analyzed in the mouse models. Transmission electron microscopy was used to detect the ultrastructure of ß-cells. The flow cytometry analysis, measurement of OCR and ROS were performed to investigate the mitochondrial function. Histological analysis, quantitative PCR and ChIP were performed to analyze the target genes of YY1 in ß-cells. RESULTS: Our results showed that loss of YY1 resulted in reduction of insulin production, ß-cell mass and glucose tolerance in mice. Ablation of YY1 led to defective ATP production and mitochondrial ROS accumulation in pancreatic ß-cells. The inactivation of YY1 impaired the activity of mitochondrial oxidative phosphorylation, induced mitochondrial dysfunction and diabetes in mouse models. CONCLUSION: Our findings demonstrate that the transcriptional activity of YY1 is essential for the maintenance of mitochondrial functions and insulin secretion in ß-cells.

Transferrin receptor 1 levels at the cell surface influence the susceptibility of newborn piglets to PEDV infection.

Porcine epidemic diarrhea virus (PEDV) mainly infects the intestinal epithelial cells of newborn piglets causing acute, severe atrophic enteritis. The underlying mechanisms of PEDV infection and the reasons why newborn piglets are more susceptible than older pigs remain incompletely understood. Iron deficiency is common in newborn piglets. Here we found that high levels of transferrin receptor 1 (TfR1) distributed in the apical tissue of the intestinal villi of newborns, and intracellular iron levels influence the susceptibility of newborn piglets to PEDV. We show that iron deficiency induced by deferoxamine (DFO, an iron chelating agent) promotes PEDV infection while iron accumulation induced by ferric ammonium citrate (FAC, an iron supplement) impairs PEDV infection in vitro and in vivo. Besides, PEDV infection was inhibited by occluding TfR1 with antibodies or decreasing TfR1 expression. Additionally, PEDV infection was increased in PEDV-resistant Caco-2 and HEK 293T cells over-expressed porcine TfR1. Mechanistically, the PEDV S1 protein interacts with the extracellular region of TfR1 during PEDV entry, promotes TfR1 re-localization and clustering, then activates TfR1 tyrosine phosphorylation mediated by Src kinase, and heightens the internalization of TfR1, thereby promoting PEDV entry. Taken together, these data suggest that the higher expression of TfR1 in the apical tissue of the intestinal villi caused by iron deficiency, accounts for newborn piglets being acutely susceptible to PEDV.

Dietary quinoa (Chenopodium quinoa Willd.) polysaccharides ameliorate high-fat diet-induced hyperlipidemia and modulate gut microbiota.

As the high nutritional and functional values of quinoa acknowledged, the increasing researches focus on the bioactivities and related mechanisms of its abundant carbohydrates. Herein, the beneficial effects of the soluble polysaccharide fraction from quinoa was investigated to lower the serum lipid of rats treated by high-fat diet (HFD) and call the disordered gut microbiota back. The polysaccharide faction was firstly extracted by ultrasonic-assisted extraction technology (yield of 9.65%) and characterized of the monosaccharide composition with glucose and arabinose (1.17:1, molar ratio). And then, the oral administration of quinoa polysaccharide of 300 mg·kg-1·day-1 and 600 mg·kg-1·day-1 for 8 weeks remarkably alleviated dyslipidemia by decreasing the levels of serum total triglyceride (TG), low density lipoprotein cholesterol (LDL-C), malondialdehyde (MDA), total glutamic pyruvic transaminase (ALT) and glutamic oxaloacetic transaminase (AST) in rats fed with HFD, as well as the reduced hepatic lipid accumulation. Meanwhile, the relative abundance of gut microbiota could be disordered by the long term of HFD. Nevertheless, dietary supplementation of quinoa polysaccharide could enhance species richness and regulate the gut microbiota community structure, reducing the ratio of Firmicutes and Bacteroides, the relative abundance of Proteobacteria. Meanwhile, Sequencing of 16S rRNA gene revealed that intake of quinoa polysaccharide decreased the relative abundances of Desulfovibrio and Allobaculum, which were positively correlated with serum lipid profiles and beneficial to lessen intestinal inflammation. Taken together, the present study demonstrated that quinoa polysaccharide supplementation could ameliorate the hyperlipidemia induced by HFD in association with modulating gut microbiota in a positive way.

Dietary microbial phytase exerts mixed effects on the gut health of tilapia: a possible reason for the null effect on growth promotion.

The present study evaluated the effects of dietary microbial phytase on the growth and gut health of hybrid tilapia (Oreochromis niloticus ♀×Oreochromis aureus ♂), focusing on the effect on intestinal histology, adhesive microbiota and expression of immune-related cytokine genes. Tilapia were fed either control diet or diet supplemented with microbial phytase (1000 U/kg). Each diet was randomly assigned to four groups of fish reared in cages (3×3×2 m). After 12 weeks of feeding, weight gain and feed conversion ratio of tilapia were not significantly improved by dietary microbial phytase supplementation. However, significantly higher level of P content in the scales, tighter and more regular intestinal mucosa folds were observed in the microbial phytase group and the microvilli density was significantly increased. The adhesive gut bacterial communities were strikingly altered by microbial phytase supplementation (0·41

Whole exome sequencing of insulinoma reveals recurrent T372R mutations in YY1.

Functional pancreatic neuroendocrine tumours (PNETs) are mainly represented by insulinoma, which secrete insulin independent of glucose and cause hypoglycaemia. The major genetic alterations in sporadic insulinomas are still unknown. Here we identify recurrent somatic T372R mutations in YY1 by whole exome sequencing of 10 sporadic insulinomas. Further screening in 103 additional insulinomas reveals this hotspot mutation in 30% (34/113) of all tumours. T372R mutation alters the expression of YY1 target genes in insulinomas. Clinically, the T372R mutation is associated with the later onset of tumours. Genotyping of YY1, a target of mTOR inhibitors, may contribute to medical treatment of insulinomas. Our findings highlight the importance of YY1 in pancreatic ß-cells and may provide therapeutic targets for PNETs.