Unknown,Transcriptomics,Genomics,Proteomics

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Genome-wide expression profile of livers from mice fed HFD,SO-HFD or Viv chow [RNAseq]

ABSTRACT: Purpose: Aim of the study is to identify changes in hepatic gene expression induced by either a 40kcal% coconut oil rich high fat diet (HFD), a 40kcal% soybean oil plus coconut oil high fat diet (SO-HFD) or a low fat vivarium chow diet (Viv). Methods: Livers from mice that had been fed one of the above mentioned diets for 35 weeks, were used to make cDNA libraries that were then sent for deep sequencing, using the Illumina TruSeq RNA. Result: Many genes involved in metabolism, lipid binding, transport and storage and many Cyp genes are dysregulated in the two high fat diets as compared to Viv HFDs in SO-HFD mice. Comparing the two HFDs shows more metabolism and disease related genes dysregulated in SO-HFD vs HFD. Conclusion: A diet high in soybean oil may be more detrimental to metabolic health than a diet high in saturated fats. cDNA isolated from livers from mice fed HFD, SO-HFD or Viv for 35 weeks, were 50bp pair-ended sequenced in triplicate using Illumina TruSeq RNA Sample Prep v2 Kit.

ORGANISM(S): Mus musculus

SUBMITTER: joseph dhahbi

PROVIDER: E-GEOD-68360 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Carotenoids are naturally occurring pigments in plants responsible for the orange, yellow, and red color of fruits and vegetables. Carrots are one of the primary dietary sources of carotenoids. The biological activities of carotenoids in higher organisms are well documented in most tissues but not the large intestine. The gastrointestinal barrier acts as a line of defense against the systemic invasion of pathogenic bacteria, especially at the colonic level. Proteins involved in tight junction assembly between epithelial cells and mucus secretion from goblet cells are essential for maintaining intestinal barrier homeostasis. A high-fat diet can cause gut impairment by inducing barrier permeability, leading to low-grade chronic inflammation via metabolic endotoxemia. Our hypothesis for this study is that the dietary intake of carotenoid-rich foods can alleviate obesity-associated gut inflammation and strengthen the intestinal barrier function. Male C57BL/6J mice were randomized to one of four experimental diets for 20 weeks (n = 20 animals/group): Low-fat diet (LFD, 10% calories from fat), high-fat diet (HFD, 45% calories from fat), HFD with white carrot powder (HFD + WC), or HFD with orange carrot powder (HFD + OC). Colon tissues were harvested to analyze the biochemical effects of carotenoids in carrots. The distal sections were subjected to isobaric labeling-based quantitative proteomics in which tryptic peptides were labeled with tandem mass tags, followed by fractionation and LC-MS/MS analysis in an Orbitrap Eclipse Tribrid instrument. High-performance liquid chromatography results depicted that the HFD+WC pellets were carotenoid-deficient, and the HFD+OC pellets contained high concentrations of provitamin A carotenoids, specifically α-carotene and β-carotene. As a result of the quantitative proteomics, a total of 4410 differentially expressed proteins were identified. Intestinal barrier-associated proteins were highly upregulated in the HFD+OC group, particularly mucin-2 (MUC-2). Upon closer investigation into mucosal activity, other proteins related to MUC-2 functionality and tight junction management were upregulated by the HFD+OC dietary intervention. Carotenoid-rich foods may prevent high-fat diet-induced intestinal barrier disruption by promoting colonic mucus synthesis and secretion in mammalian organisms.

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Genome-wide expression profile of livers from mice fed HFD,SO-HFD or Viv chow [RNAseq]

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