Project description:We aim to study the unusual TMA metabolism mechanism of ducks, and further explore the hidden reasons that led to the weakening TMA metabolism ability. To achieve this, transcriptome, proteome, and metagenome analyses were integrated based on the constructed duck populations with high TMA metabolism ability and low TMA metabolism ability. In addition, further experiments were followed to validate the hypothesis on the limited flavin-containing monooxygenase 3 (FMO3) metabolism ability of ducks. The study demonstrated that both cecal microbe, including Akkermansia and Mucispirillum, and liver FMO3 participated in the TMA metabolism process of ducks. The limited oxidation ability of FMO3 explained the weakening TMA metabolism ability of ducks. Nevertheless, it contributed to the duck’s survival and reproduction during the evolutional adaption process.
Project description:To explore the influence of maternal choline intake on placental gene expression, we employed whole genome microarray expression profiling to identify genes that were differentially expressed in placental tissues obtained from women consuming two different doses (480 vs. 930 mg/d) of choline throughout the third trimester of pregnancy. Healthy third trimester (gestational week 26-29) pregnant women were randomized to a 12-week choline controlled feeding study. The participants consumed either 480 (n=6) or 930 (n=6) mg choline/d. Full thickness placental samples were collected at delivery to extract RNA and perform the arrays. Healthy third trimester (gestational week 26-29) pregnant women were randomized to a 12-week choline controlled feeding study. The participants consumed either 480 (n=6) or 930 (n=6) mg choline/d for 12 weeks. Placental samples were obtained at delivery
Project description:To explore the influence of choline intake and pregnancy status on gene expression, we employed whole genome microarray expression profiling to identify genes that were differentially expressed between two choline intake groups and between pregnant and non-pregnant women. Healthy third trimester (gestational week 26-29) pregnant women and non-pregnant women were randomized to a 12-week choline controlled feeding study. The participants consumed either 480 (n=6 pregnant and n=5 non-pregnant) or 930 (n=6 pregnant and n=5 non-pregnant) mg choline/d. Fasting peripheral blood leukocyte samples were collected at week 0 and week 12 to extract RNA and perform the arrays. Healthy third trimester (gestational week 26-29) pregnant women and non-pregnant women were randomized to a 12-week choline controlled feeding study. The participants consumed either 480 (n=6 pregnant and n=5 non-pregnant) or 930 (n=6 pregnant and n=5 non-pregnant) mg choline/d for 12 weeks. Fasting (10-h) peripheral blood leukocyte gene expression were measured at week 0 and week 12.
Project description:Choline and methionine/choline deficient diets are widely used to generate severe rodent hepatic steatosis and steatohepatitis in an attempt to reflect stages of human non-alcoholic fatty liver disease (NAFLD). The underlying mechanism of hepatic injury in these models, and how this reflects human disease remains incompletely understood. We used detailed transcriptional analysis to interrogate the molecular mechanisms of this intervention and its similarity to human disease. Adult C57Bl/6J mice were maintained on control, choline deficient (CDD) or methionine/choline deficient (MCDD) diets for 4 weeks. Isolated liver RNA was used for transcriptional profiling by micro array analysis.
Project description:To explore the influence of maternal choline intake on placental gene expression, we employed whole genome microarray expression profiling to identify genes that were differentially expressed in placental tissues obtained from women consuming two different doses (480 vs. 930 mg/d) of choline throughout the third trimester of pregnancy. Healthy third trimester (gestational week 26-29) pregnant women were randomized to a 12-week choline controlled feeding study. The participants consumed either 480 (n=6) or 930 (n=6) mg choline/d. Full thickness placental samples were collected at delivery to extract RNA and perform the arrays.
Project description:The feeding/fasting cycles controlled by our circadian clock impose great daily metabolic and physiological changes, and yet investigations into the consequences of metabolic deficiencies, either dietary or genetic, have often ignored the time of day or the circadian time of the animals or subjects. In addition, these deficiencies may themselves disrupt our circadian clock, causing secondary metabolic, physiological and behavioural disorders. Dietary methionine/choline deficiency in rodents is a common model for human non-alcoholic steatohepatitis, but methionine and choline are nutrients essential for many other processes beyond fatty acid synthesis in the liver, including biological methylations and 1-carbon metabolism, regulation of translation notably via the mTOR pathway, phospholipid synthesis, polyamine pathway and glutathione synthesis. We have previously shown that circadian rhythms in many organisms are highly sensitive to deficiency or excesses of 1-carbon metabolites. Using a methionine/choline deficient diet in mice, we illustrate the nutrigenomic crosstalk between circadian rhythms and 1-carbon metabolism. We show not only that circadian locomotor activity behaviour is profoundly, rapidly and reversibly affected by methionine/choline deficiency, but also that the effects of methionine/choline deficiency on gene expression and 1-carbon metabolites are dependent on circadian time, illustrating the importance of considering circadian rhythms in metabolic studies. This study also highlights the impact of what we eat, or don't, on our behaviour and biological rhythms.
Project description:To explore the influence of choline intake and pregnancy status on gene expression, we employed whole genome microarray expression profiling to identify genes that were differentially expressed between two choline intake groups and between pregnant and non-pregnant women. Healthy third trimester (gestational week 26-29) pregnant women and non-pregnant women were randomized to a 12-week choline controlled feeding study. The participants consumed either 480 (n=6 pregnant and n=5 non-pregnant) or 930 (n=6 pregnant and n=5 non-pregnant) mg choline/d. Fasting peripheral blood leukocyte samples were collected at week 0 and week 12 to extract RNA and perform the arrays.
Project description:The objective of this study is to explore gene expression profiles of liver tissues in response to choline defficient diet by DNA microarray data analysis. Male CD-1mice (5 weeks) were fed either a choline-deficient diet (F2CDD, Oriental Yeast) or F2CDD plus 0.2% choline bitartrate for 3 weeks. Liver tissue from control versus choline-deficient samples were analyzed for gene expression on an Agilent Whole Mouse Genome Microarray.
Project description:Purpose:To understand the transcriptome regulator of duck spleen infected with duck enteritis virus (DEV).Methods:50-day-old ducks were inoculated with 100 titer (The TCID50 of DEV was 10-9/0.1mL) and 10-2 titer two different viral titer of DEV in leg muscle for different durations (66 h, 90 h and 114 h) and seronegative control (0 h) were analyzed using next-generation RNA sequencing.Furthermore, the data were validated using quantitative real-time PCR.Results:There were 534, 685 and 580 genes differentially expressed in 100 titer, moreover, 511, 485 and 531 differentially expressed genes (DEGs) were obtained from 10-2 titer for 66 h, 90 h and 114 h, respectively. These genes were mainly involved in functional categories including immune response, extracellular space, heparin binding, oxygen transport, extracellular region, cellular response to interleukin-4, MHC class II protein complex, antigen processing and presentation of peptide or polysaccharide antigen via MHC class II, and pathways such as ribosome, ECM-receptor interaction, cell adhesion molecules, JAk-STAT signaling pathway, PPAR signaling pathway, neuroactive ligand-receptor interaction, phagosome.Conclusions: Different titers of DEV infection can stimulate different biological processes and signaling pathways in the spleen, and regulated the complex biological processes, metabolic and signaling pathways in the process of DEV infection.This transcriptome analysis of duck spleen infected with DEV in different time points is reported for the first time, it laid the foundation for further understanding of interactions between DEV and duck spleen tissue, molecular mechanisms of duck defend against DEV infection, and screening key functional genes.