Thymol and carvacrol alleviate intestinal inflammation in lambs via the Romboutsia maritimum-benzyl cinnamate-GALNT7/MUC2 axis
Ontology highlight
ABSTRACT:
ORGANISM(S): Capra Hircus
SUBMITTER: 
Yuxin Yang
PROVIDER: PXD070212 | iProX | Mon Nov 03 00:00:00 GMT 2025
REPOSITORIES: iProX
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Project description:Here we show that the Drosophila nuclear receptor E78A regulates transcription in adult animals facilitating dietary lipid uptake. E78A mutant adults are viable with normal developmental timing, locomotor activity, female fecundity, but have significantly reduced stored triglycerides. This reduction in whole body triglyceride stores appears to originate from the midgut, using neutral lipid stainings we determined lipid levels in the midgut were greatly reduced. Upon examining our RNA-seq analysis we found that a gastric lipase, CG17192, is transcriptionally coordinated by E78A. CG17192 is expressed in an adult, intestinal specific fashion within control flies, and has a human ortholog. Through dietary supplementation and genetic testing we determined that the whole body hypolipidemia seen within E78A mutants is dependent on CG17192 expression within the intestine. Restoration of this lipase in the intestine of mutant flies is sufficient to restore normal lipid levels. Our data support the model that E78A contributes to a transcriptional regulation of the gastric lipase, CG17192, thus directing dietary triglyceride uptake in the adult fly.
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Project description:Enterocyte Iron Mucosal Block
This is a model of enterocyte iron absorption, consisting of iron uptake (movement of iron from intestinal lumen into cytplasm), and transfer (transport of iron from cytoplasm to blood/plasma). The model was created by Joseph Masison and Pedro Mendes.
Intestinal mucosal block is a cellular phenomenon defined by a transient reduction in iron absorption by intestinal epithelial cells following previous iron exposures. Understanding what controls the mucosal block is central to understanding how intestinal iron absorption contributes to pathological iron states. Three mechanisms implicated in driving mucosal block are the endocytosis of divalent metal transporter 1 (DMT1), sequestration of iron by cytosolic ferritin, and iron regulatory proteins (IRPs) regulation of ferritin expression.
Here, we build a model that reproduces the mucosal block phenomena, based on published experimental data, and use it to quantify the contribution of each mechanism to the block. Model analysis shows ferritin and IRPs regulation have the largest quantitative impact on the mucosal block. Lastly, DMT1 endocytosis is shown to play a role in limiting total enterocyte iron uptake, protecting the cell against oxidative stress, but does not contribute to the decrease in total iron transfer seen in mucosal block.
CC0 1.0 Universal: To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. You can copy, modify, distribute and perform the work, even for commercial purposes, all without asking permission. Please refer to CC0 Public Domain Dedication for more information.
2025-02-11 | MODEL2405170001 | BioModels
Project description:There is increased interest in the potential protective role of dietary Ca in the development of metabolic disorders related to the metabolic syndrome. Ca-induced intestinal precipitation of fatty acids and bile acids as well as systemic metabolic effects of Ca on adipose tissue is proposed to play a causal role. In this experiment, we have studied all these aspects to validate the suggested protective effect of Ca supplementation, independent of other dietary changes, on the development of diet-induced obesity and insulin resistance. In our diet intervention study, C57BL/6J mice were fed high-fat diets differing in Ca concentrations (50 v. 150 mmol/kg). Faecal excretion analyses showed an elevated precipitation of intestinal fatty acids (2·3-fold; P < 0·01) and bile acids (2-fold; P < 0·01) on the high-Ca diet. However, this only led to a slight reduction in fat absorption (from 98 to 95 %; P < 0·01), mainly in the distal small intestine as indicated by gene expression changes. We found no effect on body-weight gain. Lipolysis and lipogenesis-related parameters in adipose tissue also showed no significant changes on the high-Ca diet, indicating no systemic effects of dietary Ca on adiposity. Furthermore, early gene expression changes of intestinal signaling molecules predicted no protective effect of dietary Ca on the development of insulin resistance, which was confirmed by equal values for insulin sensitivity on both diets. Taken together, our data do not support the proposed protective effect of dietary Ca on the development of obesity and/or insulin resistance, despite a significant increase in fecal excretion of fatty acids and bile acids. Keywords: Diet intervention study Nine-week-old mice were fed a high fat purified diet with a low calcium concentration of 50mmol/kg (LCa diet) or a high calcium concentration of 150mmol/kg (HCa diet) for 8 weeks. Body weight was recorded weekly and after 7 weeks of diet intervention an oral glucose tolerance test was performed. For microarray analysis, after 2 weeks of diet intervention, 6 mice per diet group were anaesthetized with a mixture of isofluorane (1.5%), nitrous oxide (70%) and oxygen (30%) and the small intestines were excised. Adhering fat and pancreatic tissue were carefully removed. The small intestines were divided in three equal parts along the proximal to distal axis (SI 1, SI 2 and SI 3) and microarray analysis was performed on pooled mucosal scrapings.
