Transcriptomic analysis of colonic epithelial cells in adult rats born with intra-uterine growth retardation.
Ontology highlight
ABSTRACT: The impact of intra-uterine growth retardation (IUGR) was analyzed on gene expression of the colonic epithelial cells from adults rats fed a standard or a high-fat diet. The hypothesis tested in this study was that IUGR induces sustainable effects on colonocyte transcriptome that may alter further nutritional adaptations at adulthood, especially to high-fat diet. Total RNA extracted from control (C) and IUGR (R) rats fed chow (Normal Diet, ND) or high-fat diet (HFD).
Project description:The impact of intra-uterine growth retardation (IUGR) was analyzed on gene expression of the colonic epithelial cells from adults rats fed a standard or a high-fat diet. The hypothesis tested in this study was that IUGR induces sustainable effects on colonocyte transcriptome that may alter further nutritional adaptations at adulthood, especially to high-fat diet.
Project description:Resistant starches (RS), fed as high amylose maize starch (HAMS) or butyrylated HAMS (HAMSB), oppose dietary protein-induced colonocyte DNA damage in rats. In this study, rats were fed diets high in fat (19%) and protein (20%) with different forms of digestible starch (low amylose maize starch (LAMS) or low amylose whole wheat (LAW)) or RS (HAMS, HAMSB, or a whole high amylose wheat (HAW) generated by RNA interference (RNAi)) for 11 wk. A control diet contained 7% fat, 13% protein and LAMS. The aim of this study was to detect changes in the expression of DNA damage and repair genes in response to the above dietary treatments.
Project description:The purpose of this study was to investigate whether paternal high-fat diet (HFD) transgenerationally remodeled the hepatic transcriptome of F2 female rats Liver mRNA expression profiling of F2-female from F0-founders fed either a chow or a chronic HFD challenged. Adult females were challenge or not a high-fat diet for 12 weeks. Liver was dissected at an endpoint experiment. Rats were subjected to 4 hours fasting prior to anesthesia with pentobarbital and tissue collection.
Project description:In the animal study, both a decrease of serum alanine aminotransferase level and whole blood gene expression changes were observed in rats fed a MLP-containing high-fat diet compared with rats fed a high-fat diet.
Project description:In the animal study, both a decrease of serum alanine aminotransferase level and whole blood gene expression changes were observed in rats fed a MLP-containing high-fat diet compared with rats fed a high-fat diet.
Project description:Insulin resistance drives the development of type 2 diabetes (T2D). In liver, diacylglycerol (DAG) is a key mediator of lipid-induced insulin resistance. DAG activates protein kinase C epsilon (PKCε), which phosphorylates and inhibits the insulin receptor. In rats, a 3-day high fat diet produces hepatic insulin resistance through this mechanism, and knockdown of hepatic PKCε protects against high fat diet-induced hepatic insulin resistance. Here we employ a systems level approach to uncover additional signaling pathways involved in high fat diet-induced hepatic insulin resistance. We used quantitative phosphoproteomics to map global in vivo changes in hepatic protein phosphorylation in chow-fed, high fat-fed, and high fat-fed with PKCε knockdown rats to distinguish the impact of lipid- and PKCε-induced protein phosphorylation.
Project description:Potential mechanism was discovered through expression profiling of a total of 3545 miRNAs in liver of rats fed with high fat diet after HTG treatment. MiRNAs in liver of rats(3 group, normal fat diet group, 3, high fat diet group, 3, high fat diet + HTG treatment, 3) were detected, and differentially expressed miRNAs were analyzed to reveal potential mechanism of HTG in treating dyslipidaemia.