2011-03-03 | E-GEOD-18581 | biostudies-arrayexpress
Project description:High dietary consumption of red or processed meat is associated with increased risk of colorectal cancer (CRC), likely through the presence of dietary carcinogens. Tyramine is a biogenic amine commonly found in processed food and can be produced by the gut bacteria from tyrosine. However, the role of tyramine in intestinal mucosal health has not been studied. Therefore, we used the human colonic HCT116 cell line to investigate the role of tyramine in modulating CRC risk and development
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Project description:Background and Aims: We have shown in several controlled rat and human infection studies that dietary calcium improves intestinal resistance and strengthens the mucosal barrier. Reinforcement of gut barrier function is also relevant for inflammatory bowel disease (IBD). Therefore, we investigated the effect of supplemental calcium on spontaneous colitis development in HLA-B27 transgenic rats, an experimental animal model of IBD. Methods: HLA-B27 transgenic rats were fed a purified high-fat diet containing either a low or high calcium content (30 and 120 mmol CaHPO4/kg diet, respectively) for almost 7 weeks. Inert chromium ethylenediamine-tetraacetic acid (CrEDTA) was added to the diets to quantify intestinal permeability by measuring urinary CrEDTA excretion. Relative fecal dry-weight was determined to quantify diarrhea. Colonic inflammation was determined histologically, and by measuring mucosal interleukin-1β. In addition, colonic mucosal gene expression of individual rats was analyzed, using whole genome microarrays. Interesting results were verified by Q-PCR. Results: The high-calcium diet significantly prevented the increase in intestinal permeability and diarrhea with time in HLA-B27 rats developing colitis as compared to the low-calcium group. The histological colitis score and mucosal interleukin-1β levels were lower in high-calcium fed rats. Supplemental calcium prevented the colitis-induced increase in the expression of extracellular matrix remodeling genes (e.g. matrix metalloproteinases, procollagens and fibronectin), which was confirmed by Q-PCR. Conclusions: Dietary calcium inhibits colitis development in HLA-B27 transgenic rats. Calcium prevents the colitis-related increase in intestinal permeability, diminishes diarrhea, and lowers the inflammatory response in the mucosa, resulting in less extracellular matrix breakdown. Keywords: nutritional intervention
2009-07-17 | GSE11022 | GEO
Project description:Little is known regarding the relationship between Selenium (Se) concentrations in the liver and liver gene expression. Because most cow-calf operations in Se-poor soils provide enough Se in mineral mixes to avoid deficiency, the aim of this study was to determine the effects of 4 Se form supplementation strategies (none or inorganic, organic, or 1:1 inorganic:organic mix) on liver gene expression profiles using a Se-adequate model. Microarray analysis was conducted using the custom WT Btau 4.0 Array (version 1; GeneChip, Affymetrix, Inc., Santa Clara, CA, USA) to determine if dietary Se supplementation form differentially affects the hepatic gene expression profiles of maturing beef heifers. Sodium selenite was used as the source of inorganic Se and Se-enriched yeast was the source of organic selenium. Thirty-six Angus heifers (BW 400 ± 9.0 kg) were ranked on the Se concentration of their biopsied (day -14) liver sample and randomly assigned to one of four dietary Se treatments: Control (Ctrl) group received no exogenous dietary Se supplementation; inorganic (ISe) treatment group received daily dietary Se supplementation at 3 mg/ animal of the ISe form; organic (OSe) treatment group received daily dietary Se supplementation of 3 mg/ animal of OSe form; and the mix (1:1 ISe:OSe) received daily dietary Se supplementation of 3 mg/ animal of 50:50 mix of ISe and OSe forms. RNA was extracted from biopsied liver samples taken 168 days after initiation of Se supplementation and microarray analyses were conducted.
2013-06-01 | E-GEOD-44680 | biostudies-arrayexpress
Project description:Selenium (Se) is an essential nutrient for beef cattle health and commercial production. The molecular mechanisms responsible for physiological responses of the animal to dietary Se supplementation, however, have not been evaluated. Furthermore, the potential effect of two chemical forms (organic vs. inorganic) of Se on gene expression by Se-sufficient cattle has not been evaluated. Microarray analysis using the GeneChip Bovine Genome Array (Affymetrix, Inc., Santa Clara, CA) was conducted to determine if dietary Se supplementation in organic vs. inorganic form (OSe vs. ISe) differentially affects the liver gene expression profile in growing beef heifers. Sodium selenite (Prince Se Concentrate; Prince Agri Products, Inc., Quincy, IL) was used as the source of ISe form. Se-enriched yeast (Sel-Plex; Alltech, Inc., Nicholasville, KY) was used as the source of OSe form. Thirty Angus heifers (BW 393 ± 9 kg) were randomly assigned to 3 dietary treatments (n = 10): Control (Ctrl) group received no dietary Se supplementation; ISe treatment group daily received dietary supplementation of Se at 3 mg/animal from ISe source; OSe treatment group daily received dietary supplementation of Se at 3 mg/animal from OSe source. Six animals were randomly selected from each of 3 treatment groups for RNA extraction and microarray analysis.
2010-04-28 | E-GEOD-19696 | biostudies-arrayexpress